Stress Flashcards
What is stress? When do you experience it?
A state of physiological or psychological strain, caused by a stressor, that disturbs the functioning of the body - it’s the body’s reaction to an event.
-You experience stress when there is a mismatch between the demands made upon an individual and their ability to meet these demands.
What causes stress?
Stressors - anything that induces stress.
-E.g an event.
How can stress be a good thing? What can excessive stress lead to? Why are psychologists interested in stress?
A little bit of stress can be a good thing - it can boost performance, give you motivation and increase productivity.
-However, different people have different thresholds and excessive stress can be unhealthy for mind and body, leading to long term illness. E.g many cases of depression and anxiety are due to stress.
-Ultimately, if psychologists can better understand stress and how to treat it, there will be a less stressed workforce and society - positive implications on the economy.
What 2 pathways of the ANS are involved in the physiological stress response?
1) SAM - Sympathomedullary Pathway
2) HPA / PAS - Hypothalamic-Pituitary-Adrenal System / Pituitary Adrenal System
What is the function of each pathway? How do the 2 pathways differ?
-SAM pathway - activates the sympathetic branch of the ANS - controls the body’s initial response to an acute stressor (short-term) - triggers fight or flight response.
-HPA / PAS - activates the parasympathetic branch of the ANS - controls the body’s response to a chronic stressor (long-term) - helps the body to cope with the demands of a persistent stressor and to eventually bring about a normal state (homeostasis) - rest and digest system.
-The SAM and HPA / PAS pathways actually start at the same time - but the PAS takes longer to activate as it involves hormones which travel via the blood, as opposed to the electrical signals involved in the SAM system.
How does the SAM pathway work? How fast is it?
SAM - acute stressor perceived - fight or flight response triggered:
1) The amygdala sends a distress signal to the hypothalamus.
2) The hypothalamus sends an electrical signal to the pituitary gland.
3) The pituitary gland transmits the electrical signal to the adrenal medulla, via the sympathetic ganglia.
4) The adrenal medulla is stimulated (sympathetic arousal) and releases adrenaline (and also noradrenaline) into the bloodstream.
5) Adrenaline travels to the vital organs via the bloodstream - a sympathetic state is induced.
-It’s faster acting (instantaneous) than HPA / PAS (because electrical signals are involved), but doesn’t stay around for long.
What physical state does adrenaline cause? What are the physical effects?
Sympathetic state:
-Increased heart rate/breathing rate - greater flow of oxygenated blood.
-Dilated pupils - get as much light as possible.
-Glycogen rapidly converted into glucose.
-Sweat production increases.
-Inhibited digestion - diverts blood away.
-Inhibited saliva production - dry mouth.
-Contracts the rectum.
When does the sympathetic response to a stressor end?
Either when the parasympathetic system takes over (no longer a threat), or if the stress becomes chronic.
How does the HPA system work? How fast is it? How does the HPA system use a negative feedback loop to self-regulate?
HPA - activated by a long-term stressor:
1) Hypothalamus releases corticotropin-releasing factor (CRF).
2) CRF triggers/stimulates the anterior lobe of the pituitary gland to release adrenocorticotropic hormone (ACTH) into the bloodstream.
3) ACTH levels are detected by the adrenal cortex which secretes corticosteroids such as the the hormone cortisol in response.
4) A parasympathetic state is induced - any fight or flight response is reversed - rest and digest response activated as priority is for energy conservation.
-Think about HPA or PAS as the resting state - but its initial effects are actually to help prepare the body for the fight or flight system.
-HPA takes longer to activate (20 minutes) compared to SAM because it is slower as endocrine glands and hormones involved - the HPA and SAM response actually start at the same time. The effects of the HPA response are longer-lasting however, persisting for several hours or longer.
-Negative feedback loop - levels of cortisol in the bloodstream are then monitored back to the hypothalamus and pituitary gland, which can then inhibit the production of CRF (also known as CRH) and ACTH if cortisol levels are too high.
What physical state does the HPA system eventually cause when there is no longer a threat? What happens to control the body’s longer response to stress?
Parasympathetic state:
-Decreased heart rate/breathing rate - normal flow of blood.
-Constricted pupils.
-Sweat production decreases.
-Stimulates digestion - blood needed for digestion.
-Stimulates saliva production.
-Relaxes the rectum.
-However, if the stressor is chronic or long-term, primarily the HPA system needs to help the body cope with the demands of the stressor - it does this through the role of cortisol.
What is cortisol? What are some of its general functions?
Cortisol is a hormone produced by the adrenal cortex.
-It is often called the stress hormone, due to its central role in helping the body cope with stressors by controlling the body’s use of energy - it also has a number of other general functions.
Functions:
-Regulates the body’s use and metabolism of fats, proteins and carbohydrates.
-Regulates blood glucose - a glucocorticoid.
-Maintains blood pressure and cardiovascular functions.
-Helps reduce inflammation - it does this by slowing down the immune system (suppressing it) - cortisol suppresses leucocyte activity and reduces the production of T cells.
How are cortisol levels monitored? What can happen if levels are too high or too low?
Cortisol is always in the blood - its levels are monitored by the hypothalamus and pituitary gland - but cortisol levels can be too high or too low.
-Too low = Addison’s disease - adrenal cortex cannot produce any or enough cortisol so the body cannot mobilise energy to deal with the stressor.
-Too high = Cushing’s syndrome - body makes too much cortisol over a long period of time - i.e in response to long-term stressors (chronic stressors).
What is the role of cortisol in the stress response? How is this advantageous in the short-term?
-Cortisol provides a quick burst of energy and permits a steady supply of blood sugar - as a glucocorticoid it increases the availability of blood glucose to the brain - this increases blood sugar levels and restores energy supplies to power the stress response.
-Constricts the blood vessels to increase blood pressure so that oxygenated blood can be delivered to the muscles.
-In the short-term this is advantageous for fight or flight and is not a problem.
What happens if there are high cortisol levels over a long period of time? How can it be damaging?
If the body is consistently responding to stress (i.e when chronic stress is experienced), high cortisol levels can be damaging:
-Elevated cortisol over the long-term consistently leads to increased blood sugar levels (which can lead to impaired cognitive ability), disruption of sleep, reduced immune functioning (cortisol suppresses leucocyte activity and reduces the production of T cells) and type 2 diabetes (which in turn can lead to atherosclerosis and CHD).
-Arterial constriction and high blood pressure can lead to blood vessel damage and the build up of plaque - this can lead to cardiovascular disorders as not enough blood can get through.
-Also, by suppressing the immune system to reduce inflammation, over time cortisol can reduce immune functioning.
What 2 studies show how increased levels of cortisol can cause problems?
1) Newcomer et Al (1999) - gave participants cortisol to replicate blood sugar levels similar to those experiencing major stress events - found that their ability to recall prose passages was poorer compared to those only given cortisol to produce a stress response similar to minor events.
2) Vgontzas et Al (2013) - found that chronic insomniacs had increased activity of their PAS - proves that high cortisol levels can lead to sleep disruption.
What are the strengths and limitations of research into the physiological stress response?
Strengths:
-Treatment of Addison’s disease - adrenal glands cannot produce cortisol so the body cannot mobilise energy to deal with the stressor - individuals can self-administer hydrocortisone daily and must be aware of stressful situation when they might need an extra injection.
Limitations:
-Physiological explanations ignore psychological factors - e.g cognitive appraisal - working out whether a stressor is a threat.
-Speisman et Al (1964) - changes to heart rate whilst watching a gruesome medical procedure depended on the students interpretation of what was happening - i.e heart rate increased if they believed it to be traumatic, and heart rate decreased if they were told that the procedure was part of a voluntary and joyful rite of passage - these findings suggest that these changes cannot purely be explained a physiological theory, but also by psychological factors like cognitive appraisal.
What model did Hans Selye develop in 1936?
The General Adaptation Syndrome (1936), or GAS model.
*Likely to come up
How did Selye view stress? What did he believe was the purpose of this adaptation?
Selye viewed stress as the body’s attempt to adapt to a stressor - a non-specific response to any stressor.
-In the short-term (acute stressor), the adaptation protects the body.
-But in the long-term, serious damage can occur if the stressor persists.
What experiment with animals did Selye base his model on?
Rat experiments:
-Selye exposed rats to surgical injury, excessive muscular exercise or injected them with sublethal doses of various drugs.
-He found that no matter what he did to the rats, they all shared the same collective response (a syndrome), even when the rats were given harmless injections: stomach ulcers, enlarged adrenal glands and a shrunken thymus gland.
After working with hospital patients and seeing a similar pattern of results, Selye concluded that regardless of the stressor, the same general, non-specific response is the outcome - the GAS model was born.
What are the 3 stages of the General Adaptation Syndrome (GAS)?
1) Alarm reaction - threat/stressor recognised.
2) Resistance - body attempts to adapt to the stressor by resisting its impact.
-If the stress continues:
3) Exhaustion - the body cannot maintain normal functioning.
What happens at the alarm reaction stage? What happens in terms of the body’s resources?
-When a stressor is perceived, the immediate reaction is shock.
-At this time, the body’s resources (energy) are briefly decreased (i.e not used / resistance is lowered) before quickly recovering.
-Fight or flight system (SAM) deployed - adrenaline and noradrenaline produced. Heart rate, blood pressure, breathing rate and sweating increases. Sugar is released into the blood.
-PAS also deployed to help cope with the demands of the fight or flight system in response to the stressor.
What happens at the resistance stage? What happens in terms of the body’s resources?
-After the initial shock, the body begins to repair itself as the parasympathetic nervous system takes over - focus now is to conserve energy for the long term (in case the stressor persists - chronic).
-Resistance peaks at this stage as the body attempts to adapt.
-The body’s resources (sugars, neurotransmitters, proteins and hormones) are fully mobilised.
-The individual appears to be coping as the alarm symptoms disappear (heart rate reduces), but the body’s resources are being consumed at a potentially harmful rate.
-Resources begin to deplete - e.g cortisol (which is primary concerned with the body’s use of energy) produced in huge quantities to help cope, but will soon be depleted - the body cannot continue to resist the stress indefinitely because it cannot generate new resources.
What happens at the exhaustion stage? What happens in terms of the body’s resources?
-This stage is the result of chronic stress. If the stressor has continued to persist, exhaustion occurs.
-Struggling with stress for long periods leads to the depletion of the body’s resources - they are completely drained.
-Resistance plummets and gives way to exhaustion.
-Damaged and enlarged adrenal glands cause the parasympathetic branch to fail and the alarm symptoms from the first stage begin to reappear (increased cortisol can also cause problems).
-The physical effects of this stage also weaken/compromise the immune system as the production of proteins necessary for its functioning have been reduced. This puts the body at risk of stress-related illnesses, or ‘diseases of adaptation’ as Selye called them - e.g raised blood pressure, coronary heart disease, ulcers and depression.
What mistake did Selye make about the exhaustion stage?
Selye said we are depleted of resources - this is not the case.
-Whilst it may appear that way, stress only lowers immunity and does not directly cause disease.
-E.g ulcers are caused by bacteria - the bacteria can grow if the immune system is weakened - therefore stress is only linked indirectly.
What are the strengths and limitations of Selye’s GAS model (1936)?
Strengths:
-Highly scientific.
-Identified GAS as a non-specific response.
Limitations:
-Ignores individual differences - GAS may not be a general response to all stressors - different types of stressors have different effects, and also different people may react differently to the same stressor.
-E.g Mason (1971) - extreme cold increased cortisol levels, extreme heat reduced them - challenges the validity of GAS - shows that specific stressors can produce specific responses .
What cells form the basis of the immune system?
White blood cells (leucocytes) - our defensive barrier against pathogens (disease-causing microorganisms).
What are lymphocytes? What are 3 types of lymphocytes?
Lymphocytes are white blood cells that produce antibodies to destroy pathogens.
1st line of defence (pathogen not been there before):
1) Natural killer (NK) cells - destroy pathogen-infected cells - prevent viruses and cancer cells from spreading.
Second line of defence (immunity - recognises antigen):
2) T cells - Thymus gland secretes the hormone thymosin which produces T cells.
-There are several types of T cells - memory T cells recognise pathogens, killer T cells destroy infected cells by locking onto them.
3) B cells - create antibodies.
What is immunosuppression in terms of stress? What are some examples of chronic stressors?
Immunosuppression is when the immune system is prevented from working efficiently due to long-term (chronic) stress.
E.g bereavement, marital disharmony, serious work problems, exam time, carers etc…
-Whilst short-term stress is not dangerous, its the effects of long-term stress that can leave the body vulnerable to infection and disease (bacterial and viral).
How does stress cause immunosuppression? What is the role of cortisol? What type of relationship exists between stress and immunosuppression?
-PAS system produces cortisol in response to a stressor. More cortisol produced if stressor persists.
-Cortisol suppresses leucocyte activity and reduces the production of T cells.
-This is because long-term stress shrinks and damages the thymus gland, which facilitates the production of T cells.
-Therefore, the number of white blood cells available to fight foreign antigens is reduced.
-This leads to greater vulnerability to the effects of pathogens - immune functioning suppressed.
-This relationship is purely correlational - studies point to an increased risk rather than cause and effect - there are of course other mediating factors (e.g personality, lifestyle) - it would be unethical to put people under stress in experiments.
What study produced a graph showing the relationship between the duration of the stressor and immune functioning?
Merson (2001):
Which researcher conducted a number of studies into the effect of long-term stressors on immunosuppression?
Janice Kiecolt-Glaser - looked at the effect of chronic stress on immunosuppression when: preparing for exams (1984), and caring for ill relatives (1995).
How did the Kiecolt-Glaser (1984) study work? What were the findings? What are the main evaluation points?
Kiecolt-Glaser (1984) - a natural experiment - investigated the effects of exams on 75 medical students:
-The participants gave blood samples twice - one month before the exams started (low stress) and on the day of the first exam (high stress).
-They also completed questionnaires measuring sources of stress and self-report psychological symptoms.
Findings:
-The activity of NK cells and killer T cells decreased between the first and second samples - evidence of immunosuppression due to stress.
-This decline was most apparent in students who reported feeling most lonely, as well as those who were experiencing other stressful life events - evidence of other factors moderating stress.
Evaluation:
-Only shows correlation - not causation.
-Natural experiment - stress not artificially induced.
How did the Kiecolt-Glaser (1995) study work? What were the findings?
Kiecolt-Glaser (1995) - again a natural experiment - investigated the effects of stress on wound healing - compared the healing of caregivers looking after a relative with Alzheimer’s, with a matched group of non-caregivers.
-13 women in experimental group. 13 women in control group - (gender bias).
-A punch biopsy (small wound) was made on each arm and all participants were given a 10-item/question stress scale.
Findings:
-Both tests indicated that the experimental group (the caregivers) showed higher stress levels than the control group.
-Wound was photographed regularly - 48.7 days to heal for caregivers, 39.3 days for control group. The carers also had a larger average wound size.
What study did Cohen (1993) carry out into common cold virus? What did he conclude?
Cohen (1993) - investigated the role of general life stress on vulnerability to the common cold virus.
-Combined the responses of 394 participants into a stress index - participants then exposed to the common cold virus - 82% became infected.
Findings:
-Cohen found that the chance of developing a cold was significantly correlated with stress index scores - he concluded that life stress reduces the effectiveness of our immune system.
What are the strengths and weaknesses of research into immunosuppression?
Strengths:
-Kiecolt-Glaser’s research has led to students taking a relaxation training programme - their immune functioning was better.
Weaknesses:
-Correlation does not mean causation.
-Some research points to acute stress having immunoenhancing effects - different to the effects of chronic stress.
-E.g Dharbar (2008) - found that, in rats, mild stressors had a positive impact on the immune system - the bloodstream and body tissues were flooded with lymphocytes as the body was prepared for physical damage.
How does acute stress cause cardiovascular disorders?
-Acute stress activates the sympathetic branch of the nervous system - adrenaline is produced causing an increase in heart rate and blood pressure.
-The blood vessels constrict to facilitate the rise in blood pressure.
-Sudden emotional arousal is linked to heart attack (myocardial infarction), where the heart muscle is damaged due to lack of oxygen caused by blockages in coronary arteries - i.e CHD).
How does chronic stress cause cardiovascular disorders?
If a stressor persists over a long period and becomes chronic, the fight or flight system and its effects can become damaging.
-An increase in heart rate wears the blood vessels and increases heart rate.
-Repeated high levels of adrenaline affect the heart muscles directly.
Cardiovascular disorders:
-Coronary Heart Disease (CHD) - caused by atherosclerosis - the narrowing of the blood vessels due to a build up of plaque. Stress leads to increased glucose levels, leading to clumps of plaque blocking the blood vessels. CHD can lead to heart attack (myocardial infarction).
-Hypertension (high blood pressure consistently maintained over a period of time).
-Hypertension begins the process of arteriosclerosis - the hardening and thickening of the arteries due to the buildup of plaque in the inner lining of an artery caused by high blood pressure.
-Stroke - damage caused by disruption of blood supply to the brain.
Cortisol:
-Cortisol is produced by the parasympathetic branch of the nervous system - cortisol causes an increase in blood glucose levels (it’s a glucocorticoid) which causes the build up of plaque over time. As well as this, cortisol as a glucocorticoid can lead to type 2 diabetes, which in itself predisposes for atherosclerosis and CHD.
-In the short-term, cortisol constricts the blood vessels to increase blood pressure so that oxygenated blood can be delivered to the muscles. Over time, arterial constriction and high blood pressure can also lead to blood vessel damage and the build up of plaque - leads to CHD.
What lifestyle factors are implicated in cardiovascular disorders? What does this show about the relationship between stress and cardiovascular disease?
Lifestyle factors such as smoking, alcohol, diet etc - highlights that the link between stress and cardiovascular disorders is purely correlational, rather than a cause and effect relationship.
-However, because stress is associated with greater alcohol consumption, caffeine intake and smoking, this shows how stress can lead to behavioural factors linked to CHD.
What study did Williams et Al (2000) conduct looking into anger?
Williams et Al (2000) - investigated if anger was linked to heart disease.
-Gave a questionnaire to 13,000 people - none had heart disease - the questionnaire contained a 10 question anger scale.
Findings:
-After 6 years the health status of the participants was checked - 256 had developed heart attacks - those who had scored highly on the anger scale were 2.5x more likely to have had a heart attack.
-As anger is a form of stress (the ‘fight’ in fight or flight), it shows that chronic stress can cause cardiovascular problems.
What study did Wilbert-Lampen et Al (2008) conduct looking at football?
Wilbert-Lampen et Al (2008) - looked at incidences of heart attacks in German football supporters during matches played in the 1996 World Cup.
Findings:
-When Germany played, cardiac emergencies increased by 2.66 times - appears that acute emotional stress can more than double your risk of a cardiovascular event (although there could be other factors like increased alcohol consumption and drug use on match days).
What study did Yusuf et Al (2004) conduct looking into the effects of long-term stress on cardiovascular disorders (CVDs)?
Yusuf et Al (2004) - participants from from 52 countries of differing cultures included.
-15,000 people who had had a heart attack (myocardial infarction, MI) were compared with a similar number who had not.
Findings:
-Several chronic stressors linked with MIs - e.g workplace stressors and stressful life events.
-Yusuf concluded that chronic stress contributes to the onset of, and severity of, CVDs.
What are the strengths and weaknesses of research into cardiovascular disorders?
Strengths:
-Lots of research supporting the link between stress and CVDs.
Weaknesses:
-Stress increases the risk of CVDs - it is not a direct causal factor - its effect is mediated by personality type and lifestyle.
-There are genetic factors that predispose individuals to developing disorders like CHD.
What is a source of stress?
Any feature of the environment that causes stress - includes workplace stress, minor hassles and major changes in our lives.
What are life changes? What are some examples?
Significant and relatively infrequent events/changes in people’s lives - a common source of stress.
E.g marriage, divorce, a bereavement, a new arrival in the family, a better or worse financial state.
Why can life changes cause stress? What do life changes require us to do?
Life changes can be major stressors because they are not everyday events.
-They are stressful because they cause us to make some kind of psychological adjustment to adapt to changed circumstances.
-The bigger the changes, the greater the adjustment and associated stress.
*Note - it’s not about a life change requiring more psychological energy, it’s about it requiring a psychological adjustment.
What happens when multiple life changes happen at once? How do the effects of positive and negative life changes compare?
The effects are cumulative - all the life changes add together because, jointly, they require more change/adjustment to adapt.
-It doesn’t matter if the life change is positive or negative - both are stressful because they place new demands on the individual, who has to make a significant adjustment in order to adapt.
-However, of course, some life changes and events mean different things for different people.
What were Holmes and Rahe curious about? What did they believe?
Holmes and Rahe were both heart doctors.
-They were interested in the impact of life changes (the source of stress) on illness - they believed that people were more likely to show symptoms of illness following a period of stress.
What did Holmes and Rahe (1967) do? How did they begin to devise a scale?
-Holmes and Rahe (1967) examined the records of 5000 patients and made a list of 43 life events/changes of varying seriousness which seemed to cluster in the months preceding the onset of the patients’ illness (heart disease).
SRRS:
-To make their observations objective, Holmes and Rahe needed to devise a scale.
-They assigned marriage an arbitrary value of 500 and then asked 400 ‘judges’ to assign a number to each of the other life events in terms of the intensity and the length of time necessary to accommodate regardless of the desirability of the event relative to marriage.
-Holmes and Rahe took the average (mean) values assigned to each event and divided by 10.
-Each of the 43 life events was ranked in a scale knows as the Social Readjustment Rating Scale (SRRS).
What did Holmes and Rahe’s Social Readjustment Rating Scale (SRRS) look like? What are some of the key life changes in the scale?
The Social Readjustment Rating Scale (SRRS) - a self-report method of measuring life changes in relation to stress.
Each of the 43 life changes was accorded a value known as a life change unit (LCU) - a number corresponding to the intensity and the length of time necessary to accommodate/adjust - not to do with how desirable the event is.
-Death of spouse - 100 LCUs (highest on scale - so most amount of adjustment needed - twice as much as marriage).
-Minor violations of the law - 11 LCUs (lowest on scale - so least amount of adjustment needed).
-Marriage - 50 LCUs - only 6 events judged to be more stressful than marriage.
-Changing job - 36 LCUs.
-Christmas - 12 LCUs - not everyone celebrates Christmas (westernised scale).
How did Holmes and Rahe (1967) apply the scale to their patients? What were the findings?
Holmes and Rahe added up the experiences of the patients in the 12 months preceding their illness (heart disease), to form an overall LCU score.
This overall LCU score was essentially a measure of life stress that patient had experienced in the preceding year.
Findings:
-An LCU score of under 150 (for the preceding 12 months) increases the chance of stress-related illness by 30%.
-An LCU score of 200-300 increases the chance of stress-related illness to 50%.
-An LCU score of over 300 increases the chance of stress-related illness to 80%.
-The range of health problems included sudden cardiac death, heart attacks, tuberculosis, diabetes, leukaemia and sports injuries.
What did Holmes and Rahe (1967) conclude?
Holmes and Rahe (1967) concluded that:
-Stress can be measured objectively as an LCU score - the amount of change a person has had to adjust to during a 12-month period.
-A person’s chance of becoming ill following this period corresponds to a probability. This probability is a risk factor. E.g LCU over 300 = 80% risk.
What are the strengths and weaknesses of Holmes and Rahe (1967) and the SRRS for studying life changes as a source of stress?
Strengths:
-Validity - self-report measures like questionnaires have high validity - stress is a very personal experience and therefore self-report is very appropriate.
-SRRS still used in some form today - easy to use - participants simply indicate which life changes apply in the period of time - typically 12 months.
Weaknesses:
-The SRRS is a self-report measure and is retrospective - has problems with social desirability and accuracy of recall, which reduces the reliability of the scale for measuring life changes.
-The SRRS does not show that the life events cause illness - life events are correlated with illness - the calculated probability is only a risk factor - other factors may be involved.
-Individual differences not acknowledged - some people see different events in different ways - so to broadly assign a value is problematic - e.g some people might celebrate a divorce.
-Validity - internal validity questionable as the SRRS does not distinguish between positive and negative events.
-Reliability - test-retest varies - could be because of all the factors linked to retrospective data - e.g social desirability.
-The controllability of the life change might also cause stress rather than just the level of adjustment needed - changes in our control may be less stress-inducing.
-Culture - SRRS is a fairly westernised scale - e.g some find Christmas stressful, some find it relaxing, some don’t even celebrate it. Collectivist cultures don’t even recognise divorce.
-SRRS may not be suitable for young people - items like marriage or divorce don’t really apply.
-SRRS tend to mix together the causes and effects of stress - sometimes an illness may actually cause stress, not the other way around.
Why did Rahe conduct a further study in 1970?
Rahe et Al (1970) - wanted to investigate whether scores on the SRRS were correlated with the subsequent onset of illness in a PROSPECTIVE study (rather than retrospective).
-In other words, trying to establish a link between life changes and susceptibility to stress-related illness.
What was the procedure for Rahe et Al (1970)?
-Rahe took 2500 males serving in the US Navy, who were about to go on a tour of duty, and gave them the SRRS questionnaire to assess their experiences in the past 6 months.
-A total stress score (total LCUs) was calculated for each participant.
-Then, over the following 6-month tour of duty, detailed records on the sailor’s health were kept (no matter how minor the issue was) - afterwards an illness score was calculated.
-The stress scores (number of LCUs) were correlated with the sailors’ illness scores.
What were the findings for Rahe et Al (1970)? What was the correlation? Why was such a small correlation still statistically significant?
-Rahe found a very small (weak) positive correlation between life change scores (LCUs) before the tour and illness scores once aboard the ship.
-As life change units increased, so did the frequency of illness.
-There was a correlation coefficient of +0.118 - the only reason this correlation was found to be statistically significant was because of the large sample size (2500).
What did Rahe et Al (1970) conclude?
-Experiencing life events increases the chance of stress-related illness - life changes a robust predictor of later illness.
-As +0.118 is not a perfect correlation of +1, clearly other factors must also play a role.
What are the strengths and weaknesses of Rahe et Al (1970) in studying life changes as a source of stress?
Strengths:
-Correlation (albeit small).
-Very large sample size - 2500 men - the reason why the correlation is significant.
Weaknesses:
-Hard to generalise people’s every day lives to US Navy personnel - unique, high-stress job.
-The sample was restricted to males - this is androcentric (focused/centred on men) which could mean the study is beta biased (ignores differences between men and women).
-Research suggests that men and women use different strategies to cope with life changes.
-American - ethnocentric - SRRS is perhaps only appropriate for western, individualistic cultures.
-Controllability of different life changes not taken into account - life changes in our control may be less stress-inducing.
-Individual differences, such as personality, not taken into account in relation to stress.
-LCUs do not distinguish between positive and negative changes.
What 2 smaller studies demonstrate the fact life changes can only be correlated to stress-related illness?
-Thomas et Al (1997) - higher LCU scores predicted a greater mortality risk in heart patients - shows that heart problems (an existing issue) influences illness.
-Rosengren et Al (1993) - higher LCU scores associated with higher mortality risk in elderly participants - shows that age is another factor that influences illness.
Other factors clearly involved in increasing risk to illness - not just stress.
What are daily hassles? What are some examples? How do they compare to life changes?
Daily hassles are the minor but frequent annoyances and frustrations of everyday life.
E.g misplacing things, missing the bus or train, falling out with a friend, weight issues, household chores.
-Hassles range from trivial inconveniences to greater pressures, but don’t approach the significance of major life changes.
-Life changes are distal sources of stress - the effects are indirect, whereas hassles are proximal sources of stress - the effects are direct and immediate.
-Life changes exert their effects on well-being through daily hassles.
*Likely to come up
Why do daily hassles cause stress? What are the 2 explanations?
Daily hassles are usually short-lived, but if unresolved, the after effects may intensify and accumulate with subsequent hassles.
2 explanations:
1) The accumulation effect - minor hassles build up and multiply, leading to a stress reaction.
2) The amplification effect - minor hassles amplified by chronic stress from life changes. Major life changes exert their effects on well-being through daily hassles. E.g exam stress might lead to an inability to cope with small disagreements with friends.
What did Lazarus et Al (1980) say about daily hassles?
Lazarus et Al (1980) - argued that we experience two phases when we experience a hassle.
1) Primary appraisal - we subjectively assess how threatening a hassle is to our psychological health.
2) Secondary appraisal - if this hassle is perceived as threatening, we subjectively assess how well equipped we are to cope with the hassle.
What is a daily uplift? What are some examples? How can uplifts affect daily hassles?
A minor positive or desirable experience that makes a daily hassle more bearable.
E.g spending time with family, completing a task, sleeping well, keeping in touch with a friend.
-Uplifts can counteract the effects of hassles, thus reducing stress - although there are mixed findings on this.
How are hassles and uplifts measured?
The Hassles and Uplifts scale (HSUP).
-The HSUP scales measures how many hassles a person experiences in a given time period, and how severe the hassles are.
-It also measures how many uplifts a person experiences in this period.
What did Kanner et Al (1981) want to investigate? What was the procedure? What were the findings?
Whether daily hassles were a better predictor of psychological illness than life changes - i.e which source of stress is the most stressful.
Procedure:
-100 participants (48 men and 52 women - no beta bias) aged 45-67 each completed a 117-item hassles scale.
-Each participant completed the scale for hassles once at the end of every month for 9 months. (Uplifts NOT assessed).
-They also completed a life events scale on two occasions - before and during the study.
-Finally, each participant completed the Hopkins Symptom Checklist to assess symptoms of anxiety and depression.
Findings:
-Significant positive correlation between frequency of hassles and psychological symptoms of depression and anxiety.
-The more hassles a participant experienced, the more severe their symptoms were.
-No correlation between life events during the study and health.
-Therefore, hassles were found to be a stronger predictor of psychological symptoms than life changes.
What does the skin-conductance response (SCR) typically look like on a graph?
-The onset of a response results in a rise of conductance until it reaches a peak. There is then a gradual decay.
-The whole response can typically last 4 or 5 seconds.
