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Evolution and Mental Health > Midterm 1 > Flashcards

Midterm 1 Flashcards

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1
Q

What, fundamentally, did the Greeks believe about mental disorder?

A

That mental disorder was a product of thought–the separation between reason and emotion (irrationality).

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2
Q

What did St. Thomas Aquinas say about suicide?

A

That it violates the laws of life:

  • Nature: will to live
  • Man: community
  • God: only god can take away life
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3
Q

What did Theophrastus and Rufus of Ephesus say about melancholia?

A

That great minds are susceptible to melanchola; that melancholia is often associated with deep thought.

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4
Q

What big change did Henry Maudsley make to melancholia?

A

Mental disorder switched from a disorder of thought to mood/affect.

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5
Q

How did Freud discuss melancholia?

A

As a “keener eye for the truth”.

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6
Q

When was depression first acknowledged as a normal irrationality?

A

Either Freud or Beck.

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7
Q

Who devised the idea that depression is systematic irrationality?

A

Beck.

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8
Q

What influence did William Paley have on Darwin?

A

Formed the per saltum, all at once, argument for development. Led Darwin to think deeply about how functional complexity might form.

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9
Q

What was Darwin’s initial hypothesis surrounding the 15 species of finch on the Galapagos islands.

A

That there used to be one, and it diversified over time. Spent the next year trying to explain speciation and adaptation.

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10
Q

Briefly state Darwin’s three questions, and how they showcase his evolving thought.

A

1) Evolve from one species (speciation and adaptation)
2) Species can be linked through gradual changes in history.
3) How do species change with their environment (species won’t adapt to rapid environmental change)?

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11
Q

How do the terms ‘monstrosities’ and ‘picked’ outline an important development in Darwin’s logic? Wilkinson was involved in this.

A

Darwin began investigating the strategies of cattle breeders. These promote the idea that traits can be selected to promulgate on to the next generation.

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12
Q

How did the William Macleay essay inspire Darwin? What did he not agree with?

A

Made Darwin realize that per saltum explanations did not work–an eye can develop gradually.

However, Macleay claimed that each trait must improve reproduction. This is false. Traits can be maladaptive, yet be slowly selected against; or, traits can improve direct fitness in other ways (called indirect effects).

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13
Q

What does natural selection maximize?

A

Inclusive fitness measurable through Hamilton’s rule.

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14
Q

What is a precondition for indirect fitness?

A

Kin recognition.

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15
Q

How does worker bee drone preference vary based on queen mating habits? What was Hamilton’s prediction here?

A

Worker bees prefer drones most related to them. In the case of a monogamous queen, the drones will prefer kin produced by their sister–as it is more related to them than the queen’s kin.

Hamilton predicted that workers reproduce more when queen mates multiple times

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16
Q

What were two ideas that Darwin could not explain?

A

Blended inheritance and eusociality.

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17
Q

What is the relatedness of workers in a nest to each other?

A

r = 0.75

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18
Q

Apoptosis is what?

A

Neuronal suicide.

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19
Q

What did our mechanisms evolve for?

A

Our EEA.

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20
Q

What is our best explanation for aposematicism?

A

Fitness improvements can be indirect.

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21
Q

What does natural selection teach us about complexity?

A

That complexity is always reducible (in the case of the bacterial flagellum) and understandable through the gradual progression via a stepwise fashion.

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22
Q

What does entropy tell us about complexity?

A

Closed systems trend away from functional complexity. We need a system, natural selection, that moves against disorder.

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23
Q

Why is reverse engineering in evolutionary thought useful?

A

First, and quite importantly, we must identify non-random arrangement in nature. If we are able to determine the function of a process then we can determine malfunction. One of Wakefield’s disorder criterion was malfunction.

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24
Q

When might you attribute a trait to exaptation, constraint, and byproduct, respectively?

A

Exaptation: It fails to show evidence of non-random organization or coordination for the beneficial effect.
Constraint: Deviates from a more optimal design.
Byproduct: Fails to show non-random structure and lacks any beneficial effect.

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25
Define diagnosis:
Accurately differentiating between normal and abnormal mental states.
26
Define treatment:
Depends on having a good diagnostic and mechanistic understanding.
27
How can you best determine if natural selection has occurred?
By identifying non-random organization.
28
Who's theoretical beliefs was the current DSM based upon?
Emil Kraepelin.
29
What benefit did the initial DSM-I and DSM-II offer?
Disorders were dimensional: clinicians recognized a normal distribution of behavioural proclivity.
30
Who removed homosexuality as a disorder? What broader implications did this have?
Robert Spitzer. It led to an overhaul of the DSM in the 1980s.
31
What were the two main issue of the DSM-I and DSM-II?
1) Lack of reliability | 2) Too much psychoanalysis
32
What is the lifetime and annual prevalence for a DSM diagnosis?
50% and 30% respectively.
33
What was the clinical response to the DSM's high prevalence rates, and what was the outcome?
Added the clinical significance criterion. It hardly lowered prevalence--50% to 46%. Annual prevalence for college students is 50%.
34
Describe the role of ghostwriting in psychiatry.
Pharmaceutical companies will pay physicians to write under their name. They will in turn only publish positive results about their drug.
35
What is the nature of the pharmaceutical publication bias?
Positive/Negative Odds Ratio Published: 94/6 Negative: 51/49
36
When did the conception of disorder as a form of dysfunction first arise?
From Emil Kraepelin in 1907.
37
How did Wakefield and Spitzer differ in their conception of dysfunction?
Wakefield: A malfunction in an adapted mechanism that is socially not accepted. Spitzer: Distress and impairment.
38
How does Wakefield define a function?
An effect that explains the structure and operation of a trait/object.
39
What are the two major implication of Wakefield's definition.
1) A properly functioning mechanism cannot be disordered. | 2) We cannot determine how a 'disorder' best be treated.
40
What does Dr. Andrews describe as the course principle, and how does etiology relate to it?
The course principle is that mechanisms have involved to accomplish a purpose. When we suppress the mechanisms, we suppress the purpose (i.e. fever). **He claims that we can only decide when to intervene if we know the associated etiology. "Etiology is crucial to treatment."**
41
The heritability coefficient is what?
The proportion of variability that is attributable to genetics.
42
Describe how a Mendelian disorder and mental disorder differ.
Mendelian disorders: Rare and can be explained by random mutation. Mental disorders: Common, harmful, and heritable.
43
What term explains the high prevalence of sickle cell anemia as a Mendelian disorder?
Heterozygote advantage.
44
What does the CDRV hypothesis say about allele contribution?
Most of the mutations that contribute to the variability of a trait are rare and differ across individuals (does not occur in the same location across individuals).
45
Provide an example of and explain antagonistic pleiotropy.
Ex. Schizophrenia is often associated with the up-regulation of immune functioning. Antagonistic pleiotropy says that the same allele both increases the risk of disorder and improves fitness with another trait.
46
What does a GWAS study do? Why is it flawed?
It correlates gene variants across individuals with and without a disorder. Unfortunately, you will get a statistical effect by chance rather consistently as it relies on frequentest statistics. To prevent this, you must 1) use a Bonferroni correction, which results in a p-value too low to detect anything. 2) run a GWAS study with too high of a p-value. Take those alleles and run a separate study on them alone (narrowed down). See if those alleles replicate results.
47
How effective are GWAS studies?
Not effective. If you take the thousands of alleles slightly implicated in schizophrenia, researchers are only able to account for 23% of the genetic variance; however, 80% of the variance could be explained in intelligence.
48
How does chromosome length relate to genetic variability?
Larger chromosomes have more SNPs. With more SNPs, more genetic variability can be explained.
49
Which chromosome is depression associated with in the Han Chinese?
Chromosome 10.
50
Summarize the idea behind the watershed model. What are the implications of this?
Many inconsequential alleles combine to form traits which then create behaviours. These behaviours have fitness outcomes which are heavily polygenic due to their widely sourced origin.
51
Why are polygenic traits genetically persistent? Provide multiple reasons.
1) Mutations can affect hundreds of potential source alleles. 2) Slightly deleterious alleles take longer to select against. 3) **Recessive alleles do not always express so they are often propagated. ** 4) Chance/drift can maintain these alleles over time.
52
How much variability does a polygenic trait have? Why should we care?
Substantially high variability. Most of the traits that encode for our fitness are polygenic, and thus incredibly variable.
53
What is the solution to the lek paradox? 'Why do females continue to pay attention to a male's tail when selecting a mate, despite the decrease in variability of generations?'
Courtship and mating traits will be polygenic. Because they are polygenic, we can expect them to have enough variability (via mutation) between generations to sustain competition and difference.
54
How is inbreeding a useful indicator for geneticists?
If we see increased levels of disorder in inbred children then we know that recessive alleles are implicated.
55
How are runs of homozygosity useful?
They are a measure of inbreeding. The longer a run, the more recent the breeding was. Each 1% increase in the risk of schizophrenia by 17%.
56
Why does depression peak in prevalence during reproductive years?
There is evidence that depressive phenotypes increase fitness. Depressed men have the same fitness; depressed women have higher fitness. The siblings of depressed people also have higher levels of fitness.
57
What theory of selection best explains the depressive peak during adolescence?
Directional selection.
58
How does REM sleep vary across the three depressive phenotypes.
Decreases in both starvation and sickness; increases in the melancholic phenotype.
59
How does motor activity vary across the three depressive phenotypes.
Decreases in both melancholia and sickness; increases in the starvation phenotype.
60
How does core body temperature vary across the three depressive phenotypes.
Decreases in the starvation condition; increases in both the starvation and melancholic phenotype.
61
What is the relationship between 'fever of unknown origin' and 'endogenous depression'?
Individuals with a 'fever of unknown origin' show symptoms of depression. They may falsely be diagnosed with endogenous depression.
62
Why is cortisol released during depression? Provide evidence for this.
To facilitate glucose release and insulin resistance, which then redirects energy from extra-muscular systems to the brain for intense ruminative thought. Cortisol shows a correlation with ruminative thought.
63
Explain the pathos D. hypothesis.
"Depression is an adaptive response to social stressors that put one at increased risk of infection."
64
What would Maier say about the relationship between depressive phenotypes?
"Depression co-opted the machinery involved in sickness behavior and may serve a similar function--to converse energy." Dr. Andrews changed this to REALLOCATE ENERGY in his own theory.
65
Explain the 'Energy Reallocation Hypothesis'
"Depressive phenotypes evolved in response to stressors that required prolonged energetically expensive responses"
66
How does the melancholic phenotype differ in the 'Energy Reallocation Hypothesis'?
They show more REM sleep. We know that REM sleep increases our retention of complex information. Depressive rumination is the repeated consideration of complex information.
67
How would you best describe analytical thought?
You break complex issues into their smaller components.
68
How do depressed individuals feel about their ruminations?
They feel positively about them, i.e. they are important.
69
People with PTSD show uniquely unmethylated genes. What were these responsible for? What implications does this have?
Immune functioning. People with PTSD show a compromised immunoresponse due to the misallocation of immune system resources (same response as depression).
70
Explain the lesion account of mental disorder from Wakefield's paper. How was it countered?
"mental disorders exist only if the very same concept of disorder that applies to physical conditions also applies to the mental conditions labeled as disorders." 1) Lesions are inaccurate due to individual variance. 2) There are not lesions in all mental disorder.
71
What is the major disadvantage of the value view of disorder?
1) Uses purely culture-relative norms that ignore scientific context. 2) Some symptoms have evolved to produce socially undesirable responses.
72
What is the primary argument against the 'Whatever Professionals Treat' view of disorder?
"equating illness with 'therapeutic concern' implies that no one can be ill until he has been recognized as such, and also gives doctors, and society, free rein to label all deviants as ill."
73
What is the primary argument against the 'Statistical' view of disorder?
Any deviation could, then, be a disorder--implies another value judgement. For example, shortness in height.
74
Why is the Scadding, Kendell, and Boorse, view of dysfunction as an evolution-derived criterion for lowered survival or lowered reproductive fitness incorrect?
It does not consider how maladaptive systems might not be malfunctioning.
75
What should individuals be evolved to maximize?
Their inclusive fitness.

Evolution and Mental Health (3 decks)

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