The role of stress in illness, including reference to immunosuppression and cardiovascular disorders.

AO1, Description: The Role of Stress in Illness

Definition: Immune System: The body’s main way of defending itself against millions of antigens (i.e. bacteria, viruses, toxins and parasites) that would otherwise invade it. None of these things are able to affect the body when the immune system is working effectively. The moment the immune system stops functioning properly, the body becomes at risk of infection and illness.

Immunosuppression:

Stress may have a general impact on the immune system, i.e. leading to overall suppression of immune function (immunosuppression) which can cause individuals to develop illness.

In a meta-analysis of 293 studies, Segerstrom and Miller (2004) concluded that acute stressors (short-lasting) can actually lead to an upregulation (increased strength) of natural immunity.

However, It was concluded that chronic stressors (long-lasting), however, can lead to downregulation (or suppression) of most measures of immune functioning.

* For example, chronic stressors can lead to continuous production of corticosteroids (through constant activation of the Hypothalamic-Pituitary-Adrenal system).

Furthermore, chronic stress has also been shown to affect the body’s ability to carry out other processes such as wound healing. Research has shown chronic stress can mean wounds take much longer to heal and this might also affect the body’s ability to fight infection.

Description, AO1 – Research into Immunosuppression: (Janice Kiecolt-Glaser et al 1995)

Aim: Kiecolt-Glaser et al (1995) sought to demonstrate the direct effects of stress on the immune system by looking at how quickly wounds heal.

Procedure:

  • In a field experiment, Kiecolt-Glaser obtained a group of 13 female participants (using a volunteer sample) who were caring for relatives suffering from senile dementia (a task which has shown to be associated with chronic stress).
  • The experimental designed used was a matched-participant design, the 13 female volunteers were placed in the experimental condition and a further 13 females were matched with the carers on the basis of age and income but not marital status (this was the control group).
  • All participants were given a wound (a puncture biopsy), which is a cut of 3.5mm just below the elbow. The wounds were dressed and treated by a nurse in the same way for each participant.
  • In addition, a second measure of immune response was taken. The researchers assessed levels of cytokines (a biochemical substance involved in regulating the body’s immune response). Participants were also given a 10 item perceived stress scale to check how stressed they actually did feel.

Findings:

  • Kiecolt-Glaser found that complete wound healing took significantly longer in the carers than in the control group (an average of 9 days – 24% longer in the carers).
  • It was also found that cytokine levels were lower in the carers than the control group and on the perceived stress scale, the carers did actually indicate they were feeling more stressed.

Conclusion: The findings support the view that chronic stress depresses the functioning of the immune system (immunosuppression), which in turn increases vulnerability to illness.

 

Stress and Immunosuppression – Evaluation, AO3 Kiecolt-Glaser et al (1995):

Strengths:

(1) POINT: There is research to support the idea that chronic stress can lead to immunosuppression (a depletion of the functioning of the immune system). EXAMPLE: For example, Marucha et al (1998) inflicted a punch biopsy in the mouths of students either during the summer holidays or 3 days before an exam’. The wounds given before the exam’ took 40% longer to heal than the wounds during the holidays. EVALUATION: This is a strength because the findings from Marucha’s study indicates that prolonged stress and the production of cortisol can have a negative/depleting effect on the immune system (immunosuppression) causing illness to develop/healing time to increase.

Weaknesses:

(1) POINT: This study can be criticised for having a bias sample. EXAMPLE: For example,  Kiecolt-Glaser uses all females taken from a volunteer sample. EVALUATION: This is problematic because the all female sample means that the findings relating to the effects of stress on the immune system are not able to be generalised to the effects of stress on the male immune system as males and females are physiologically different and may respond to stress in every different ways as a result of their different biological make up (for example, women have different hormonal releases in comparison to men etc…). Furthermore, the sample used was volunteer, typically individuals who volunteer tend to be more confident and outgoing than non-volunteers which may mean that their reaction to stress is very different to a non-volunteer (who my be less outgoing and confident). As a result, such findings cannot be generalised passed Kiecolt-Glaser’s sample.

 

(2) POINT: Evidence has suggested that stress does not always have a negative effect on the immune system. EVIDENCE: For example, research has suggested that stress can sometimes enhance the activity of the immune system. Evans (1984) looked at the activity of an antibody (slgA) which helps protect from infection. Evans arranged for students to give talks to other students (immediate stress). These students showed an increase in slgA whereas levels of slgA decreased during examination periods which stretched over several weeks. EVALUATION: This shows that stress can have two effects on the immune system: up-regulation (increase efficiency) for short term acute stress, and down regulation (decreased efficiency) for chronic stress and therefore indicates that stress does not always lead to immunosuppression.

 

Description, AO1 – Research into Cardiovascular Disorders and Stress

There is evidence that stress may contribute to the development of various cardiovascular disorders such as heart disease and strokes.

Immediate Stress: Adrenaline and Cardiovascular Disorder:

Stress activates the sympathetic branch (SNS) of the autonomic nervous system leading to the production of adrenaline and noradrenaline. High levels of adrenaline will have the following effects:

  • Increased heart rate causes the heart to work harder and takes a toll over time.
  • Constriction of the blood vessels increase blood pressure, which puts tension of the blood vessels causing them to wear away.
  • Increased pressure can also dislodge plaques on the walls of the blood vessels, and this leads to blocked arteries. This may cause a heart attack or stroke.

 

Aims: Williams et al (2000) conducted a study to see whether anger was linked to heart disease (anger, like stress also activates the SNS).

Procedure:

  • About 13,000 people completed a 10-question anger scale, including questions on whether they were hot-headed, if they felt like hitting someone when they got angry, or whether they got annoyed when not getting recognition for doing good work.
  • None of the participants suffered from heart disease at the onset of the study.

 

Findings:

  • Six years later the health of the participants were checked.
  • 256 had experienced heart attacks
  • Those who had scored highest on the anger scale were over two-and-a-half more likely to have had a heart attack than those with the lowest anger ratings.
  • People who scored ‘moderate’ in the anger ratings were 35% more likely to experience a coronary event than those with lower ratings.

Conclusions: The findings from William’s et al study suggests that the SNS arousal is closely associated with cardiovascular disorders.

 

Stress and Cardiovascular Disorders – Evaluation, AO3 Williams (2000)

Strengths:

(1) POINT: There is research to support the idea that stress and cardiovascular disease is linked. EXAMPLE: For example, Sheps et al (2000) focused their research on volunteers who suffered from reduced blood flow to the heart. They gave 173 men and women a variety of psychological tests, including a public speaking test. Their blood pressure typically soared dramatically, and in half of them, sections of the muscles of the left ventricle began to beat erratically. Of all the participants, 44% of those who had shown erratic heart beats died within 4 years, compared to just 18% who had not. EVALUATION: This is a strength because the findings from Sheps study showed that psychological stress can dramatically increase the risk of death in people with poor coronary artery circulation.

Weaknesses:

(1) POINT: This study can be criticised for using a volunteer sample. EXAMPLE: For example, individuals completing this study self-selected and agreed to take part in the study. EVALUATION: This is problematic because research has suggested that volunteers tend to hold very different traits to non-volunteers in that they tend to be more confident and outgoing. In terms of stress, volunteers holding these personality types are said to respond in a different way than non-volunteers (volunteers/confident people may be more immune to the negative effects that stress can have on health in comparison to non-volunteers). This means that such findings cannot be generalised to the wider population and therefore the study lacks population validity.

 

(2) POINT: Evidence has suggested that there are individual differences in cardiovascular effects. EVIDENCE: For example, Rozanski et al (1999) conducted research which suggested that the sympathetic branch of the ANS in some individuals is more reactive than in others. This shows that some individuals (described as hyper-responsive) respond to stress with greater increases in blood pressure and heart rate than others, this would lead to more damage to the cardiovascular system in hyper-responsive individuals EVALUATION: This is a weakness because such findings suggest that stress does not have the exact same effect on all individuals and therefore, research into stress can be criticised for adopting a nomothetic approach.

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