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MAPD 1 > L5: Biological Models > Flashcards

L5: Biological Models Flashcards

1
Q

MAPD: nature vs nurture?

A

false opposition - behaviour is always nature AND nurture
more useful: ultimate vs proximal causes

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2
Q

what are the 3 key concepts in evolution?

A
  • theres variation in traits within a group
  • natural selection (adaptive differences): certain variants should increase your chances to reproduce
  • the traits are heritable
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3
Q

do psych mechanisms work n the same evolutionary way as other traits?

A

to some extent: (negative) emotions, but not DSM diagnoses

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4
Q

is there one “optimal” adaptation?

A

No, it is all depends on the context, and changes in context and individual
differences: ‘smoke detector principle’

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5
Q

what is the smoke detector principle?

A

we vary in how likely we are to detect threats in our environment.
It all depends on:
* How probable the event is (in nl you are probably not very likely to be likely to detect a snake cus its not very probable)
* False negative; e.g. the cost of missing a dangerous situation (what would happen if you missed a potential snake in the environment? if very dangerous consequences then more likely to detect)
* False positive; e.g. the cost of wrongly identifying something as dangerous (thinking that theres a threat when theres nothing can also have a cost, like u wouldnt scream in the middle of a lecture cus u think theres a snake)
so u weigh the them
and …true negatives, true positives.
* Changes in the environment (how likely is an event today to predict an event tomorrow)

Negative emotions like fear and anxiety follow the “smoke detector principle,” prioritizing avoidance of false negatives even at the cost of more false positives.

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6
Q

why is the adaptation-interpretation of psych constructs (including MAPD) criticized?

A

cause quantitative research is needed!
for example: are MAPD heritable

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7
Q

what does DNA consist of?

A

Only <2% of DNA are genes! - rest “junk” DNA?
-> No, rest of DNA can influence gene expression..

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8
Q

what is epigenetics?

A

environment influences gene expression

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9
Q

what are the research methods of behavioural genetics?

A
  • Family studies
  • Adoption research
  • Twin research: Monozygotic (MZ); 100% genetical identical
    or Dizygotic (DZ); on average 50% genetical identical
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10
Q

how does twin research go?

A
  • calculate correlation r between mental disorder scores of dizygotic twins and monozygotic twins (rMZ and rDZ)
  • estimate Additive influence genes (A: 2(rMZ - rDZ)) vs Common environment (C: rMZ - A) vs unique Experience (or Error) (E: 1-rMZ) aka genetic influence vs common environment influence vs individual differences influence
    -> compare how similar dizygotic twins vs monozygotic twins are: if the r between MZ twins is stronger than the r between DZ twins, than that must be due to genetics
    aka Heritability = statistical estimate
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11
Q

twin research - are depressive episodes heritable? what about anxiety?

A

DE: party heritable (40%), partly unique experience (55%) (rest is common environment)
Anxiety: partly heritable (44%), partly unique experience (45%) (rest is common environment)

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12
Q

what has been shown about MAPD heritability?

A

partially heritable… but environment also heritable? (6-39%)

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13
Q

what environmental factors are also heritable and to what extent?

A

6-39% heritable
- marital quality (monozygotic twins have more similar marriage quality than dizygotic)
- social support
- parental discipline and warmth (that u give ur own kids)
- family environment
- peer relationships

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14
Q

how come some environmental factors are heritable?

A

genes & environment interact and correlate
correlations: genes->environment
- passive
- reactive
- active
interactions: environment->genes
- through epigenetics (but replication problem here)

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15
Q

what is the relation between allele frequency & effect size in MAPDs?

A

negative correlation: so the rarer an allele the bigger the effect on psychiatric disorders, while very common alleles have only a small effect

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16
Q

what is meant with polygenetic effects?

A

that MAPDs ar partially heritable but that they usually arent related to a few genes, but to multiple genes (and gene-environment correlations & interactions)
unclear how the genetic mechanism works exactly

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17
Q

what are the 3 major neurotransmitter systems?

A
  1. Amino Acids (glutamate, GABA)
  2. Mono-amines (serotonin, dopamine, norepienphrine) MOST IMPORTANT
  3. Peptides (opioids)
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18
Q

where do the 3 major mono-amines originate in the brain?

A

dopamine - Ventral Tegmental Area
norepinephrine - Locus Coeruleus
serotonin - raphe nucleus
-> all originate in the prefrontal cortex and spread from there

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19
Q

what are the main function sof the 3 major mono-amines?

A

dopamine: pleasure drive, motivation, appetite, sex, aggression, cognitive function, mood, emotion
norepinephrine: ergotrophic vigilance, anxiety, irritability, motivation, cognitive function, mood, emotion
serotonin: trophotropic impulse, appetite, sex, aggression, cognttive function, mood, emotion, anxiety, irritability

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20
Q

what has been the development of psychopharmacology for antidepressants?

A

1950s: monoamine oxidase inhibitors (MAOIS), tricyclic antidepressants (TCAs)
1980s: selective serotonin reputake inhibitors (SSRIs), bupropion
1990s: serotonin norepinephrine reuptake inhibitors (SNRIs), mirtazapine

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21
Q

what is the function of antidepressants? and what is common misconception resulting from it?

A

affect levels/activity of serotonin, norephineprine, and dopamine
thus: depression is disorder of the neurotransmitter systems (“chemical disbalance” or “monoamine theory of depression”, ppl tend to think that depression = chemical imbalance/lack of serotonin etc, but this isnt not clear at all!)

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22
Q

how do antidepressants work?

A

some theories
SSRI -> block serotonin reuptake -> more NT
SSRI -> less (senstivie) autoreceptors -> more NT
Neuroplasiticity: SSRIs -> more Brain Deried Neurotrophic Factor -> Hippocampus growth -> better stress regulation

23
Q

do we know how antidepressants work?

A

increase serotonin levels but we dont know if this is the mechanism by which depression symptoms alleviate
so we dont really know… but they are used a lot

24
Q

how are antidepressants effects studied?

A

randomized controlled trials: measure depressive symptoms pre and post treatment (eg SSRI) compare w placebo
outcome measure: the higher the pre-post score on depression rating scale, the better (more symmptom reduction this can be standardized: cohens d)

25
Q

how effective are antidepressants?

A

Effect size for depression and anxiety disorders, compare to placebo D = 0.3
But the total effect (not compared to placebo) is much larger D = 0.8-1.4
-> this might explain why doctors & researchers think differently about antidepressants

26
Q

what is the difference between the pre-post effectiveness between antidepressants & placebos?

A

effectiveness for placebo
+ effect of clinical management
+ expectations (placebo effect)
+ natural course
+ regression towards the mean
effectiveness for antidepressant, all of the above
+ specific pharmacological effect

27
Q

is placebo effect real?

A

yes!
not a biological active substance, but it does have a biological effect! it changes stuff in ur brain without having any active substance

28
Q

should placebos be presribed? how do they compare to other treatments?

A
  • might not be ethical (but open labelled placebo might also work!)
  • not as effective as psychotherapy
29
Q

why has it taken so long to realize the limitations of antidepressants?

A
  • study publication bias: which studies were not published at all?
  • outcome reporting bias: which (negative) studies were published but with suddenly positive results?
  • spin: which (negative) trials were published w negative results, but somehow still concluded that the drug is effective?
  • citation bias
30
Q

so overall conclusion, do antidepressants work?

A

mainstream conclusion: yes, a bit better compared to placebo, comparable to psychotherapy! and combined it works better
but the use of and knowledge about antidepressants is not balanced
critical conclusion: still not sure/no, theres no clear evidence in favor of ADs
Treatment response depends on likelihood of receiving a real drug
* Placebo-run in phases: selection of patients in clinical trials who don’t respond to placebo.
* Active placebo effect; larger AD-placebo difference when perceived being on active treatment.
* Effects of AD are only shown on short term.
* Side-effects can be severe

31
Q

how has the faith in antidepressants changed in the last 20 years?

A

Early antidepressant trials, from 20 years ago, showed substantial drug-placebo differences (70% vs. 30%). Since then, however, several important changes have occurred, challenging the assumptions about the effectiveness of antidepressants. Specifically, it became evident that the drug-placebo difference was much smaller (40% vs. 30%).

32
Q

what did kahns data analysis of antidepressants vs placebo in major depression reveal?

A
  1. symptom reduction with placebo was larger in non-pharmaceutical depression trials compared to FDA (pharmaceutical trials), not suprising since antidepressants are commercial
  2. when its difficult for investigators and patients to guess treatment assignment (blind trials), the differences between treatments, controls, and placebo become quite small. EXPECTATION BIAS BIG FACTOR
33
Q

what can non-specific treatment effects aka placebo effects be explained by?

A

the apparent therapeutic effect is influenced by factors involved in any treatment, regardless of the actual drug efficacy
in other words, patients w depression are prone to non specific therapeutic effects: whatever treatment a patient receives (placebo or drug) there are still common components (thorough evaluation, explanation for distress, a healers commitment) that can have their effect

34
Q

what is placebo risk exposure?

A

the more placebo group included, the higher this risk (3 groups of which one is placebo: 33% placebo exposure risk)
the higher the PRE, the lower the therapeutic effect of the drug/placebo.
in other words: if the patient & clinician know theres a high chance of getting a placebo, the less they will actually improve (even tho drug is just as effective)

35
Q

what are the important changes that contributed to the narrowing of the drug-placebo efficacy difference?

A
  • DSM III: by conceptualizing a braod syndrom ecalled major depressive disorder, mildly to moderately ill patients were now also included into antidepressant trials (more likely to experience a smaller antidepressant-placebo difference)
  • Drug development regulators (eg FDA)
36
Q

what drug development regulator changes have occured that narrowed the drug-placebo efficacy difference?

A
  1. syndromal improvement: FDA requires a syndromal improvement (symptom reduction) rather than a global feeling of well being. so the depression rating scales used have much broader ranges of scores which leads to smaller antidepressant-placebo differences
  2. data analysis: the last observation carried forward (LOCF) if patient quits trial is used, as well as the mixed-effect model repeated measure analysis -> generally techniques that minimize antidepressant placebo differences
  3. number of arms aka groups: requires multiple groups & control groups not required -> nr of arms required makes antidepressants results look worse than they are & results in confusion
  4. EMA differences: uses alternate models than the FDA to evaluate new antidepressants -> the different methods are source of confusion, making interpretations hard & reulting in need for caution when doing this
37
Q

what is the scientific defintion of mood?

A

enduring affective states influenced by past experiences, affecting responses to subsequent events
- mood appears to be widespread across species suggesting an adaptive function
- a subset of emotions
- discussed in terms of its analysis as a signal detector

38
Q

how can you categorize moods in two-dimensional space?

A

sensitivity to punishment/threat on one axis, sensitivity to reward on the other

39
Q

what is the adaptive function of mood?

A

aid decision making based on environmental conditions and your’ physical state

40
Q

what are emotions?

A

encompass cognitive, motivational, and physiological changes triggered by appraisal of specific environmental situations

41
Q

what is the function of emotions?

A
  • they are adaptive, allocating cognitvie & behavioural resources to address immediate fitness-relevant priorities
  • can be viewed as detectors, identifying situations and prompting suitable responses, with an optimal detection threshold determined by the probability of the event and the costs of different outcomes.
  • Core emotions like fear have highly conserved neural and hormonal mechanisms across species.
  • Negative emotions like fear and anxiety follow the “smoke detector principle,” prioritizing avoidance of false negatives even at the cost of more false positives.
42
Q

how do moods differ from acute emotinoal states?

A

moods have longer duration & detachment form immediate triggers, reflecting an integrative function of past emotional experiences

43
Q

what does the horizontal axis represent in the mood two dimensional space?

A

the threshold for responding to reward cues, with optimism and approach behavior associated with lower thresholds and depressed mood associated with higher thresholds.

44
Q

what does the vertical axis represent in the mood two dimensional space?

A

the threshold for responding to punishment cues, with anxious mood characterized by a low threshold and a focus on potential dangers.

45
Q

how do these mood axes provide an orthogonal classification system?

A

the overall subjective valence of mood captured by the line y = x, where unpleasant moods are toward the bottom left and pleasant moods are toward the top right.

46
Q

what is our mood architecture like?

A

we integrate each experience, adjusting our treshhold for detecting rewards & punishments (aka we adjust our mood)

47
Q

what is the alternative to our mood architecture?

A

to not adjust our treshholds with each experinece: so a system where there would be fixed tresholds for reward detection & for punishment detection, and the individual returns to these at the end of each bout of experience regardless of what happened
aka a fixed emotion architeture

48
Q

why would it be adaptive to adjust treshholds in the way we do (mood) instead of this fixed emotion architecture?

A

the optimal treshold for a detector depends on:
1. probability of event to the next: experiences from one period can inform expectations for the next, making mood adjustments advantageous.
2. physical condition: like bein gwell nourished, also affects the optimal treshholds for emotion detection
3. the interaction between environmental state x physical condition further justifies the need for mood systems to dynamically adjust detection treshholds
ALL OF THESE FACTORS CONSTANTLY UPDATE/CHANGE SO ITS USEFUL TO ADJUST MOOD AS WELL

49
Q

does the adaptive framework of mood fit real life?

A
  • adaptive framework predicts mood responses based on recent experiences: non-reward increases depressed mood, while punishment increases anxious mood.
  • Human evidence supports these predictions, life events like loss trigger depression and danger triggers anxiety while Positive life events like marriage have an antidepressant effect
  • Changes in physical condition affecting the outcomes of detection also alter thresholds and mood. Physical infirmity or limitation is associated with both anxious and depressed mood.
  • Circumstances like poverty and social isolation in humans have depressogenic and anxiogenic effects for similar reasons.
  • animal findings also support this
  • generally increasing negative events or impairing physical conditions result in mood changes
  • Comorbidity of depression and anxiety may be explained by shared predictors related to deteriorations in physical condition, making both threat detection and reward approach more costly
50
Q

how does cognitive bias relate to mood?

A
  • Mood changes alter the perception of ambiguous stimuli, impacting the interpretation of ‘threat’ and ‘reward’.
  • shown in anxious/depressed ppl more likely to intepret amibigious stimuli negatively (similar effects shown in animals)
51
Q

how do antidepressants impact the treshholds of mood?

A

normalize altered thresholds for detecting rewards and punishment, suggesting a central role of changed thresholds in mood across different species.

52
Q

what are the implications for mood disorders by the signal detection mood system?

A
  • mood, including depression & anxiety, is see as fulfilling their evolved function
  • but defining the boundary between normal & pathological mood responses is challenging (DSM does it arbitrarly)
  • evolutionary thinking suggests disorders occur when a biological system fails to produce effects that led to its evolutionary selection, causing harm
  • mood disorders can result from adverse life experiences or dysregulated neurobio mechanisms (which is what therapeutic interventions focus on)
  • changing environments to be less punishing & more rewarding could reduce the burden of mood disorders
53
Q

what are 2 ways to study the genetic basis of (ie) social anxiety?

A
  1. Single Nucleotide Polymorhpism (SNP): have two groups (social anxiety group & control group) and they are tested on a specific gene
  2. GWAS study: can identify the effects of thousands of genes and compare their relation to a trait

MAPD 1 (6 decks)

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