8. Evolution and Psychopathology/ Mental health Core Flashcards

1
Q

what is evolutionary psychopathology?

A

• Field of study which applies basic evolutionary principles to the investigation of mental health disorders (Nesse & Williams, 1995; Stevens & Price, 1996)

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2
Q

what is EP concerned with explaining?

A

• Concerned with explaining the adaptive origins of these disorders

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3
Q

why does it seem to make sense that something evolutionary is going on with disorders?

A

• Vast majority of mental health disorders have at least some genetic component- seems to make sense something evolutionary going on

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4
Q

what does EP allow?

A

• Allows us to move beyond proximate causation to the ultimate causation.

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5
Q

what are the implications of EP?

A

• Give context of psychopathology within the ‘bigger picture’
• Move from a dichotomous medical model of psychopathology to a more fluid continuum model. Medical model is a very black and white view or presence or absence. If you use distribution you can have non-clinical to clinical on a continuum and seeing those who lie in between these points rather than just present or absence.
• May help inform current treatments and aid in the development of new interventions.
o Determine the appropriateness of a response and therefore tailor medical interventions to that response.
o At present the long term consequences of supressing potentially adaptive responses is unclear (Nesse & Berridge, 1997). Adaptive responses are meant to be there to help us. this is quite a worrying question more caution when approaching pathologies
o Preliminary analyses seem to suggest that some medications impact other adaptive processes over time (Andrews et al., 2012)

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6
Q

heritability of mental illnesses stats

A

o Depression: 40-66% (de Geus & Middeldorp, 2013)
o Schizophrenia: ~70% (Sullivan et al., 2003; Lichtenstein et al., 2009)
o Bipolar: 70-80% (Edvardsen et al., 2008)
o Anxiety disorders: 32-43% (Hettema et al., 2001)

these are too high to suggest anything else

• Can not be explained by genetic mutation
o Exceeds 1% threshold model (Hyxley et al., 1964)

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7
Q

what happens to bad polymorphisms?

A

• Purely deleterious genetic polymorphisms are candidates for removal through natural selection (Homberg & Lesch, 2011).

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8
Q

what two hypotheses are there for continued presence of mental health disorders?

A

1) the mismatch hypothesis

2) Adaptive persistence

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9
Q

what does the mismatch hypothesis poster?

A
  • Mental health disorders were once adaptive- as humans if we look back at our supposed evolutionary environment it would have looked very different to now .
  • However, our environment is now radically different to our ancestral one
  • Our psychological adaptions for the previous environment have not caught up with the current on
  • Therefore, they are no longer appropriate, malfunction and ultimately cause distress (Auld et al., 2010; DeWitt et al., 1998; Frankenhuis & Del Giudice, 2012)
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10
Q

example for the mismatch hypothesis

A

Example- prenatal stress response and ADHD/ Anxiety (Glover, 2011)
• Heightened prenatal stress levels results in foetal exposure to cortisol
• In the EEA, heightened foetal cortisol levels may have been an indicator that the immediate environment was dangerous (i.e. high predator load)
• Therefore, child develops traits which promote vigilance (anxiety) and rapid percpetual awareness (ADHD).
• Fitness increased as child is more aware of dangers in the environment, and acts more readily due to lower fight/ flight response.
SO…
• Heightened prenatal stress levels does not necessarily indicate a dangerous environment today
• Thus, these adaptions for surviving in a dangerous environment are inappropriate and are mismatched with our modern environment.
• This results in behaviour problems in the child:
o Lower flight/ fight threshold  Anxiety
o Rapid perceptual awareness  inability to focus (ADHD)

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11
Q

what may serve as further evidence to the missmatch hypothesis

A

The concept of mismatch between former adaptation and current environment can be readily observed also in physical behaviour. E.G. Preference for glucose rich foods is now doing us harm is resulting in rise in obesity.

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12
Q

what are issues with the missmatch hypothesis?

A

• Makes all-or-nothing assumptions
o E.g. any level of expression of a given trait is detrimental.
• Doesn’t explain why some and not all individuals succumb to disorder if, historically speaking, a given trait increases fitness- would expect to see higher rates nowadays. But on the face of it reported rates of psychopathologies are increasing, which is something we need to explain also.

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13
Q

what does the adaptive persistence hypothesis poster?

A
  • Underlying genetic material associated with psychopathology is at some level beneficial
  • Therefore, psychopathologies persist in the gene pool as the associated genetic material is not intrinsically pathological.
  • Potential adaptive mechanisms do not malfunction in the present environment, and are in fact still helpful, despite distress caused (evolution doesn’t really care how you feel- e.g. having a fever but serves a biological function to raise body temp to fight infection and is doing more good than harm. Thus the same thing can be served to psychological mechanisms, just because it doesn’t feel good doesn’t necessarily mean that it is completely bad for you).
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14
Q

example for adaptive persistence

but what does this leave out

A

risky and anti-social adolescent behaviour (ellis et al., 2012)
• Adolescence marks an important transitional period in human development
• This transitional period promotes risky behaviour due uncertain social (and sometimes physical) environment.
• Anti-social behaviour (e.g. bullying) promoted in order to assert social dominance.
• While socially undesirable, these behaviours are still somewhat adaptively relevant:
o E.g. social dominance associated with control of physical, sexual and social resources. Observed in social animal species (Chimpanzees- Goodall, 1986; wolves- Mech 1970)
• Thus, anti-social and risky behaviour are not selected out as they still convey some advantage in spite of cultural objections.

this however leaves out extreme manifestations in this model

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15
Q

how have extreme manifestations been explained in terms of the adaptive persistence model?

A

With Cliff-edged fitness- Nesse, 2004

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16
Q

what does cliff edged fitness purport?

A

• Purports that expression of a given adaptive trait increases fitness exponentially.
o I.e. the more you have of x trait, the greater levels of fitness you have
• But
• After a critical point, expression of X is associated with decrease in fitness
• Distribution of trait in population from non-clinical to clinical, expression increases then at a certain point there is a fitness plateau, then there is a rapid drop as the trait x increases past this fitness plateau point.

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17
Q

give an example of cliff-edged fitness in humans (non mental health)

A
  • Ulric acid has been shown to protect against oxidative tissue damage in humans (Ames et al., 1981; Becker, 1993)
  • Reduced oxidative stress has been associated with likelihood of developing cancer (Droge, 2002; Valko et al., 2007) and cardiovascular diseases (Cai & Harrison, 2000; Stocker & Keaney, 2004).  thus good it increases our fitness.
  • But.. elevated uric acid levels have been linked with the development of gout (Choi et al., 2003)- painful and inhibits movement.
  • Therefore, the ability to produce uric acid has profound fitness benefits, up to a point, after which it becomes detrimental to produce efficiently.
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18
Q

why is schizophrenia so controversial?

A

• One of the most controversial disorders to have evolutionary theory applied to
• Multitude of cognitive deficits
o Attentional (e.g. Braff, 1993)
o Working memory (e.g. Lee & Park, 2005)
o Language Processing (e.g. Banger et al., 2003)
o Motor Deficits (e.g. Manschreck et al., 1982)
• Associated with auditory verbal hallucinations, inappropriate affect and delusions (Andreasen, 1995)
• So trying to apply an evolutionary theory can be controversial because how can this be argued to be good.

19
Q

what are arguments for the existence of schizophrenia?

A

1) Schizophrenia as an evolutionary cost
2) the shaman hypothesis
3) Schizotypy and creativity

20
Q

talk about schizophrenia as an evolutionary cost

A
  • The brain is highly lateralised with respect to functional organisation. E.g. left hemisphere is dominant for language, right hemisphere for spatial cognition.
  • This degree of organisation is what allowed language to evolve
  • However, the organisation is so complex, that when something goes wrong, the consequences are severe and this is what we see in the case of schizophrenia.
  • Schizophrenia associated with anomalies in normal functional lateralisation (e.g. sommer et al., 2001)—e.g. sig proportion of schizophrenic patients have reversed lateralisation and majority are true left handers.
  • The benefits of language outweigh the costs of schizophrenia, and so schizophrenia persists. To be without language would be horrific it is too valuable to humans and thus evolution doesn’t care.
21
Q

talk about the shaman hypothesis

A

Polimeni & Reiss, 2002
• Broadly refers to the idea that the persistence of schizophrenia may be linked to certain sociocultural benefis
• In many hunter-gatherer societies, spiritualism and religion have been key forces in uniting many individuals to form communities.
• Cultural data suggests that many hunter-gathered societies have variations on ‘shamans’
• Behavioural similarities between ‘shamans’ and schizophrenics has led to speculations that schizophrenia has been propagated by high social standing for these individuals.
• Some evidence that suggests that schizophrenics have visual halucinations but mostly voice.
• Idea that these shamans would have more food +better access to mates as higher in society.

22
Q

talk about schizotypy and creativity

A

• Functional account of how schizophrenia arises
• Adopts the continuum view, such that schizophrenia is an extreme manifestation of an otherwise adaptive trait.
• Schiztypy is a collection of personality traits which are functionally similar to, but phenomenologically distinct from schizophrenia.
• Question becomes what is the adaptive significant of schizotypy?
Nettle & Clegg, 2006
• Looked for associations between levels of shizotypy, self-reported creativity and reported mating success
• Recruited 425 participants (156 male, 269 female, mean age = 40.5 years)
o Came mostly from general population
o Also recruited from ‘creative sources’ e.g. art magazines
• Administered the O-LIFE schizotypy inventory (Mason et al., 1995)
• Also asked participants to self-report levels of creative activity
• Took record of various demographic details (job history ect.) including relationship success.
• Classed individuals based on their creativity levels e.g. ‘serious’ or ‘professional’ producers had significantly larger numbers of sexual partners than non-producers and ‘hobby’ producers (controlling for sex and age).
• No interaction found between sex and creative activity- pattern is the same for both males and females
• Path analysis also found that creative activity significantly mediated the link between unusual experiences and number of partners. So basically, the number of unusual experiences you had had a direct response on the number of partners greater experiences greater creativity  greater partners.
• Results suggest that schizotypy is associated with increased levels of creativity and in turn, mating success (as measured by number of partners).
• Preliminary support for the idea that schizotypy facilitates a peacock-like mating strategy (creative display)
• As such, schizophrenia may be the most extreme manifestation of these traits.
• Has since been replicated and extended by (Beaussart et al., 2012- read
o Found associations between everyday creative activity and mating success.
o They found the Association to be true for men only, but linked with short term mating strategies.

23
Q

what is the potential difficulties with schizotypy data

A

o We don’t know the quality of the mates- we don’t know whether it is just sex for the sake or whether they are having better sexual partners
o If people are professionals they could be more likely to have greater resources.
• but generally, is very interesting research and study.

24
Q

what is general consensus on the evolutionary origins of anxiety disorders?

A
  • Appears to be some consensus on the evolutionary origins of anxiety
  • Largely thought to be associated with improving an individual’s vigilance in the face of potential threats
  • Heightened vigilance leads to heightened preparedness of the fight/ flight response when required.
  • Should vary as a function of threat probability in a given environment.
25
Q

what principle has been put forward to explain evolutionary theory of anxiety disorders? and what does this poster?

A

The smoke detector Principle- Nesse 2001

• Suggests that it is more cost effective (in terms of fitness) to overestimate threats than to underestimate
o Better to expend energy running away from a rustle of the bushes than it is to assume that there is nothing there and then get eaten.
• Therefore, it is better to detect ‘threats’ which are not really there.
o Those who ran away more readily were around to pass on their genes.
• Over time, this trait is compounded until fight/ flight thresholds are reduced to such a point, that everything may be perceived as a threat in some generations and this is where we see anxiety disorders emerge.

26
Q

what predictions can be made based upon the smoke detector hypothesis?

A

• 1) Individuals who are highly anxious are better at detecting threats
o BUT, they may overestimate threats more generally, and rate something as threatening when it is not.
o Example of an interpretation bias.
• 2) We should also see levels of anxiety vary as a function of threat probability

27
Q

evidence for prediction 1 of smoke detector hypothesis

A

• 1) Individuals who are highly anxious are better at detecting threats

• Individuals who load more highly on trait anxiety measures are better able to detect angry faces compared to happy faces, using fewer eye movements (Richards et al., 2011)
o Also better at detecting multiple targets vs single targets!
• Similarly those higher in trait anxiety are also better at detecting fearful faces (Doty et al., 2013)
• Interpretation bias- Children loading highly on trait anxiety scales also interpret stories as more threatening than low trait anxiety children (Muris et al., 2000).- e.g. triangle chasing the square (because it is angry in high anxious children)

28
Q

evidence for prediction 2 of smoke detector hypothesis

A

2) should also see levels of anxiety vary as a function of threat probability

Epidemiological data supports link between threat probability and levels of anxiety
• Low birth weight predicts higher trait anxiety (Lahti et al., 2010)
• Low SES associated with heightened anxiety (Najman et al., 2010)- fewer resources available if threat does occur.
• Individuals with injuries or disabilities have higher levels of anxiety, which is independent of the association between depression and physical conditions (Cano et al., 2010)- cant deal with threats.
• More anxiety among women than men (Breslau et al., 1995)- vulnerability issue men are more likely to be violent and aggressors
• Different levels of threat evoke different levels of anxiety dependant on background and situation.

29
Q

what are evolutionary theories of depression?

A
  • Disengagement theory
  • PATHOS-D hypothesis Raison & Miller, 2013
  • Analytical Rumination Hypothesis Andrews and Thompson, 2009- ARH revised- a balanced view
30
Q

what is disengagement theory?

A

• Purports that depression is an evolved mechanism at the population level as a means of population regulation
o An adaptation which may be maladaptive for the individual is ultimately adaptive for the population
• Depression is a state brought about during the pursuit of a given goal. When this goal is not achieved on a number of occasions, depression manifests as a means to discourage pursuit of what now appears to be an unattainable goal.
• Finally, individuals who experience multiple depressive episodes are unable to attain their goals consistently, and are subsequently removed from the population via social withdrawal, eventually leading to death.

31
Q

what is support for disengagement theory?

A

• There is support or the idea that depressed individuals experience greater levels of mortality (Cuijpers & Smit, 2002)

32
Q

issues with the disengagement theory?

A

• But concept of group selection is still heavily debated within the literature
• Does not deal particularly well with how the trait is transmitted.
o I.e. if all those carrying the gene die more quickly than any other member of the population, how does the gene propagate? If it is promoting with withdrawal from society and die more quickly then where is a person going to get the opportunity to mate and pass on these genes.

33
Q

who developed the PATHOS-D hypothesis and what does it stand for?

A

Raison & Miller, 2013

refers to pathogen host defence

34
Q

what does PATHOS-D posit?

A
  • Suggests that depression evolved as a mechanism for combating bacterial infection.
  • Halts the spread of disease at the behavioural level through social withdrawal (Anders, Tanak & Kinney, 2013)

• Suggests that alleles associated with immunological response and those associated with depressive responses are in fact one in the same.

35
Q

support for PATHOS-D hypothesis

A
  • Evidence of an increase in reported depression following sickness (Dantzer, 2009; Wichers et al., 2006)
  • Also evidence of persistent inflammatory response in depressed individuals (Dowlati et al., 2010
36
Q

what is good about the PATHOS-D hypothesis?

A

• Only hypothesis to try and account for the novel observation of enhanced inflammatory response in depressed individuals

37
Q

issues with PATHOS-D hypothesis

A
  • Cannot account for depressive episodes triggered by non-immunological events
  • Not necessarily incompatible with another account, if we accept that depression alleles and immunological alleles are one and the same.
  • Really nice way for accounting for immunological findings can be integrated with another theory.
38
Q

who developed the Analytical Rumination Hypothesis? and what does it posit?

A

Andrews & Thomson, 2009
• Depression is a mechanism for when we encounter problems which leads to rumination which then results in a solution.
• Purports than depression is an evolved mechanism for the promotion of rumination
• Occurs in the face of complex problems (predominantly social), but can occur whenever some environmental change arises
• Depression is an ‘involuntary brake’ and so symptoms reflect a cessation in engagement of survival activities
• Rumination is then promoted as a means of dedicating cognitive resources to the problem encountered.

39
Q

what predictions can be made based on the Analytical Rumination Hypothesis

A

1) Rumination varies as a function of low mood and depression
2) Rumination should also vary as a function of task difficulty
3) those who engage more frequently in rumination will be better problem solvers

40
Q

evidence to support Analytical rumination hypothesis

A

some evidence to support prediction 3- that those who engage more frequently in rumination will be better problem solvers.

o Financial trends analysis and mood (Au et al., 2003)- individuals who experienced low mood were better at financial trends analysis and made better decisions.
o Ability in a modified Prisoner’s dilemma (Hokanson et al., 1980)- those with low mood/ some depressed patients did better.

41
Q

what was issue with indirect evidence supporting prediction 3 (those who engage more frequently in rumination will be better problem solvers.) of rumination hypothesis & what has been done

A

• Problem is that they did not measure rumination directly but depression assuming that rumination is a property of depression…
So….to solve this…

Birch, Dharam & Boothroyd unpublished dissertation data- Preliminary study suggests there is some direct link between problem solving and rumination.

• Looked for a direct association between rumination and problem solving across a range of tasks.
o Modified prisoner’s dilemma paradigm (social problem)- saw computer (participant) response before you make ow decision so can reward/ punish/ be equal.
o Modified Iowa Gambling task (risk problem)- different decks have different values (2 bad decks two good decks) modified so that had to make a decision about each deck for each trial.
o Raven’s advanced Progressive Matrices (abstract problem)
• Multiple measures of rumination
o Ruminative response scale
o Distressing thoughts questionnaire- rumination subscale.

Findings
• Significant associations between levels of rumination and problem solving ability in two out of three tasks (prisoners and gambling).
• No association between rumination and abstract problem solving
o See arguments of evolutionary appropriateness and task design- does it actually tap into something that is evolutionary relevant?
• Problem solving ability in the tasks could be differentiated by the type of rumination
o Reflective- more adaptive very concrete thought selection and problem – associated with giving self more money in prisoners and avoid large punishment in Iwoah.
o Brooding- what if thinking more destructive e.g. what if this hadn’t happened to me. People avoid more subtle punishments- better in Iwoah finding subtle decks that slowly chip away at money.
o Anxious – external focus more association with punishing others in the prisoners task more focus on external sources.

42
Q

What ultimately needs to be considered when revisiting the Analytical Rumination Hypothesis

A

The ARH- revisited
• Rumination may indeed promote problem solving ability, but it is critical to consider the type of rumination involved, and the relative frequency of this rumination.
• Not all ‘maladaptive’ ruminations may be maladaptive.
• So long as reflective rumination is the dominant process, maladaptive ruminations (i.e. brooding, anxious) may in fact have some benefits
• Negative impact of ‘maladaptive’ ruminations attenuated by reflextion
• Low mood serves to promote reflective rumination predominantly, but when transitioning to depression, there is a breakdown in the ability to attenuate maladaptive ruminations.

43
Q

what needs to be done in future for Evolutionary Explainations to psychopathologies?

A

Seeing more and more research which is taking account of evolutionary models. Even if some of the theories don’t hold true there is such implications and power it is important