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Stress: Illness and Coping - Coggle Diagram
Stress: Illness and Coping
Definition of stress
The physiological or psychological response to internal or external stressors. Stress involves changes affecting nearly every system of the body, influencing how people feel and behave. By causing these mind-body changes, stress contributes directly to psychological and physiological disorders and disease and affects mental and physical health, reducing quality of life.
Discriminating
between stimulus -
process - response
Stress can be a stimulus, process, and response.
Major life events, every day stressors
A very well-developed stress response that is unsuitable for the things we experience in daily life.
Psychosocial determinants of stressful events:
Environmental: overcrowding, noise, SES, pollution, traffic
Family: new members, divorce, illness, relationship breakdown
Social: employment demands, multiple roles, discrimination, status, loneliness, social isolation, rejection- social pain, acculturation (moving cultural contexts)
Individual: performance, illness, time pressure, individual characteristics (experience, resilience).
Stress as a stimulus
Traumatic, catastrophic, crisis events
A traumatic event is an event where the individual is exposed to death, threatened death, actual or threatened serious injury or sexual violence.
Direct exposure: experiencing in person.
Indirect exposure: happened to a loved one; repeated indirect exposure due to profession (first responders, journalists, etc.)
How stressful events impact health
What type of stressor has the most impact on health?
Daily hassles are stronger predictors of psychological well-being than major life events
Cumulative stress exposure increases the risk of harm to health.
Impact of trauma on health:
Impact of multiple traumas (compound-trauma)
Every exposure to a new traumatic event increases the risk for mental and physical health problems
Dose-response relationship.
ACE = adverse childhood experiences > health is better when you have no ACE, and health is worse + likelihood of bad health outcomes is increased by 5+ ACE.
Increases depressive symptoms, anxiety, alcohol use, etc
Multifinal risk factor > multiple resulting outcomes
Populations with high exposure to trauma have higher rates of ptsd
Homeless people = 27.38% prevalence
First Nations people = 19-55% prevalence
refugees/asylum seekers = 31% prevalence
Prevalence in the general population = 3-5% prevalence.
interaction between categories of stressful events
Psychiatric epidemiology studies risk factors for psychological disorders
Trauma is a risk factor for poor mental health > has a direct effect, but can increase the effect of daily stressors, leading to mental health problems.
Acute vs long-term stressors
Acute stress response to trauma is associated with poorer general physical health, increased pain and disability, lower quality of life, higher all-cause mortality, and more cumulative psychiatric disorders.
Chronic stress has been associated with lower survival rates, higher heart rate and blood pressure (poorer cardiac health), age-related diseases such as alzheimers, and psychological disorders (esp depression, anxiety and ptsd).
Positive events can also be stressors.
Stress as a process
Factors that influence appraisals:
We start to think about our resources when we get to appraisal.
Support, financial, resilience, etc.
Make an appraisal of how well-equipped you are to deal with the stressor.
Situational characteristics like
uncertainty, timing, controllability,
and social factors
uncertainty
Uncertainty stress is more strongly associated with all categories of unintentional injury; life stress only with traffic injury.
Walking into things, tripping, etc.
The time refugees spend exposed to uncertain stress (migration status uncertainty) predicts physical and emotional health.
Chronic stress and uncertainty:
Understanding the maintenance of uncertainty under neutral or event circumstances > uncertainty about your SAFETY not about a THREAT
As a species, this is our default response > evolutionarily, it was better to be safe than sorry. Only once we have repeated experiences of safety do we downregulate this response.
Being constantly ready to ensure safety is not always metabolically costly, because it's INHIBITORY instead of EXCITATORY.
The activation of a response is more metabolically costly than the constant running of a response.
“Off” periods are much shorter > when there is TRUE safety.
More likely to perceive something neutral as negative instead of positive
timing of events
Events occur earlier or later than expected, like the death of a child
Compounding events, like getting sick during exam week
Developmental stage of stress response > early life stress can have detrimental effects
controllability
Differentiating between objective and perceived controllability.
Perceptions of controllability influence coping
If a stressor is perceived as controllable, individuals will adopt more problem-focused strategies compared to emotion-focused coping strategies.
Controllability and related choice of coping strategies are also influenced by causal attribution
Attribution of cause to the self leads to more problem-focused vs more avoidant coping for unknown causes.
We can exert control in different ways:
Personal control: feeling that one can make decisions to produce desirable outcomes and avoid undesirable ones
Behavioural control: concrete action to reduce the impact of a stressor
Cognitive control: engage in thought processes to modify the impact of a stressor, more effective in a low control environment.
If perceived to have some control, it is protective against traumatic stress amongst torture survivors > perceived controllability is more strongly related to ptsd than the severity of the torture.
Individual characteristics like self-efficacy,
personality traits, and capabilities
like experience with effective
stress management.
Self-efficacy:
Perceived ability to organise thoughts and behaviours in a way to cope with potentially ambiguous and stressful situations.
Following acute stress induction > the cold pressor
Randomly assigned to
Cognitive pain control intervention > enhancing self-efficacy to deal with stressors
Placebo analgesic
No instruction control
Self-efficacy causes a significant change > boosts capacity to tolerate physical stressors
Self-efficacy shows moderate associations between health-related intentions and behaviours.
Better health-related quality of life in cardiovascular disease and chronic obstructive pulmonary disease, and shows large associations with distress in cancer patients.
Self-efficacy can be improved with interventions.
personality
Personality characteristics can impact on primary secondary appraisals
Self-esteem > whether an event is appraised as a challenge vs a threat
Motivation > whether the event is appraised as harmful or a challenge according to whether the stressor will impact on realisation of goals
Belief system or cultural values > what is considered stressful
Hardiness and optimism > recognising internal resources to cope
Personality types.
Stress as a response
Neurobiology of stress
Fight, flight or freeze
immediate response to a threat from the hypothalamus, which then activates the sympathetic nervous system, which activates the adrenal medulla, releasing norepinephrine and epinephrine and adrenaline.
Activation of the sympathetic nervous system activates glands and smooth muscles.
Bodily impact of hormones: Faster breathing, bladder relaxation, pupil dilation, digestion slows, and heart rate accelerates.
The longer you’re in fight or flight, the worse your health can become.
Cortisol
Operates through a feedback loop with the HPA axis.
Turns the sympathetic nervous system off.
Cortisol can be problematic if it doesn’t send the signal to reduce fight or flight behaviours.
The suprachiasmatic nucleus central clock receives light–dark signals that, in turn, influence hypothalamic–pituitary–adrenal [HPA] and sympatho–adrenomedullary activity leading to circadian CORT[ISOL] production.
CORT activates glucocorticoid receptors in peripheral tissues, which synchronises peripheral clocks and downstream metabolic, cardiovascular, neuronal and immune pathways.
Other Zeitgebers such as food, temperature and social cues can also entrain or influence the entrainment of clocks and can alter the output of these downstream pathways.
Cortisol is secreted in a circadian rhythm characterised by a nadir or quiescent phase during the inactive period (overnight while sleeping in humans). An anticipatory rise in CORT levels occurs before waking, followed by the circadian peak of secretion at the start of the active period.
Stress as allostatic load:
Repeated hits from multiple or chronic stressors > no chance to recover
Poor adaptation to repeated stressors leads to sustained stress over time, with no adjustment
No recovery following stress means a maintained high physiological response
Unable to respond effectively to stressors in the first place causes maladaptive compensatory mechanisms.
Diathesis stress model:
When the environment is positive and there is no stress, the vulnerable and resilient individuals are at equal health, but when there is stress, the vulnerable individual is worse off.
Stress and immune system reactivity
Acute and chronic stress can suppress immune system function inflammation leading to health issues & disease
Cytokines: chemicals released by immune system and communicate with nervous system (e.g. proinflammatory cytokines, incl. interleukins) feeling sick, glum, social withdrawal, fatigue, malaise
May be the key mechanism linking immune and nervous systems
Stress can also affect recovery and healing rates
healing from physical wound took 40% longer during a stressful (i.e., exam) period vs. non-stressful (i.e., holiday) period
Positive affect appears to have a buffering effect on the impact of stress on inflammation
Associations between affective states and inflammation are complex, timing of affect and inflammation measurement matters
Preliminary evidence that greater emodiversity is associated with lower markers of inflammation
Sustained HPA-axis engagement suppresses immune system lymphocytes (T-cells: Identify germs; B-cells: Attack germs)
Stress and infectious disease
When under stress, more likely to develop infectious diseases (e.g. flu, cold, virus).
Duration of stressor – chronic stressors > 1 month increased risk for colds
Stress can weaken the strength of vaccination response, including flu vax
Stress can influence the progression of infectious disease, including HIV, herpes, respiratory diseases
Can predict symptom outbreaks and treatment success
Stress and cardiovascular disease
Higher heart rate and blood pressure during stress and recovery increased risk of CVD
Stress causes increased:
Platelets & clotting factors in blood > raises stroke risk
high blood cholesterol > raises stroke risk
Atherosclerosis (thickening arteries): Animal studies show major social changes (i.e., stress) led to atherosclerosis due to repeated SNS activation
Rigid/low heart rate variability (also associated with poor emotion regulation and mental health)
Stress contributes to CVD via:
Increased inflammatory markers, stress hormones and CV reactivity
Cardiac arrhythmia
Poor lifestyle choices (i.e., indirect pathways)
Type d- distressed personality
Increased risk for illness: 1 in 4 coronary hear disease patients have Type D personality
Type D is part of the European Cardiovascular prevention guidelines to screen for risk
Measuring stress
Physiological arousal: objective markers
systolic/diastolic blood pressure
Heart rate/heart rate variability
Skin conductance response
Stress hormones such as salivary cortisol
Self-reported stress
Coping
with stress
The process by which people try to manage the perceived discrepancy between the demands of a situation and the resources available to them.
Problem-focused coping:
Direct action
Reduce demands of the stress or increase resources
Emotion-focused coping:
Adjust perceptions of risk or emotional reactions via behavioural or cognitive strategies
Hundreds of emotion-focused strategies
Many known as emotion-regulation strategies, including: cognitive reappraisal, acceptance, suppression, avoidance, rumination
Some appear more adaptive and others more maladaptive
Strong association between habitual ER strategy use and mental and physical health (via inflammation)
Avoidant coping:
Denying, ignoring, neglecting problem
Occasionally effective in the shortterm, but not the long-term
Buffering hypothesis of social support:
Social support provides protection against the negative effects of high stress, reducing its impact on health (little effect during low stress)
Changes primary appraisal
Enhances coping (i.e., secondary appraisal) – Provides social resources to assist coping with stress
Direct effects hypothesis:
Social support has benefits for health and well-being regardless of level of stress
Builds self-esteem & sense of belonging
Health benefits independent of stress
Can lead to healthier lifestyle (e.g., staying well for loved one)
Harmful effects of lack of social support
Ongoing loneliness increases risk of cardiovascular disease
Cultural differences:
Collectivistic cultures prefer to preserve social harmony and reduce the impact of personal stress on others
Individualistic cultures like to share the burden of stressful circumstances for personal benefit
Stress
management
strategies
What doesn’t work:
‘Just think positively’ ‘Stop worrying’
Avoidance, distraction and numbing
Anti-anxiety medication > temporary
Benzodiazepines – reduce anxiety, panic, insomnia
Beta-blockers – reduced arousal not stress
What works:
Cognitive restructuring: > Getting evidence for and against a negative thought.
Guided problem solving
Guided muscle relaxation: > systematic tensing and relaxing of muscle groups
Increases awareness of muscle tension
Daily practice associated with decreased muscle tension
Health benefits in patients with COVID-19; cancer; mental health problems; chronic obstructive pulmonary disease; abdomical surgery
Decreased pain, Improved sleep, Decreased fatigue, Reduced stress & anxiety, Improved quality of life