Week 2: Stress and the Mechanisms of Stress Flashcards

1
Q

Applications of the TSST

A

This test measures people’s ‘stress reactivity’ - that is, how strongly they react and how quickly they return to baseline. Reactivity profiles can be measures physiologically, hormonally, or via self-report over time

-it tests how other factors can predict stress reactivity (eg. genes, early-live experiences, psychological characterisitcs) or test how patterns of stress reactivity predict other outcomes (eg. metnal resilience, physical health) – these studies can be retrospective or prospective

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2
Q

Prolonged SAM activation and Cardiovascular Reactivity

A

Cardiovascular reactivity = changes in cardiovascular function, measured by increases in heart rate, blood pressure, peripheral resistance, which occurs in response to short term stressors

  • if stress doesn’t go away our bp just remains high. Which can lead to the narrowing of arteries and therefore athlerosclerosis (thickening or hardening of the arteries caused by a build up of plaque in the inner lining of an artery)
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3
Q

Define Eustress

A

Eustress = positive stress that motivates and focuses energy; improves performance; is perceived as being within our coping abilities ; it feels exciting ; is a short-term experience

Eustress is more akin to challenge - like euphoric stress

Shows that not all stress is bad and that stress is a part of living

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4
Q

What are the Major Life Stressors According to the Social Re-adjustment Rating Scale (Holmes and Rahe, 1967)

A

Major life events are those like graduating, getting married, jail etc
Experiencing multiple or many negative major life events can increase ones risk of stress related illnesses.

Holmes and Rahe, 1967 produced a list that explained how disruptive or impactful certain major stressors are

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5
Q

Correlations linked to high ACE scores and Poorer life outcomes

A

A higher ace score was associated with ;
- higher likelihood for chronic depression
- higher rates of antidepressent prescriptions
- increased likelihood of smoking as an adult
- increased likelihood of being an alcoholic

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6
Q

Developmental Literature and Major Life Stressors

A

Most studies of development look at extreme or catastrophic forms of stress (major life events, like abuse, parental divorce, alienation etc). This is often measured through the Adverse Childhood Experiences (ACE) questionaire.

More Ace’s are linked to poorer mental and physical health in childhood and adulthood.
- a higher ace score is bad an adverse childhood is linked to producing an adverse outcome for both childhood and adulthood in both mental and physical health

The questions in the questionaire are aimed to denote instances of physical neglect or abuse or emotional factors

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7
Q

Define Stress (oxford and psychology definition)

A

Oxford; A state of mental or emotional strain or tension resulting from adverse or demanding circumstances
= not very specific and negates the fact that our body physically responds to stress (it’s not just an emotional/ mental reaction)

Psyc definition; A psychological and physiological reaction that occurs in response to a threat, i.e., when an individual perceives that enviornmental demands tax or exceed his or her adaptive capacity
– the perceived risk = something in the environment that is more taxing than your capacity

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8
Q

Distress Defined

A

= a negative stress that causes anxiety or concern; decreases performance; is perceived as outside of our coping abilities; feels unpleasant; can be short-term or long-term.

Distress is more akin to threat

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9
Q

Differences in Time Course with the SAM and HPA Axis

A
  • The SAM system - is mediated neurally; is quick (milliseconds to seconds) ; mostly linked with short-term bursts of activity ; focussed consequences for the cardiovascular system
  • The HPA axis - is mediated hormonally; is slower (minutes to hours); more systematic and complex relations with body; is involved in trying to restore allostasis; widespread consequences especially for energy utilization as it goes through the blood
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10
Q

Kaplan Manuck et al., 1983 Experimental Evidence Linking Stress to Atherosclerosis

A
  • Took 30 healthy macaques
  • randomly assigned these animals to either an unstressed control group and a stressed experimental group whereby the groups of monkeys that lived together were frequently switched (which created stress for the monkeys)
  • they did this for 21 months and they maintained a healthy diet
  • Measures;
    >accessed cholestrol (with monthly blood samples)
    > Blood pressure (taken bimonthly)
    > Thickness of the coronary artery (intimal thickness measured in autopsy)

-Results;
There were significant differences in thickness of the coronary artery in the monkeys
There were no differences in circulating cholestrol levels or bimonthly blood pressure readings
The precise mechanism postulated was that the stressed animals, due to repeated ‘arterial injury’ via ‘hemodynamic alternations’ (eg. cardiovascular reactivity due to stressful circumstances)

Implications for humans;
- this study forms the basis for a large body of literature suggesting that more frequent, pronounced and prolonged increased in blood pressure and heart rate due to SAM activation - initiate atherosclerosis and can lead to coronary heart disease.
- in humans this can occur over a 10-25 yr period

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11
Q

Define Acute Stress

A

= sudden, typically short-lives, threatening events
eg. giving a presentation, doing a job interview, having a heart attack

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12
Q

Allostasis

A

= homeostasis (kind of)

Peter Sterling and Joseph Eyer of the University of Pennsylvania + Bruce McEwen of Rockefeller University adapted homeostasis to a more expansive concept called allostasis based on three problems/ observations=

  • There cannot be a single optimal level i.e. different tasks would require different blood pressure levels for example. What is ideal under basal conditions is different under stress!
  • The given set point can be regulated by multiple different mechanisms each with their own consequence (instead of just a single local regulatory system). Allostasis is about coordinating multiple body systems and often involves behaviour.

-Another allostatic concept is that the body can set about changes in anticipation of an alteration to the set point.

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13
Q

What are the symptoms of prolonged cortisol activation

A
  • Cardiovascular reactivity due to facilitation of sympathetic activation
  • Insulin resistance due to increased utilization of glucose & fatty acids into bloodstream
  • Weight loss or gain, depending upon the stressor profile
  • Immune impairment
  • Growth problems (in children and adolescents) and reproductive problems (in men and women of reproductive age) due to reduced hormone activity
  • Cognitive problems (memory, attention) via destruction of neurons in the hippocampus
  • Depression
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14
Q

Cushing’s Disease

A

is a condition driven by prolonged chronic stress and cortisol secretion

this is linked to increased weight gain and a fat pad on the bad of the neck

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15
Q

Behavioural Changes in response to stress

A
  1. Changes in lifestyle factors; which in turn scale-back our healthy lifestyle
    In response to stress there can be an changes in the big four health behaviours:
    eg. increased smoking/vaping
    eg. drink more alcohol (particularly in mid-life populations but less so for young people -as tend to drink when go out and go out to celebrate less when stressed i.e. during exam season)
    eg. decreased exercise
    eg. poor diet (as there’s less time for healthy meals when we’re stressed)

These behavioural changes towards the big four can worsen or impair our health

  1. inattention leading to carelessness
    when we are stressed we are more careless so at greater risk of carelessness driven events like falling over or a car accident
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16
Q

Define a Stressor

A

A Stimulus or event that causes a stress reaction

17
Q

Trier Social Stress Test (TSST)

A

In this, you do a test people have to do a speech in front of a ‘cold,’ ‘stony faced’ panel and doing mental arithmatic in front of this same panel (eg. counting back in 13’s)

The video we watched looked at the relative performance of people in this task depending on their childhood stressors.

The test measures stress reactivity to a standard social stressor
- social support and physical touch can help mitigate the stress and improve the recovery

18
Q

HPA Axis and the effects of hormonal changes

A

The effects of activating the HPA axis;
- enhances the effects of epinephrine and norepinephrine on the heart (CRH) (increased feelings of activation/arousal; heart rate; blood pressure; and vascular resistance

  • increased utilisation of glucose and fatty acids into the bloodstream
  • decreased growth, reproduction hormones
  • decreased immune response /inhibited inflammatory response
19
Q

What are the Big Four Health Behaviours

A
  1. Smoking and Vaping
  2. Drinking
  3. Diet
  4. Exercise
20
Q

Caveats and Complexities in Crosswell and Lockwood 2020

A
  • there is no single best way to ‘objectively’ measure the stress response (no single stress biomarker; even cortisol)
  • even biomarkers as the sole marker of stress is problematic (can be unreliable with an unknown time course)
  • phsyiological, hormonal and emotional self-report are not always correlated. We aren’t a coherent organism. Their body may be stressed but they don’t feel it
  • stress responses vary to a large extent between-people (person A very different to Person B) and within-people (Stress is different in the same person depending on situation and timing)
21
Q

Perceived Stress Scale 4 (PSS-4)

A

The Perceived Stress Scale (PSS) is the most widely used psychological instrument for measuring the perception of stress. It is a measure of the degree to which situations in one’s life are appraised as stressful.

It is a self-reported questionnaire that was designed to measure the degree to which situations in one’s life are appraised as stressful.

Responses are coded from 0 - 4 then a respondants total score indicates their perceived stress level

22
Q

What are the 4 primary pathways that stress affects health

A
  1. Behavioural Changes
  2. Neural changes
  3. Hormonal Changes
  4. Immune Changes
23
Q

Minor Life Stressors

A

= Daily Hassles, rather than large events
- are things that can occur in our day-to-day lives
- these events are less severe than major stressors but are more chronic (frequent)
- the accumulation of less severe but more frequent hassles can be as harmful or more harmful to health as major life events

eg. job challenges, emails, cooking dinner every night, annoying flatmates

These minor stressors causes harm due to the subsequent amount of time that you spend in a stressed state as a result. If you’re not getting to recover from these stress events or calming down, then damage can occur

24
Q

Measuring Stress; What is the main idea from the reading by Crosswell & Lockwood

A

Main Idea; = stress idea is important to health, yet measurement of stress is problematic in health research, which can lead to inaccurate research findings. This article provide best-practise guidance on understanding and measuring stress.

25
Q

From the Crosswell & Lockwood reading, what are the fundaments of stress measurement

A

Stressor exposure vs stress response.
- exposure via life events checklists, exposure checklists and exposure to hassles
- stress response via self-report (emotional symptoms, perceived stress scale), behavioural coding (facial expressions), physiological recording (heart rate, blood pressure) or biomarkers (cortisol)
- a common way to evoke stress in the lab is via the Trier Social Stress test which incolves preparing a speech and doing mental arithmetic in front of a stony-faced panel

26
Q

Define Chronic Stress

A

= Ongoing environmental demands that persist and cause stress responses
eg. work stress, financial hardship, caregiving, noisy vs nosey neighbours, neighbours, living near roadworks etc

27
Q

Hormonal Changes with Stress

A

With stress, the hypothalamus launches a hormonal cascade, resulting in the relase of glucocorticoids from the adrenal glands into the bloodstream

  • cortisol increases access to energy reserves - via increases in blood sugar - among other things
  • hormonal changes take longer than the neural changes eg. minutes and hours, rather than seconds
  • In relation to SAM activation, causes activation of the HPA axis (to release cortisol from teh adrenal glands)
28
Q

Physiological changes in response to stress

A

AS shown in Sapolsky, stress influences two main physiologic systems
1. The neural based Sympathetic Adrenal Medulary (SAM) system)
2. The hormone based Hypothalamic Pituitary Adrenal (HPA) axis.
These systems function to get us out of danger (fight or flight) and also restore equilibrium (allostasis)

Actually, stress influences health through ‘multiple converging systems’ - SAM and HPA are only two of these converging systems (they’re 2 methods of many)

29
Q

Short Term Vs Chronic Activation

A

Short-term acute stressors allow adequate recovery time between stressors, however, variable and chronic stressors can throw these systems of balance

An example of short term vs chronic activation of stress
- prolonged activation of the HPA axis raises cortisol
- cortisol should drop after stress, but because stress is frequent, cortisol stays high even at night
- this means the body cannot recover from the stress and places us in chronic stress

30
Q

Sympathetic-Adrenal-Medullary (SAM) system

A

The adrenal medulla in the adrenal gland (at the top of the kidneys) secretes epinephrine (or adrenaline)

This works to;
- dilate the pupils
- inhibits salivation
- accelerates the heartbeat
- inhibits digestion

31
Q

What are the 4 fundamentals of stress measurement

A

> The stressor exposure vs the stress respone
Select the most appropriate stresor exposure for a population (eg. stressors will differ for mid-life samples or youth, or youth from low or high SES environments)
Consider the timescale for the stressor (chronic stress > Life events > Traumatic life events > Daily hassles > acute stress)
Identify the stress response type you want to measure (psychological eg. PSS, behavioural eg. behavioural coding and fMRI, cognitive eg. performance testing, physiological eg. heart rate, BP, cortisol or hormonal eg. cortisol)

32
Q

Effects on the body from activation of the SAM pathway

A

effects of sympathethetic-adrenal-medullary (SAM) system; preparing the body for flight or fight

  • increased feelings of activation/arousal
  • increased heart rate
  • increased blood pressure and vascular resistance (something exercise doesn’t increase)
  • increased sweating
  • increased attention and pupil dilation
  • dicreased digestion

Activation of this pathway is very rapid - on a mS scale

33
Q

Major Life Stressors and Health Outcomes, Rahe et al., 1964

A

Rahe and Holmes 1967 checklist was also used in assessing whether people were at a greater risk of illness or disease when they’d been exposed to more stressors. This case-controlled study was one of the first to explore this

It found that people with tuberculosis were more likely to have had stressful life events in years 1-5 prior to illness onset than the controls
This is a non-causal association as it’s a case-control study and we cannot rule out confounds. Interestingly similar patterns have been found relating stress and disease/illness in cohort and prospective studies.

Since the earliest tuburculosis study, research examined a link between cardiac patients and stressors