1
Q
def stressor
A
anything that knock’s you out of your homeostatic happy place *originates from a survival mechanism
2
Q
When may your body need stress?
A
- body needs it to stay alert
- exercise
- fever
3
Q
What 2 hormones dominate the stress response?
A
adrenaline (norepinephrine) and cortisol
4
Q
Who came up with the general adaptation syndrome and what does this mean?
A
-Selye
- “A common response to all stressors that help mobilize energy to help defeat the threat.”
- proposed stress to be a general response to any unpleasantries (through dropping mice and giving them stomach ulcers)
5
Q
What physiological “fight/flight” responses do we see?
A
- increased HR
- increased BP
- increased breathing rate
*body mobilizes stored energy to convert into glucose and fuel muscles that need it
6
Q
What turns on the “startle” stress response?
A
- mediated by locus coeruleus
7
Q
What turns on the “threat” stress response?
A
- amygdala (responds to strong emotions like fear)
8
Q
describe the pathway of stress activation
A
- the amygdala or locus coeruleus independently or collectively activate the hypothalamus (this initiates 2 cascading stress axes that work simulatneously)
- one fast (SAM axis) & 1 slow (HPA axis)
9
Q
Provide the full name for the SAM axis and how it works:
A
- sympathetic adreno-medullar axis
- uses sympathetic nerves to activate the adrenal medulla
- fast (bc using nerve responses), first-acting
- activation of AM causes the rush of adrenaline/epinephrine into the blood stream
10
Q
Why might slower/deep breathing help relax/turn off stress response?
A
reactivates parasympathetic system (rest + digest)
11
Q
Provide the full name for the HPA axis and how it works:
A
- hypothalmic pituitary adrenal axis
- slower bc uses hormones
- once hypothalamus gets activated, it releases CRH (corticotropin releasing hormone) which binds to receptors onthe pituitary gland that release ACTH (adrenocorticotropic hormone)
- ACTH goes through blood to the adrenal cortex which gets activated and releases cortison
- when cortisol rushed into the blood it helps release stored energy (most in liver and fat cells) for fight + flight
*delayed response
12
Q
Can the hypothalamus and stress responses be activated without the amygdala or locus coeruleus?
A
Yes! By any alterations in homeostasis
13
Q
Exercise and psychological stress both activate the same processes… how do these differ in the way they activate it?
A
Exercise
- voluntary
- acute (mins to hours)
- minor strain
- easy to recover from
Psychological
- involuntary
- chronic - weeks, months, years (ex. money, relationship, work)
- major strain
- difficult to recover from (years with activated SAM and HPA is really straining to body, can cause brain damage)
14
Q
def the cross-stressor hypothesis
A
voluntary exercise stress induces adaptations in the stress system that makes us more resilient to all stressors, even physiological ones
15
Q
What did (Rimmele et al., 2007)’s study find in relation to cortisol, post-test anxiety and heart rate responses to psychosocial stress in trained and untrained men?
A
lower cortisol (HPA), lower anxiety and lower heart rate (SAM) in trained men
- exercise training = less reactive to stress
16
Q
what does innocuous mean?
A
harmless
17
Q
In a study on kinesophobia by (Pfingsten et al 2001), what was found as a result of telling participants certain exercises would be painful?
A
- increase in fear rating
- rating of pain increased by 20%
- did not perform as many reps
18
Q
def nocebo effect
A
negative effect produced by a sham treatment that cannot be attributed to the properties of the treatment itself and therefore, must be due to the patient’s belief in that treatment
19
Q
Fear from innocuous cues can be conditioned through _
A
experience
(ex. Albert became afraid of anything white & fluffy after terrifying noise played with white mouse apprearance)
20
Q
Equation for fear conditioning of a stress response:
A
CS (conditioned stimulus) +US (unconditioned stimulus) = CR (Conditioned Response)
CS = harmless stimulus (eventually evokes fear on it’s own)
US = thing that already has fear associated
21
Q
def generalized anxiety disorder
A
excessive and exaggerated worry about everyday events for no apparent reason
22
Q
def panic attacks
A
A sudden and intense fear that triggers a severe physical reaction when there is no real danger or threat
23
Q
def phobia
A
An intense fear or aversion to a specific object or situation that may be harmless
24
Q
def social anxiety
A
An intense fear of being negatively judged or scrutinized in a social setting even when it’s not true
25
How does the amygdala affect neurons?
Links them together strongly, makes it very hard to forget things associated with strong emotions
26
How does the amygdala function in anxiety and why might this be problematic?
- once any "threat" is detected, the stress response is activated to warn all the body tissues without delay
- the amygdala stays on until the threat is gone (but worries can sometimes never fully go away)
- amygdala also has no way of telling the body what the nature of the threat is, so there may be a heightened response to something that is not truly dangerous.
27
Are the amygdala and hippocampus necessary for fear conditioning? (Bechara et al 1995)
- Hippocampus not necessary, see similar patterns of fear responses (unless context-related fear)
- Amygdala very critical for fear conditioning
28
What are the 3 steps for basic fear conditioning?
habituation (CS), acquisition (CS + US = CS), extinction (CS)
29
What are the 5 steps for context-related fear conditioning?
habituation, acquisition, extinction (change rooms), reinstate, (change rooms), recovery
30
Linking of fear to context is largely due to _ (brain area)
hippocampus
31
describe the brain regions involved in fear conditioning
- hippocampus (context-specific threat) activates amygdala to initiate fear, which integrates info and interface with hypothalamus which starts the 2-axis stress response
- the PFC is able to control the more primitive parts of the brain (3 mentioned above) * why mindfulness can help stress, inhibits the amygdala
*in an anxiety disorder, PFC can't communicate with amygdala anymore
32
When does learned helplessness happen?
when a person is conditioned to believe that a bad situation is unchangeable or inescapable
*often occurs due to repeated stress, we get freeze instead of fight/flight
33
describe the shutter box experiment
- 1 side wired with electricity, other side is not
- dog doesn't even try to cross small barrier because of the uncontrollable stressor
*only dogs shocked without control learn helplessness
- dogs shocked with control of a red button to stop shocks escapes
34
What is the effect of exercise on learned helplessness?
exercising decreases "freeze" responses, take less time to leave (escape latency)
- mice shutter box experiment
35
More "freeze" responses are associated with _
learned helplessness
36
How does exercise affect the SAM axis?
- exercise turns the SAM axis "on" and "off"
- intensity of exercise dictates how stress-provoking it is (moderate increases adrenaline a little, high a lot)
- adrenaline drops very quickly during recovery
- cortisol takes longer to peak & drop in recovery period, stays elevated (can help turn off the sam axis & hpa to refill glycogen stores)
37
def allostasis
-stability through change
- rapid but gradual internal changes to meet demands of changing external environment
- the body is not fixed to certain homeostasis, homeostatic set point changes
38
def allostatic load
stress overload, body grows weaker rather than stronger
- more likely to occur with chronic psychological stress or combined stressors because it is involuntary and uncontrollable
39
How is cortisol production shut off? What is this calles?
-as cortisol rises, it binds to it's receptors located on the pituitary gland and hypothalamus
- when cortisol binds, it stops the next step in the cascade of cortisol production
- this is called negative feedback loop
40
Which 2 receptors can cortisol bind to?
Mineralocorticoid Receptors (MRs)
- high affinity for cortisol, occupied all the time
- sets baseline levels
- more MRs = lower baseline
Glucocorticoid Receptors (GRs)
- low affinity for cortisol (only bind when cortisol is high)
- occupied when CORT is high
- sets recovery rate
- more GR = faster recovery
41
What brain area contains the most glucocorticoid receptors?
hippocampus
42
How do GRs inhibit the 2 axes? Aka "master off-switch"
When GRs bind to the hippocampus, it inhibits the hypothalamus directly which stops the 2 stress response axes
43
Why do individuals react differently to stressors?
-some have more GRs, recover faster from stressful events and less likely to suffer from allostatic load
- earlylife stressful environment (high and low licking and grooming mouse mom crossfostering study)
*partly built into biology!
44
What effect does chronic life stress have on GR number in the brain?
reduces GRs
- GRs saturated all the time and stress "off-switch" not working, become corticoresistant and cortisol remains in the blood
*exercise can protect brain against chronic early life stress
45
What role does BDNF play in stress?
- Brain-Derived Neurotropic Factor
- works like a protective coating from stress
- surrounds the hippocampus, protecting GRs from stressor
- moderate exercise increases this a little, high intensity increases a lot BUT supressed in chronic stress
46
def epigenetics
- external modifications to DNA that turn gener "on and off"
- These modifications do not change the DNA sequence, but instead, they affect how the gene is "read"
*can be altered by phychological stress and exercise
47
Gene expression is determined by _
the packaging of DNA
- DNA tightly wound around histones, helps dna fit and express genes through allowing it to be read by transcription factors
- dna>rna>proteins>things like bdnf
48
Do epigenetic changes affect the genetic code?
No, just alter gene expression
49
What are some examples of epigenetic changes?
- adding an acetyl group, loosens chromosome structure and makes it easier to read the underlying gene
- methyl group physically inhibits gene expression by attaching to the nucleotide cytosine, gene can't be read and protein can't be made
50
What is added to the GR gene during chronic stress and what can reverse this change?
chronic stress adds CH3 to the GR gene, but exercise removes them
51
def tuberculosis
- a respiratory condition but bacteria based
- can be exposed but not get symptoms
52
Holmes et al tested if stress can impact the ability to get infected with tuberculosis, what did they find?
- studied employees of sanitoriums (20 each that did or did not get TB)
- sorted by age, sex, race
- people with stress before hand were more likely to develop TB
53
Why do stressed-out cells trick the immune system?
Body cells "know the handshake"
- Foreign cells don't, have pathogen associated molecular patterns (PAMPS)
- Stressed out cells have damage associated molecular patterns (DAMPS) that induce a sterile immune response, "too tense to perform handshake"
54
def sterile immune response
no virus, cell damage evokes immune response
55
A double-breach in immunity activates _ that _
inflammasomes
- increase inflammation a lot
- ex. stress only ok, infection only increases inflammatory cytokines, stress and infection increases cytokines by much more
56
def inflammasomes
specialized immune cells triggered by 2x immunity breach
57
Too much inflammation causes _
allostatic load
- stressed-out system more sensitive to allergens and viruses
58
What is an elevated WBC count indicative of?
an infection being fought by the body
59
Cohen et al investigated the impact of psychological rate of infection, describe some elements of the study and what they found
-420 healthy adults given nasal drops with respiratory virus
- the ppl with psych stress tended to get a cold
*WBC count didn't change tho!
60
Which cells are impacted by stress?
Th1 and Th2
61
Describe Th1/Type 1 cells:
- provide cellular immunity, can even kill cancerous cells
62
Describe Th2/Type 2 cells"
- provide humoral immunity, things that are circulating in the blood (ex. parasites, malaria)
63
What can happen if TH1 and TH2 are not in balance?
too much Th1: cellular attack mode and autoimmune responses
too much Th2: can make you more sensitive to allergies
64
Stress decreases the production of which type of cell?
Th1, decreases protection from viruses, bacteria
- can make Th2 cells more abundant, may be more succeptible to allergies
65
In the study mentioned in class by Fox and Kang, what was observed with increasing levels of stress in students during exams as compared to midterms?
- Th1 decreased (more succeptible to get sick, greater risk for infections)
- Th2 increased (greater allergy risk)
66
What influenced the western medicine and biomedical model of health for over 300 years?
Descartes mind-body dualism (treating the mind and body as seperate things)
67
How does mind-body communication work?
Mind: consciousness, perception, thinking, and memory interact with the nervous system
- the nervous system then interacts with the immune system and endocrine system
68
How can physical illness impact your physiological mood?
cause negative mood states by increasing inflammatory cytokines which interact with the amygdala to increase social withdrawal
- viruses, toxins and bacteria are sensed by TLR (toll-like receptors) and activate immune cells to produce cytokines
- the cytokines then cause inflammation (increased blood and immune cells) at the site of injury and interact with microglia in the brain, activating them to make cytokines
- brain becomes inflamed and interacts with amygdala which produces symptoms (fatigue, withdrawal, anorexia, fever)
69
How can temporary sadness and social withdrawal be adaptive?
- not gonna spread disease to other people if sickness is acute
70
What's the core neural component of pathoge-induced social withdrawal?
heightened amygdala activation
71
def depression and give an assumed biological cause
an affected state of negative mood and low arousal lasting at least 2 weeks, lack of serotonin in the forebrain
72
What are 3 factors that may lead someone to believe that physical illness causes depression?
- chronic inflammatory diseases are associated with depressive symptoms (Evan et al., 2005)
-12 weeks of cytokine therapy for cancer increased rates of mahor depression (Musselman et al., 2001)
- Depressed individuals who are otherwise healthy have higher levels of pro-inflammatory cytokines (best evidence) (Miller et al., 2002)
73
What is the mainstream treatment for depression? How does this work?
SSRIs (selective serotonin reuptake inhibitors)
- block the reabsorption of serotonin
74
Why might SSRIs not work for someone with drug-resistant depression?
- some people have persistently high levels of inflammation (higher baseline pro-inflammatory cytokine levels)
- some forms of depression may be more associated with inflammation than lack of serotonin (treating inflammation may help reduce symptoms)
75
What specific cytokine may be linked to depressive symptoms?
TNFalpha
- induces depression-like changes in brain function and behaviour
76
How does exercise affect inflammation?
- exercise is temporarily pro-inflammatory, this goes away because muscles release myokines which are anti-inflammatory
- exercise tones stress responses so that you are less reactive to stressors
77
What did the study by Rethorst et al, 2013 find in relation to exercise and clinically depressed individuals?
Clinically depressed people with high TNFalpha benefit most from exercise as compared with those with a lower TNF alpha at baseline, still saw a decrease in depressive symptoms though
78
Does the dosage of exercise affect depression and inflammation? (Emily's thesis study)
- looked at 55 uni students
- moderate intensity reduced depression, anxiety, and stress, while the control group reported increases in depression and anxiety
- HIIT increased anx and stress, but reduced depressive symptoms
- moderate intensity exercise can reduce TNF alpha to improve mood, while HIT did not.
*dose matters!
79
How can acute stress change the morphology of neurons in the brain?
- with more exposure to stress, spinal density of neurons in the amygdala increases which makes it hypersensitive to stress
- spinal density in the hippocampus and PFC, however, is reduced with chronic stress due to the chronically high levels of cortisol that change the neuroenvironment, toxic to neurons
- neurons shrink in length and branch points and neurogenesis is prevented = hippocampus not functioning properly and takes a longer time to turn off stress response
80
How is the pre-frontal cortex affected by stress?
- in a similar way to hippocampus, spinal density decreases = worse at cognitive tasks and regulating emotions (PFC usually inhibits amygdala)
- as a result, amygdala is able to launch larger and more frequent stress responses
81
Who is Chris Waddell? What happened to him and how does his story relate to resiliency?
- promising ski racer
- sustained a spinal cord injury
- became most decorated paralympic skier
- became first paraplegic to summit Mt. Kilimanjaro
- Waddell's exercise training likely buffered the effects of his trauma (exercise increases BDNF to protect brain, also helps counteract decreasing neurogenesis)
82
def resiliency
the capacity to withstand or to recover quickly from difficulties
83
Perception of Health Matters! In Keller et al.'s study, what was found in relation to percieved affects of stress on people's health vs risk of death
- those who experienced a lot of stress but believed that it had a small effect on their health has a ~20% reduced risk of death
- those who believed their stress had a large effect had a 43% increased risk of death
84
Viewing stress as positive can improve_
cognitive functioning
85
def trait mindfulness
one's ability to purposely pay attention in the present moment, non-judgementally
86
How does mindfulness meditation reduce psychological distress?
increasing PFC activity and inhibiting amygdala activity
87
Are positive affirmation helpful?
Yes, but not to everyone
88
How can CBT (cognitive behavioural therapy) help with psychological stress?
helps rewire the brain to help you rewrite the narrative about fear
Health Psychology
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