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Acute & Chronic Stress Flashcards

1
Q

STRESS

A
  • state of worry/mental tension caused by difficult situations/environments
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2
Q

HYPOTHALAMIC-PITUITARY ADRENAL (HPA) AXIS FUNCTION

A
  • hypothalamus; corticotropin releasing hormone (CRH) ->
  • anterior pituitary; adrenocorticotropic hormone (ACTH) ->
  • adrenal cortex; negative feedback -> hypothalamus/anterior pituitary
  • aka. glucocorticoid production -> increased availability of glucose to facilitate “fight VS flight”
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3
Q

“STRESS-SENSITIVE” BRAIN REGIONS

A
  • dense w/glucocorticoid receptors:
    1. prefrontal cortex
    2. amygdala
    3. hippocampus
  • development/function might be altered by environmentally-induced variation in cortisol release
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4
Q

PREFRONTAL REGULATION DURING NON-STRESS CONDITIONS

A
  • alert
    DMPFC
  • reality testing; error monitoring
    DLPFC
  • top-down guidance of attention/thought
    rIPFC
  • inhibition of inappropriate actions
    VMPFC
  • regulating emotions
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5
Q

AMYGDALA CONTROL DURING STRESS CONDITIONS

A
  • loss of prefrontal regulation
  • emotional habits
  • bottom-up attention
  • emotional reflexes
  • emotional associatons
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6
Q

ACUTE STRESS & EXECUTIVE FUNCTIONS

A
  • acute stress shown to impair working memory & cognitive flexibility
  • some effects = for inhibition
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7
Q

SUMMARY I

A
  • acute stress = adaptive response
  • leads to reduced executive functions & prefrontal brain activity
  • increased emotional & “bottom-up” control from sensory brain parts
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8
Q

CHRONIC STRESS

A
  • ongoing stress resulting in consistent sense of feeling pressured/overwhelmed over long period of time due to internal/external stressor
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9
Q

FELITTI ET AL.

A
  • enduring effects of adversity
  • relationship of childhood abuse & household dysfunction to many leading causes of death in adults
  • are adverse chilldhood experiences linked to negative health outcomes later in life?
  • found strong dose response relationship between exposure to childhood adversity & disease in adulthood/adveristy & psychological health
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10
Q

LIU ET AL. (1997)

A
  • plasticity of HPA axis
  • maternal care, hippocampal glucocorticoid receptors & hypothalamic-pituitary-adrenal responses to stress
  • more licking/grooming -> pups had reduced lvls of ACTH/CORT to acute stress
  • maternal beh serves to “program” HPA axis in offspring
  • Q: how do life-experiences impact HPA axis? do adverse life experiences result in heightened/blunted HPA axis reactivity?
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11
Q

THEORETICAL MODELS

A

SEVERITY OF ADVERSITY
- w/mental illness = positive adveristy -> HPA axis reactivity correlation
- aka. trauma = high HPA reactivity
- w/o mental illness = negative adversity -> HPA axis reactivity correlation
- aka. trauma = low HPA reactivity
DURATION OF ADVERSITY
- stage 1 = alarm; stage 2 = resistance; stage 3 = exhaustion

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12
Q

P-CURVE

A
  • p-curve = distribution of statistically sig p-values for set of studies
  • can help resolve discrepancies in literature by determining which set of conflicting findings = more likely to be correct
  • aka. could results showing hyper-reactivity of HPA be result of publication bias?
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13
Q

HOSSEINI-KAMKAR, LOWE & MORTON (2021)

A
  • dif calibration of HPA axis as function of trauma VS adversity; systematic review & p-curve meta-analyses
  • use p-curve to examine conflicting findings regarding association between early-life experiences & HPA axis reactivity
  • study 1 = trauma; study 2 = adversity
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14
Q

HOSSEINI-KAMKAR, LOWE & MORTON (2021): METHODS

A
  • separated articles based on whether they found cortisol HYPER/HYPO reactivity
    1. PSYCINFO RECORDS
  • records entered into cortisol hyper/hypo/both-reactivity p-curve
    2. PUBMED RECORDS
  • records entered into cortisol hyper/hypo-reactivity p-curve
    3. REFERENCE SECTION
  • articles entered into cortisol hypo-reactivity p-curve
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15
Q

HOSSEINI-KAMKAR, LOWE & MORTON (2021): STUDY 1 (TRAUMA) HYPER RESULTS

A
  • cort hyper reactivity
  • evidential value if:
    1. half p-curve (p-values below .025) = sig right-skewed at p < .05 OR…
    2. both half/full p-curve = sig right-skewed at p < .1
  • results: half (p = .1321); full (p = .0531)
  • aka. neither condition met aka. p-curve = NOT sig right-skewed
  • absence of evidential value ONLY if:
    1. full p-curve = sig flatter than p-curve of 33% power at p < .05 OR…
    2. both half p-curve/binomial tests = sig at p < .1
  • neither condition = met; p-curve = inconclusive
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16
Q

HOSSEINI-KAMKAR, LOWE & MORTON (2021): STUDY 1 (TRAUMA) HYPO RESULTS

A
  • evidential value if:
    1. half p-curve (p-values below .025) = sig right-skewed at p < .05 OR…
    2. if both half/full p-curve = sig right-skewed at p < .1
  • results: half = p < .0001; full = p < .0001
  • aka. both conditions met; p-curve = sig right-skewed
17
Q

HOSSEINI-KAMKAR, LOWE & MORTON (2021): STUDY 2 (ADVERSITY) HYPER RESULTS

A
  • evidential value if:
    1. half p-curve (p-value below .025) = sig right-skewed at p < .05 OR…
    2. both half/full p-curve = sig right-skewed at p < .1
  • results: half = p .0227; full = p .0598
  • aka. both conditions met; p-curve = sig right-skewed
18
Q

HOSSEINI-KAMKAR, LOWE & MORTON (2021): STUDY 2 (ADVERSITY) HYPO RESULTS

A
  • evidential value if:
    1. half p-curve (p-value below .025) = sig right-skewed at p < .05 OR…
    2. both half/full p-curve = sig right-skewed at p < .1
  • results: half = p.0572; full = .3453
  • aka. neither condition met; p-curve = NOT sig right-skewed
  • absence of evidential value ONLY if:
    1. full p-curve = sig flatter than p-curve of 33% power at p < .05 OR…
    2. both half p-curve/binomial tests = sig at p < .1
  • results: full = p.0313
  • full p-curve sig flatter than p-curve of 33%
  • aka. evidential value = absent
19
Q

HOSSEINI-KAMKAR, LOWE & MORTON (2021): SUMMARY

A
  • p-curve used to examine conflicting findings regarding association between early-life experiences & HPA axis reactivity
  • trauma = lower axis reactivity BUT…
  • adversity = higher axis reactivity
20
Q

INVERTED U-SHAPE FUNCTION

A
  • how do life-experienced become biologically embedded?
  • inverted U-shaped function explains relationship severity of adversity/cortisol reactivity
  • distinction betwen adversity/trauma = important in probing literature
21
Q

MCLAUGHLIN ET AL. (2019): AMYGDALA REACTIVITY

A
  • 11 studies = heightened amygdala reactivity to threat cues in kids exposed to adversity
  • 6 studies = NO difs in amygdala reactivity to threat cues in adversity exposure relative to controls
  • 1 study = BLUNTED amygdala activity in adversity exposure relative to controls
22
Q

MCLAUGHLIN ET AL. (2019): SALIENCE NETWORK (INSULA)

A
  • 6 studies = heightened insula reactivity to threat cues in kids exposed to adversity
  • 4 studies = NO dif in insula & dACC reactivity to threat cues in adversity exposure relative to controls
  • 4 studies = BLUNTED insula & dACC activity in adversity exposure relative to controls
23
Q

PSYCHOLOGICAL PROCESSED AFFECTED BY EARLY LIFE ADVERSITY & UNDERLYING NEURAL SUBSTRATES

A
  • prefrontal cortex = cognitive control
  • emotion regulation -> amygdala = emotional processing (aka. emotional reactivity)
  • delay discounting -> striatum = reward processing (aka. reward responsivity)
24
Q

META-ANALYSES

A
  • help establish:
    1. likelihood of true findings
    2. generalisability of findings
    3. point to moderating variables that help explain heterogeneity across studies
25
Q

WAGER, LINDQUIST & KAPLAN (2007): LITERATURE SEARCH SUMMARY

A
  • meta-analysis of functional neuroimaging data; current/future directions
  • 1984 abstracts reviewed
  • 83 studies included
  • 5242 pps
  • 801 xyz coordinates entered
  • studies separated: emotion processing; reward processing; memory processing; inhibitory control tasks
  • ONLY whole-brain results
26
Q

WAGER, LINDQUIST & KAPLAN (2007): RESULTS

A
  • sig result = area where consistency of activation across studies exceeds chance expectation; aka. where chance = random even distribution across whole brain
    ACROSS ALL TASK DOMAINS
  • higher amygdala activity in adversity VS controls
  • higher PFC activity in controls VS adversity
    EMOTION PROCESSING TASKS
  • higher amygdala activity in adversity VS controls
  • higher PFC activity in controls VS adversity
    INHIBITORY CONTROL TASKS
  • higher ACC/insula activity in adversity VS controls
27
Q

WAGER, LINDQUIST & KAPLAN (2007): CONCLUSIONS

A
  • MKDA used to help synthesise conclusions from large literature body
  • individuals w.adversity exposure may have:
    1. exaggerated neural response to threatening stimuli (aka. heightened amygdala activity)
    2. reduction in top-down control (aka. downregulation) of limbin response to threat (aka. blunted PFC activity)
  • might help better identify how early adversity diminishes ability to cope w/later stressors; heightened susceptibility to diverse mental health issues
28
Q

CROSS-DOMAIN TRANSFER EFFECTS

A
  • acute stress reduces food-related self-control
  • stress -> increase in ventral striatum & amygdala activity -> people select “tastier food”
29
Q

CDTE: ENVIRONMENTAL STRESS MODELS

A
  • inform WHO might need intervention:
    1. CUMULATIVE RISK
  • ie. psychopathology x number of stressors
    2. SPECIFIC STRESSORS
  • ie. economic stress; daily disruption; threat
    3. STRESS SENSITISATION
  • ie. psychopathology x stress = history of adversity
30
Q

CDTE: STRESS PATHWAY MODELS

A
  • inform HOW to intervene:
    1. STRESS APPRAISAL
  • ie. psychopathology -> stress -> appraisal -> reappraisal -> psychopathology etc.
    2. STRESS BUFFERS
  • ie. social support; physical activity; structured daily routine
    3. STRESS MECHANISMS
  • ie. sleep; emotion regulation; reward processing
31
Q

EFFECT OF MULTIPLE DIMENSIONS ON BRAIN DEVELOPMENT

A

EARLY LIFE ADVERSITY
- threat
- deprivation
NEURAL ADAPTATIONS
- emotional processing
- executive function
- reward processing
PSYCHOLOGICAL CHANGES
- heightened emotional reactivity
- poorer emotion regulation
- increased delay discounting
- blunted reward responsivity
ADDICTIVE BEHAVIOURS
- smoking cigarettes
- drinking alcohol
- overeating high-sugar/fat foods

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