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Evolution and Mental Health > Midterm 2 > Flashcards

Midterm 2 Flashcards

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1
Q

How does the DSM-5 conceptualize anxiety?

A

Excessive anxiety (dysfunction) that causes clinically significant distress.

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2
Q

What is an issue with the distress criterion for disorder?

A

Distress occurs when a phenotype does not fit well into MODERN day society. These systems did not evolve for modern day organization.

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3
Q

What did Paz say about understanding anxiety?

A

We need to understand the purpose (origin) of anxiety to make sense of dysfunction.

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4
Q

What type of anxiety system was functional in our EEA?

A

An overly sensitive anxiety system. The better-safe-than-sorry system.

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5
Q

How sensitive would you expect an anxiety system to be when the cost of a miss is low?

A

The system would not be sensitive.

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6
Q

Contrast a DSM-5 vs. Evolutionary view of anxiety.

A

DSM-5: “What is excessive and distressing is disorder.”

Evo: “What appears and is distressing can still represent a normally functioning system.”

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7
Q

What does evolution propose as the primary issue with anxiety?

A

An incompatibility between evolutionary evolved systems and today’s environment.

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8
Q

What does Dr. Andrews view as a key issue with the DSM diagnostic criteria?

A

That diagnosis is categorical and not dimensional.

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9
Q

What phenomenon do clinicians have a difficult time explaining?

A

Spontaneous Remission. True disorders do not heal themselves over time.

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10
Q

What does Wakefield believe about the existence of mental disorder?

A

Wakefield believes that disorder exists. Important.

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11
Q

Dr. Andrews says that medical treatment does what?

A

Expedites natural remission.

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12
Q

What are the two types of rumination as indicated by the Ruminative Response Scale (RRS)

A

1) Brooding (Worsens symptoms)

2) Reflective Pondering (Improves symptoms)

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13
Q

How does Dr. Andrews explain brooding related ruminative questions?

A

Causal questions, or comparing against an unachieved standard.

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14
Q

How does Dr. Andrews explain pondering related ruminative questions?

A

Less causal questions; ask about the nature or root of the problem.

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15
Q

What was an issue with the brooding-pondering dichotomy?

A

These two measures are strongly correlated.

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16
Q

How does mood impact type 1 vs. type 2 thinking?

A

Positive moods promote type 1; negative moods promote type 2.

Type 2 thinking is an analytical, divide and conquer, style.

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17
Q

What were the two key takeaways from the depression-breast cancer studies?

A

1) Depressive individuals are not pessimistic.

2) Depressive individuals are better at using available information.

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18
Q

What did Galen believe about Melancholia?

A

Depression was a disorder of thought caused by an imbalance in black bile.

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19
Q

Summarize the Theophrastus view of depression.

A

The depressive genius.

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20
Q

What was ruminate originally intended to mean?

A

An intensive thought.

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21
Q

What has psychiatry done to change the definition of melancholy?

A

They have added disorder to the saddened state.

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22
Q

What is recall of a depressive episode like compared to normal experience?

A

Depressive episode recall is worse than typical experience.

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23
Q

Explain the two stages of the adaptationist model of rumination.

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A

1) Causal analysis: Identify the cause of the problem.

2) Problem-Solving Analysis: Try to solve the problem.

24
Q

What is the difference between normal vs. analytical thinking?

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A

Analytical thinking involves causal analysis.

25
Why do we experience so much anxiety around potential cheating?
Because the potential fitness consequences are quite high.
26
What is an issue with the brooding-pondering dichotomy?
There is poor internal consistency; the model is a poor fit.
27
What do we learn about the brood-pondering dichotomy across different groups?
The strategies vary between sexes, across cultures, and by clinical status.
28
Explain Dr. Andrews Analytical Rumination Questionnaire.
He found strong internal consistency between two new factors: causal analysis and problem-solving analysis.
29
Explain the relationship between the stages of the adaptationist model of rumination.
Depression is related with positively related with casual analysis; causal analysis is positively correlated with problem solving analysis; problem solving analysis is negatively correlated with depression. Here we see a circular model whereby problem solving seems to lower depression.
30
How commonly do depressed individuals think about their symptoms and sad state?
Not very often.
31
What do individuals with depression most think about?
Problem-solving thoughts and their current circumstance.
32
Explain the origin of the low serotonin hypothesis (called the monoamine hypothesis now).
Found that reserpine, a drug known to use up monoamines, increases depressive symptoms. Hypothesized, then, based on transporter blocking data, that depression is caused by an excessive breakdown of monoamine neurotransmitters (low monoamine levels).
33
What is the most problematic issue with SSRIs?
SSRIs immediately increase extracellular serotonin levels, yet symptom alleviation takes 3 to 4 weeks.
34
What sort of trend do we typically see when somebody first takes SSRIs?
Initially, within the first week, depressive symptoms become worse than controls—later alleviating.
35
How do we presently measure 5-HT?
To measure serotonin itself we must use cellular recording. Thus, human studies of serotonin are not possible.
36
What happens to the serotonin levels of rats during inescapable shock.
Serotonin levels increase during shock.
37
How do concentration levels differ from transmission levels?
Concentration is a measure which adds both transmission and reuptake levels. It is also the measure which we have access to.
38
What is the best proxy measure of serotonin transmission?
The 5HIAA/5-HT ratio; this ratio is sensitive to both intensity and duration.
39
An increase in the 5HIAA/5-HT ratio indicates what?
Greater levels of stimulation.
40
What is the consensus on serotonin level change when rats are put in stressful scenarios?
Levels consistently rise.
41
Lesioning the dorsal raphe nucleus (DRN) has what outcome?
DRN lesions inhibit the development of depressive symptoms. Hence, serotonin is necessary for the development of depressive symptoms.
42
We see what levels of 5-HIAA in the jugular veins of patients with MDD?
Elevated levels. Provides evidence that the rat trends seem to carry over to humans.
43
How do 5-HIAA levels in humans seem to change when MDD is treated?
Levels decrease.
44
What does it mean to say that serotonin is under homeostatic control?
Serotonin is ‘set’ at a certain level, and the body will alter other functions to maintain this (compensatory response).
45
Steve Hyman made a claim about serotonin, homeostatic control, and therapeutic outcomes. What did he say?
“Adaptations are needed to trigger therapeutic effects.”
46
Favia also made a claim about serotonin and compensatory responses. What did he say?
“Adaptations are responsible for the drug’s loss of efficacy.”
47
How would you define hormesis?
A biphasic response to a drug. Biphasic: A drug or toxin can elicit different responses by dose level.
48
Here are some symptoms that demonstrate biphasic effects: aggression, anxiety, BDNF expression, and motor excitability. Outline the nature of these in both acute and chronic treatments.
Aggression: decreases; increases. Anxiety: increases; decreases. BDNF Expression: decreases; increases. Motor Excitability: increases; decreases.
49
Explain the perturbation trajectory for most biological systems. Why might this be advantageous?
There is an initial overshoot caused by a drug. Then, an undershoot occurs from an oppositional tolerance response. We then see future dampened oscillations. Systems like these allow for a mechanism to return back to baseline faster.
50
How does cellular serotonin change after taking a single SSRI? Outline both pre- and post-conditions.
Begin with more intracellular serotonin; following SSRI usage, extracellular serotonin increases.
51
How does acute versus chronic SSRI usage change cellular serotonin levels?
Chronic SSRI use lowers overall serotonin production. This occurs because extracellular levels begin to match that of a stimulated neuron; the neuron then 'assumes' that no more serotonin is required, thus resulting in extremely low intracellular serotonin.
52
How might serotonin production look during one's first month of SSRI use.
There will be an initial spike (extracellular build-up), then the levels will dramatically drop (halt in production), and, finally, the levels will middle out at a homeostatic balance.
53
What happens to serotonin transmission--as measured by the 5-HIAA/5-HT ratio-- upon sustained SSRI use?
The ratio decreases as there is fewer neuronal firing. Can also be explained in that less NTs are being metabolized.
54
What would you expect to occur when a chronic SSRI user stops?
Increased firing, low extracellular serotonin concentration, and excitation of synthesis. Will eventually return to baseline.
55
How does SSRI dose influence the symptoms that one experiences when discontinuing their medication?
The onset of symptoms is delayed; the oscillations are delayed.
56
What happens to infant rats whose mothers took anti-depressants?
The infant rats are lighter, less successful in mating, and unable to hold territory.

Evolution and Mental Health (3 decks)

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