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Stress, Health & Disease - IBP Year 2 - Lecture notes

General information

- Course objective: Knowledge and understanding of the most important psychological and biological models of stress and stress management.

- Skills learnt during the WG’s: answering research questions on the basis of systematic investigation of academic literature. We will give an oral presentation including a review and discussion. We will end with trying out a mobile stress intervention program. 

- The workgroups will not match the content of the lectures.

- The upcoming five lectures will deal with the question of how purely psychological stress can make us bodily sick. 

 


Lecture 1: Stress Responses and Evolution

- We don’t have a conclusive definition of stress. Sapolsky, for example, refers to the relation of stress with the disturbance of the homeostatic balance. 

- Stressor = every possible threat to the attainment of psychobiological goals. Stress response = adaptive psychobiological reaction to a stressor. It is a negative emotional psychobiological response; it has psychological stress responses, such as negative emotions, and bodily stress responses; such as heart palpitations.

- Stress is a wide-scaled problem; it increases the chances of getting a disease.

- An important example is that stress increases the risk of contracting a cardiovascular disease. 

- Stress can cause us to contract a bodily disease through the direct route via psychobiological mediators.Stress can also cause impaired cognitive performance, which affects our health behaviors, and eventually causes bodily diseases: this is the indirect route.

 

- An acute stress response occurs when our primary appraisal of a stressor is threatening. A chronic stress response occurs when oursecondary appraisal of the stressor is that we cannot cope with the situation.

- Chronic stress can lead to disregulation in the body, leading to organic diseases. All these three factors can also cause psychological complaints.

- According to William James “no mental modification ever occurs which is not accompanied or followed by bodily change”.

- A biological theory of stress by Cannon is the following: a psychological threat leads to the ‘fight or flight’ response; a fast reaction caused by the involvement of epinephrine (adrenaline). A stress response is functional.

- In contemporary society, we do not ‘fight or flight’. This results in prolonged or even chronic stress responses; which are not functional anymore. “Chronic stress is a recent invention of mankind”.

Main message 1: Brief stress response is good; it is an emergency response and functional. Prolonged or frequent stress responses are bad; not functional and lead to disease.

 

- Selye discovered the ‘general adaptation syndrome’: 1. alarm stage --> 2. stage of resistance --> and if you do not successfully cope: 3. stage of exhaustion (which we now refer to as prolonged/chronic stress). In the stage of exhaustion, we risk contracting physical diseases.

- He discovered that the stress response is non-specific. He also found out about the involvement of glucocorticosteroids (cortisol) in stress.

- The stress response is one that has existed for a very long time; since the beginning of life. All species have a stress response.

Main message 2: The stress response is phylogenetically old; which implies that it is generally the same for all animals including humans. The stress response is a functional reaction to any conceivable threat.

 

- Without doubt, our ancestors faced very different stressors than we do nowadays.

- There are three consequences of the phylogentic age of the stress response: 

1. The function of the stress response is still; we remove the threat or escape.

2. The effects on the body of animal and men follow old biological routes that we share with other animals. However, we face more complex or culturally determined stressors.

3. The effects of stress on the body of animals and men are also caused by the same basal psychological factors.

Basal psychological stress factorscan be divided into three stressor dimensions(1. adversityor nature of the threat 2. uncontrollability and unpredictability; the psychological core of stressand 3. duration of the response), and two response patterns (1.defenceand 2. defeat).

 

- The stressor’s dimensions:

1. The adversity/nature of a stressor: we distinguish physical and psychological threats; the latter is divided into threats to our physical integrity and threats to our psychosocial integrity. Most of the threats we face nowadays are social in nature.

2. The uncontrollability and unpredictability of a stressor (main message 3).

3. The duration of the threat (see main message 1).

Main message 3: The psychological core of stressors is their uncontrollability and/or unpredictability.

- A classical experiment involving the uncontrollability of stress is the Yoked control experiment. One rat has control over an electric current; another does not. In this experiment, the adversity is kept constant while a psychological factor; the uncontrollability of unpredictability, is manipulated. The rat that has no controllability over the stressor will start to suffer from many physical diseases.

- Any type of human stressor, no matter how complex, can be formulated in terms of the uncontrollability and unpredictability.

- The higher the uncontrollability, the higher the risk for disease.

 

- The stressor’s response patterns:

1. Defence; fight, flight, fear. It occurs when there’s lesscontrol over stressors. Our goals is to obtain control.

2. Defeat; give up. It occurs when there’s a lossof control over stressors. The goal is to conserve energy and withdraw from the situation.

- So, how can purely psychological stress make us bodily sick? Stress results in negative emotions. Negative emotions are associated with action tendencies: fight (in the case of anger), flight (anxiety or fear) or give up and withdraw (depression).

- An action tendency is a physiological preparation. The psychological stress response is at its core equivalent to the exercise response; as during heavy physical activity. 

- However, the psychological stress response also involves perceived adversity and decreased control, leading to negative emotions.

 

- The autonomic nervous system is divided into the sympathetic nervous system (SNS; mobilises the body for action) and the parasympathetic nervous system (PNS; maintains and restores; ‘rest-and-digest’).

- During a stress response, the activity of the PNS is decreased very quickly in order to increase the activity of the SNS. Adrenaline levels go up due to the increased activity of the SNS. Also, cortisol levels go up. 

- The hypothalamus increases levels of CRH, which stimulates the pituitary gland to produce ACTH. Consequently, in the adrenal, cortisol is produced. This process is called the HPAC system (Hypothalamus Pituitary Adrenal Cortical system).

- The SAM system (Sympathetic Adrenal Medullary system) makes sure that the activity of the PNS is decreased, in order to increase the SNS’s activity. Adrenaline is produced to go to specific target organs.

- The SAM system is much quicker than the HPAC; but the latter lasts longer.

- The immediate consequences of SAM system: increased heart rate and blood pressure, more blood to muscles; preparation for action, more glucose; fuel, and increased sweating; cooling and better grip during the fight/flight response.

- The consequences of HPAC system: sustaining the SAM system’s effects, suppressing immune activity and other ‘non-essential’ activity in order to conserve energy to support the fight/flight action. Also, it buffers against SAM induced tissue damage and causes the body to return to a steady state. It suppresses pain via endorphins, so the experience of pain does not interfere with our action.

Main message 4: The function of the biological stress response (‘fight or flight response’) is to: 1. transport more oxygen and fuel muscles 2. save fuel and building material by suppressing other bodily activity 3. limiting damage and negative sensations.

 

- The body prepares for more action during the biological stress response. When we encounter prolonged or chronic stress, this can endanger health.

- Three types of prolonged/frequent stress response:

1. Chronic or highly frequent response

2. Slow recovery

3. Anticipatory responses

- Accumulation of stress leads to damage to organs and tissue and the dysregulation of the bodily system.

- The SAM system plays a mediating role between stress and disease; it increases the blood pressure, raises the heart rhythm, results in more lipids and fatty acids in the blood and impairs cellular immunity.

- The HPAC system also plays a mediating role between stress and disease; it causes prolonged immunosuppression, slows down growth and speeds up the aging process, and it is responsible for hippocampal damage by deregulating the production of cortisol.

- Humans are constantly preparing for the ‘fight or flight’-response. 

Main message 5: Stress response in humans: preparation but without action.

- Prolonged preparation-without-action can lead to the response pattern of defeat.

- The human brain differs from other animal’s brains: We make vivid representations of past and possible future scenarios. A disadvantage is that this can lead to chronic stress.

 


Lecture 2: Stress and Disease: Who falls ill and from which stress?

- This lecture started with an intriguing example of a study that showed people with certain initials in their names had an increased risk on disease and mortality. 

- Another example: the prevalence of heart rhythm diseases doubled in the area of New York after the event of 9/11.

 

- Frequent causes of disease/health complaints stem from:

Biological vulnerabilities:

> Heritable factors

> Acquired bodily conditions (obesity, pregnancy, old age, deficiencies in early           immunological stimulation, fitness level)

> Disease agents & other direct disease triggers (viruses, bacteria,

et cetera)

Physical vulnerabilities:

> Physical stressors (extreme temperatures, dangerous chemical environment, physical violence, accidents, undernourishment)

Psychological vulnerabilities:

> Psychological stressors (social-economical living conditions, life events,daily hassles, emotions, worry)

> Health cognitions (symptom perception; illness interpretation of bodily signals; and beliefs about risks)

> Health behavior (alcohol, drugs, smoking, riskful sports, sexual habits)

- Health behavior is involved in a very important indirect route of stress (lecture 1).

 

- Repetition: 

Main message 1:Brief stress response is good; it is an emergency response and functional. Prolonged or frequent stress responses are bad; not functional and lead to disease.

Main message 2:The stress response is phylogenetically old; which implies that it is generally the same for all animals including humans. The stress response is a functional reaction to any conceivable threat.

Main message 3:The psychological core of stressors is their uncontrollability and/or unpredictability.

Main message 4:The function of the biological stress response (‘fight or flight response’) is to: 1. transport more oxygen and fuel muscles 2. save fuel and building material by suppressing other bodily activity 3. limiting damage and negative sensations.

Main message 5:Stress response in humans: preparation but without action.

 

- Overview of this lecture: 

Types of stressors, modulators of the stress response (what and for whom?), worry.

 

Types of stressors

- Stressors are, for a large part, culturally determined. 

- Selye: The chief and primary causes of the very rapid increase of nervousness are modern civilization; caused by steam power, the periodical press, the telegraph, the sciences and the mental activity of women.

- Different types of stressors:

> Psychological traumas

> Life changes / life events

- The classic method, by Holmes & Rahe, measured ‘life change units’; they asked the question how long it took people to adapt to the new situation. Different life changes were listed in order of scores; representing the difficulty of adaptation. The death of your spouse was apparently the hardest situation to adapt to.

> Daily hassles

- Daily problems are better predictors of disease than life changes.

- Modern stressors are not yet on the list of common daily stressors; think of computer and smartphone-related stressors, social network stress, stress in children due to performance pressures and homework.

- A study found that cell phone use increases anxiety and lowers satisfaction with life and academic performance; presumably due to the felt obligation to remain constantly connected.

- Daily hassles presumably cause disease since they are characterized by uncontrollability and unpredictability. 

- Daily hassles are also mediators: life events --> daily hassles --> physiology and/or health-behavior; disease.

> Chronic stressors

- Chronic stressors are also mediators in the latter causal chain.

- Examples: low social economic status (SES), environmental stress (traffic; neighbors), work stress, marital stress, caregiving and psychopathological   conditions (suffering from an anxiety disorders, depression, PTSD, OCD, et    cetera).

 

- Example to show the effects of low social-economic status: We viewed a clip of a study in which two monkeys were treated unfairly; causing significant stress in the underpaid monkey.

- ‘With every step on the SES ladder, your disease risk drops’.

- Is stress the most important factors in this? People with low SES have daily hassles, life events and chronic stressors. Moderators in this issue are less social support, less controllability and predictability of life in general.

 

Modulators of stress responses

- Psychological variables can modulate/moderate the effect of stressors on disease: They change the effect of A on B.

 

Social support:

- Many social contacts and a stable social network are related to lower mortality, fewer cardiovascular diseases, less depression, et cetera.

- Support has effects in different intensities on stress:

> Strong effects: bereavement and loneliness

> Average effects: not many friends, no relationship

> Small effects: stress experiments with/without a supporting friend

> Very subtle effects: stepchild in family with biological children

Direct types of routes from social support on health: social support --> general improvement in wellbeing, independent of stressors (‘Always Good’ Hypothesis)

Indirect effect of social support on health: 

1. Social support --> stimulates healthy behavior (The Healthier Life Style Hypothesis).

2. Social support--> good during stressors (The Buffer Hypothesis).

- Example: a baby rat that had not been licked by its mother for 1 day had higher stress levels even until 3 years later.

 

Perceived controllability & predictability:

- Example: a rat that is able to control a lever that reduces the strength of an electrical current experiences less stress. Even when the lever is not even attached, the rat perceives it has control over the current, so it suffers from less stress.

 

Outlet for frustration:

- Expressing your negative emotion with anger or aggression in fact does not relieve stress but only accelerates it. We only ‘rehearse’ our anger, which only stimulates it. We train our brains to experience anger, so we encourage it.

Catharsis is abreacting your tension; is based on the hydraulic metaphor: emotion must come out somewhere! However, this comparison is wrong:

1. The stress response will not be changed, since the perceived threat continues. 

2. Only when the perceived threat stops, the stress response recovers. 

3. Faster recovery only occurs when we remove the perceive threat or avoid it. 

4. Quick recovery occurs due to opportunity to retaliate, not necessarily through the act of aggression itself. The possibility to react, or get control again, is sufficient to lower blood pressure.

5. What helps is to change the message of the brain to the rest of the body: ‘the threat is over’.

- Bodily exercise helps to relieve stress; it works as a distractor and it has positive cognitive effects. Also, it works as a peripheral physiological buffer; it lowers the stres response in the body.

 

- Risk factors: Hostility, dispositional anger and Type A personality; dispositional anxiety; depression; and defensivity.

- Type A personality is characterized by being under time pressure, being extremely competitive and being hostile. In the 60s, Type A personalities were found to have an increased risk on cardiovascular diseases. However, in the 80s, this effect was found to be absent. Later on, science found that it was the characteristic of hostility that has the effect of increasing the risk on cardiovascular diseases.

- Anxiety and hostility are in fact very similar to each other. Both show defensive characteristics; a loss of control. 

- Anxiety disorders are characterized by thinking about possible future stressors; worry. Depression is characterized by thinking about past (& future) stressors; rumination.

- Hopelessness predicts disease.

 


Lecture 3: Stress, Heart Attacks and Killer Cells

- Stress increases the chance of contracting a cardiovascular disease.

- In this lecture, we’ll discuss about stress and cardiovascular diseases, the role of immuno-suppression in the stress-disease model, some basic knowledge of the immune system, the routes form psychological factors to changes in immune system, and the influence on disease.

 

Stress and cardiovascular diseases

- The SAM system is important in mediating between stress and disease. Excessive sympathetic arousal and (nor)adrenalin distorts heart rhythm, blood pressure regulation, cellular immunity and the traffic of lipids through the blood.

- High blood pressure --> hypertension --> growth of vascular muscles --> raising resistance within these vessels --> even higher blood pressure (vicious circle). - Hypertension also leads to ventricular hypertrophy (left part of the heart, where the blood enters, increases in size). This can lead to heart attacks or cardiac ischemia.  

- Heart dysrhythmia can lead to sudden death.

- Increased blood pressure leads to damage to the vessels, in particular the branching points in the vessels. This can lead to formation of plaques and atherosclerosis. 

- During prolonged activation of the SAM system, the blood gets thicker, leading to increased formation of plaques and atherosclerosis.

- The risk of atherosclerosis is that arteries get narrower; leading to increased blood pressure again (vicious circle again).

- When these plaques torn loose and obstruct e.g. coronary arteries (called thrombus); this can lead to a heart attack. 

- Simple acute stress, which is okay for the majority of people, can lead to vascular resistance in people who already have narrower arteries.

 

The role of immuno-suppression in the stress model

- The immune system was always thought to work autonomously. In the 70s, experiments showed that the immune system could be conditioned. So, the nervous system and the immune system appeared to be linked to one another. 

- Through the results of these experiments, the field of psycho-neuro-immunology (PNI) was developed.

- The immune system is an important mediating factor in stress leading to disease.

- An example: Only showing a photo of someone sneezing could already alert the immune system of participants and increase its activity.

 

- A chronic stress response leads to immune suppression. By interaction of disease agents, this can lead to a disease. This is called the interaction route.

- The main route displays that a chronic stress response leads to disregulation and tissue damage directly.

- The last route is that chronic stress leads to worse health behavior, leading to disease by interaction with disease agents.

 

Basic knowledge of the immune system

- The immune system is the bodily surveillance system against infection and neoplasia (new tissue; cancer). Its primary function is to distinguish bodily cells and non-self cells. It attacks and gets rid of non-self invaders.

- The first line of defense consists of physical and chemical barriers; like our skin and liquids in our ear, nose, mouth, et cetera. 

- The immune system is active in wounds; blood clotting, white blood cells, et cetera.

- The immune system can become over-active or under-active, by endogenous or exogenous factors:

 

Over-active

Under-active

Endogenous

Auto-immune diseases

Cancer

Exogenous

Allergies

Infection

 

 

 

 

 

 

- Different types of immunity; defense to injury by invading organisms/material

            - Natural immunity (inherited, acquired)

            - Artificial immunity (vaccination)

- Nonspecific immunity attacks nonspecifically: phagocytosis (direct killing by cells), antimicrobial substances, inflammation and fever.

- Specific immunity works specific to certain invaders: Cellular immunity (white blood cells; phagocytes, lymphocytes (T-cells) and natural killer cells) and humoral immunity (soluble substances; B-cells making antibodies and memory-cells).

- The immune response starts with mechanistic maneuvers (coughing, sneezing, vomiting), then phagocytosis, then the interference of macrophages; t-helper cells and lastly B-cells.

- The macrophage acquires T-helper cells, and killer cells get rid of the invader.

- B-cells then make antibodies and memory cells; so the body recognizes the invader when it enters the body a second time. The second response is then able to occur way faster.

 

Routes from psychological factors to changes in the immune system

- The central question is: How can the mind influence the cells of the immune system?

- The nervous system appears to interfere with the lymphoid organs; so with the immune system.

- Cortisol suppresses immune response in many ways: it stops forming new lymphocytes in thymus, it kills lymphocytes, remove them from blood circulation, inhibits excretion of intercellular messengers, and makes circulating lymphocytes less responsive during infection.

 

- At the start of a stress response, the immune response is increased (above 100%). After a short duration of stress, approximately 30 minutes, the immune response is lowered again. It only happens during chronic or prolonged stress, that the immune response decreases below the level of 100%.

- So, acute stress leads to increased immunity. This happens through the SAM system, but also cortisol. Chronic stress leads to decreased immunity, mainly through the HPAC system, the SAM system and cortisol.

- The immune response during an acute stress response is strengthened, because it prepares your body for externally and internally caused damage. Thereafter, during a long-term or chronic stress response, the immune response is dampened in order to save energy and fuel (main message 4). However, a lot of energy is spent during the suppression of the immune response. An alternative explanation is that the immune response is decreased in order to prevent auto-immune diseases from occurring.

- Presumably both of these explanations are partly true.

- People who find a stressor controllable have an increased level of natural killer cells in their blood, and thereafter the level decreases again. For people who think a stressor is uncontrollable; the level decreases after the occurrence of the stressor.

 

- Chronic stress can be the result of social isolation, interpersonal stressors, the loss of someone close, depression or bad caregiving; in interaction with disease agents. Wounds heal less efficient and a greater risk on infectious diseases is developed.

 


Lecture 4: Stress and the Life Cycle; Metabolism, Sex & Reproduction, Growth, Aging...

- Repetition of the five main messages.

- This lecture will focus on stress in relation to the life cycle; metabolism, aging, sex & reproduction, growth, et cetera.

 

Stress and metabolism

- Insulin is created in the pancreas, through parasympathetic activation. It plans for metabolic future; future need of fuel and building materials. Insulin is stored in fat cells and muscles.

- Fat storage is limited.

- Metabolism under stress works as follows: the insulin effects are reversed. Insulin becomes proteins, glycogen and triglycerides again and is released in the blood stream. They serve as fuel in the fight/flight response.

- The storage of fat is blocked under stressful conditions by cortisol, adrenaline and noradrenaline. This process is called insulin resistance.

- On top of that, energy goes from inactive to active muscles.

- And, there is more ‘bad’ cholesterol (LDL) and less ‘good’ cholesterol (HDL); increasing the risk on atherosclerosis.

- In case of a long-term preparation for a fight/flight response; a diabetic state develops. 

- Diabetes type 1 is an autoimmune disease; the immune system attacks pancreas cells so there is no sufficient production of insulin; too little insulin. Diabetes type 2 occurs through obesity; fat cells are fully stored, so they respond less to insulin. Too much insulin can cause damage to brain cells.

- Also non-diabetics can suffer from damage to their blood vessels when their blood levels of glucose are continually high.

- Obese people’s existing risk for diabetic episodes is even higher during stressful periods. Smoking is also an important factor.

- Obesity interacting with an unhealthy lifestyle leads to more severe effects and an increased mortality risk.

 

Summary Metabolism & Stress

- Food broken down and stored as i.a. glycogen, triglycerides and proteins.

- Under stress this storage process is being reversed: more fuel in blood stream: (glucose,  fatty acids, amino acids) for ‘active’ muscles

Human stress = only preparation (main message 5): Long-term increase of glucose etc.: damage in body (i.a. atherosclerosis)

- Bigger risk for diabetes (type 1 & 2) and obesitas: already a disturbed/increased glucose level

 

- Under stressful conditions, the activity of the PNS goes down, while the activity of the SNS goes up. This causes the digestion process to stop. The reason for this is to save fuel (main message 4).

- What happens then: Less saliva --> dry mouth, less appetite, stomach stops movement, less mucus & acid buffer, stomach secretes less enzymes and acids, small intestine stops with its peristaltic movements, absorption in the intestines stops, there is reduced blood supply to the stomach and intestines, and quick emptying of the colon and bladder can occur.

 

- Two stress hormones play a role in appetite, yet they have opposite effects. CRF dampens the appetite and cortisol stimulates appetite.

- During frequent stress there is a chronically high level of cortisol, leading to more appetite, so obesity.

 

- Immense stress, sometimes in interaction with the Helicobacter Pylori bacterium, can lead to stomach ulcers (peptic ulcers), duodenal ulcers (which are most common) and esophageal (gullet) ulcers.

- Other factors were also theorized to be of influence: 

1. During stress, there is less stomach acid, mucus and bicarbonate. After the stress response, people tend to eat a lot, so there will be more acid, but there is still too little mucus and bicarbonate. This leads to damage of the stomach and intestinal walls. Combined with frequent stress and a bacterial infection, an ulcer can occur.

2. During stress, there is low blood supply and fewer free radicals. After the stress response there are more free radicals, but still too few buffers. This leads to damage of the stomach and intestinal walls. 

3. Too little prostaglandins (that repair small damage to the stomach and intestinal walls).

4. Slow rhythmic stomach contraction under stress, leading to damage to the stomach and intestinal walls.

5. Immunosuppression leads to fewer antibodies against Helicobacter Pylori, which causes an increase in these bacteria and an increased risk of developing an ulcer.

 

- The Irritable Bowel Syndrome (IBS) is the most prevalent stress-related disorders; characterized by frequent diarrhea, constipation, flatulence, belching, feeling bloated/swollen, et cetera.

- Theories about IBS:

1. Prolonged or frequent stress leads to specific intestinal problems.

2. Prolonged or frequent stress leads to intestinal desynchronisation.

3. Traumatic early stress leads to higher reactivity and sensitivity to stress; leading to intestinal problems.

 

Stress and aging

- An optimistic, hopeful and positive outlook on life has a beneficial effect on aging and life expectancy.

- Theories:

1. Bodily coping with stress becomes less efficient: slower recovery of temperature, lesser intellectual power under pressure and slower recovery of stress hormones (adrenaline, noradrenalin, cortisol) and heart activity. A higher resting level of stress hormones occurs with age.

2. Stress can accelerate aging. Excessive cortisol levels can result in immunosuppression and other diseases.

The set-point level of cortisol can shift; chronically higher stress. The hippocampus is important in this process; it is the location of cortisol-negative feedback.

 

- The glucocorticoid neurotoxicity hypothesis displays the vicious circle or aging:

Stress can cause excessive cortisol secretion --> the hippocampus loses neurons during these period of excessive stress --> cortisol excretion is dysregulated --> even higher levels of cortisol. 

- Cell aging through chronic stress can happen through the shortening of telomeres; which stabilize the chromosomes in cells.

 

Stress, sex & reproduction

- Stress inhibits libido in both sexes. But in humans, in contrast to some animal species, social and psychological factors are much more important.

- Impotence is the inability to get an erection, often related to excessive stress.

- During sexual arousal, the sympathetic nervous system’s activity goes up. Then the parasympathetic nervous system goes up during an erection. At the point of ejaculation, the sympathetic nervous system’s activity goes up again.

- Premature ejaculation or impotence can occur when the parasympathetic nervous system’s activity goes down too soon. 

 

- Miscarriages can occur through repeated stress responses that cause diminished blood supply to the fetus.

- Stress may also be the cause of many failed IVF attempts.

 

Stress and growth

- The presence of parental love, touch and cuddling is crucial for a child’s growth.


Lecture 5 (officially lecture 6): Stress, Pain and Subjective Health Complaints

- Notes from the previous lectures:

- Chronic stress can lead to disease or illness, or to the deterioration thereof, through psychological and physiological mechanisms.

- In this lecture we focus on subjective physical symptoms that are part of major illnesses and diseases.

 

- A chronic stress response can lead to psychological complaints and subjective somatic complaints. Think of pain, fatigue, nausea, shortness of breath, et cetera. 

- The biopsychosocial adjustment model: 

Personality, stressors and social factors --> emotions, cognitions and behaviors. Cognitions --> psycho-physiological response

Emotions, behaviors and psychophysiological response --> quality of life & disease outcome.

 

- In contrast to acute pain, that does not last long, chronic pain lasts for more 3-6 months. It is often very complex. The brain keeps on sending pain signals although in fact the body is completely fine. 

- Reducing stress can help to reduce pain by calming down the nervous system. Stress is often a major contributor to chronic pain.

 

 

- Examples of types of pain:

--> Rheumatoid arthritis.

This is an autoimmune disease; characterized by chronic inflammation of the joints. It leads to physical disabilities. Chronic medication use leads to side effects. The disease has an unpredictable course. It can have psychological consequences, such as depression.

 

--> Fibromyalgia

This disease is characterized by generalized pain across the entire body. It has no clear somatic cause. It leads to physical disabilities. There is no evidence-based treatment. The disease has an unpredictable course and psychological consequences.

 

- The number of medically unexplained symptoms (MUS) at a GP’s office is higher than the number of medically explained symptoms (MES). This leads to high medical costs.

 

- According to the biomedical pain model “pain is a reflex-like response to noxious internal or external stimuli. Nerve impulses from the damaged site to the brain determine the pain’s severity”. 

- The main point of criticism here is that pain is seen as a purely sensory phenomenon. Also, there is no 1-to-1 correspondence between tissue damage / inflammatory activity and reported levels of pain.

- According to the biopsychosocial pain model, it is more multidimensional. Physical factors involve the detection and perception of pain, psychological factors involve the negative affective response and social factors are about the pain behavior of the individual. 

- The Gate Control theory and Neuromatric model of pain state that “pain is a multidimensional experience produced by patterns of nerve impulses generated by a widely distributed neural network in the brain, of which the somatic sensory input is only a part”.

 

- Acute, sharp pain serves as a warning of potential danger. It motivates an individual to move away from the source of the pain. After the activation, an interneuron is activated that stops the pain signal.

- Slow, diffuse and constant pain has the function of recovery. It motivates the individual to take rest. After activation, the pain-inhibiting interneuron is not activated, leading to the pain signal remaining to be transmitted.

 

- Sometimes, the pain remains even though the damage is already gone.

- Allodynia is pain experienced in response to a non-painful stimulus (sensitization).

- Hyperalgesia is more emotional reactivity to pain; so no increased activity of pain receptors. It is often caused by psychological stress.

- Analgesia is pain decrease through endogenous (produced by the body) opioids; endorphins, which decrease the activity of neurons transmitting pain signals. One can attain this by acupuncture, placebo effects, sports and physical stress.

Main message 1: What is pain? Pain is determined multidimensional in the brain and not in the periphery. It is always a subjective experience. Stress can increase and decrease pain.

 

- Chronic pain and subjective health complaints; e.g. uncontrollability, fluctuating course, invalidation / disbelief by others, side effects of medication, an uncertain future, adjustments in work or hobbies, no cure / explanation and dependence upon other people.

- Stress can be a risk factor for the development of pain and subjective health complaints. Stress can also form a risk factor for worsening pain and subjective health complaints.

Main message 2: Stress, pain and subjective health complaints: Stress can be caused by pain or subjective health complaints. Especially chronic and major stress can contribute to, maintain, and increase pain and subjective health complaints. Mechanisms to explain the link of stress with pain and subjective health complaints include psychological and physiological pathways.

 

- Acute stress responses occur when the environment asks more than a person can offer. During this response, the threat is tried to be taken away, 

Our body produces catecholamines and cortisol, more energy is transported to muscles and the brain, and there is temporary suspension of less essential activities.

An acute stress response has an adaptive function.

- A chronic stress response occurs when it is not possible to take away the threat from the environment. Chronic stress is something typical for humans; we engage in stress anticipation (worrying) and linger in past stressors (rumination). Consequently, our stress systems become hyperactive, receptors change in their sensitivity, and chronic inflammation can occur.

 

- Repeated stimulation of the nervous system leads to habituation and a reduced response; under conditions of low arousal. 

- Under conditions of high arousal, it leads to sensitization. 

- A lower pain threshold can occur and a lower pain tolerance to the same stimulus.

- Individuals can create a ‘stress memory’.

- Cross-sensitization is what happens when stress increases the immune response in the body.

Main message 3: Physiological stress mechanisms: Stress responsiveness has become dysregulated in many patients with chronic pain or subjective health complaints. Sensitization at the somatic level increases the physiological stress response and through that, among other things, pain sensitivity and immune functioning.

 

- Anger and sadness increase the pain experience in response to an experimental pain stimulus in both patients of fibromyalgia and healthy individuals.

- Female patients of fibromyalgia engage in more emotionally avoidant strategies and experience fewer positive emotions and more negative emotions.

- Negative emotions lead to an increase in noradrenaline levels.

- The brain areas that are active during social exclusion are also activated with physical pain (like the anterior cingulate cortex (ACC)). 

Main message 4: Emotions: Negative affect strengthens the processing of stimuli in a more negative affective tone. Negative emotions lead to sympathetic activation and an increase in muscle tension. Emotional, social and physical ‘pain’ share a neural alarm system.

 

- Frequent and intense physical signals are prioritized at higher levels of information processing, leading to an attentional and memory bias for pain-related information. This leads to a long-lasting activation and continuous reactivation of pain-related cognitive networks. There is more attention to and detection of internal and external pain cues, more ambiguous internal and external information is interpreted in terms of pain; there is more misattribution of harmless signals as pain, and more and stronger pain memory traces.

Main message 5: Cognitions and behaviors: Stress-related cognitions lead to a decreased threshold to detect both stress and pain/subjective health complaints, increased interpretation of experiences as physical symptoms (cognitive sensitization), prolonged psychological and physiological stress responses. Also, cognitions influence (pain) behavior and with that can start or instantiate a vicious circle.

 

- Placebo/nocebo effect: Pain can already be reduced when only seeing a painkiller. It is about the physician’s and the individual’s expectations.

Main message 6: Expectations: Expectations can increase or decrease pain or subjective health complaints through learning (e.g. conditioning) and contextual factors (e.g. communication). Expectations of pain or pain decrease can lead to similar changes in the brain and physiological stress responses as an actual pain stimulus or painkiller.

 

- Clinical settings focus at stress-management, cognitive-behavioral, and expectation-based interventions.


Lecture 6 (officially lecture 5): Chronic Stress and Unconscious Stress

Main message 1: Brief stress = ‘emergency’; which is okay most of the time. Prolonged or frequent stress = most of the time bad for the body.

- We can get from short stress responses to long stress responses by emotional perseveration. Negative emotions increase the risk of stress leading to disease.

- Anxiety and depression do not need to be pathological to have effects on health.

- Emotions occur along a continuum. The more extreme the emotion, the more health risk. 

- Evidence that anger leads to heart disease is limited. Hostility is however a characteristic that increases the risk. There is good evidence that anxiety and fear lead to heart disease. Evidence that depression leads to heart diseases is limited; hopelessness is however found to be related.

 

- Each emotional state has a different physiological pattern, with some variables, such as blood pressure, responding stronger than others. However, most variables, such as heart rate, respond with equal magnitudes to different emotional states.

Simple self regulation model:

> The autonomic nervous system reacts to any discrepancy between ‘set values’ and ‘actual values’.

> The initial physiological response during any intense emotion is not emotion-specific. It is a nonspecific ‘alerting’ response.

Two-dimensional models:

> Two-dimensional model of emotion: arousal & valence. It is similar to the effort-control model. The risk for disease is highest with high uncontrollability and high effort. This model explains why depression has less of an effect on heart-disease risk than anxiety and anger.

Anger with challenge and anger with threat.

> In these different situations, different mechanisms come to play, but the same elevation of blood pressure occurs. Anger with challenge is the response of immediate fighting; a relatively short response (via cardiac output). Anger with threat leads to vigilance; a prolonged response (via high peripheral resistance).

 

- Another dimension of stressors we have not considered yet is the duration. (The other dimensions are adversity (nature of the threat) and uncontrollability & unpredictability).

- With negative emotions, the neutral heart rate level after the stress response is higher than with positive emotions. So, initial valence but not arousal explained a prolonged heart rate increase.

 

- Stress response during stressor --> prolonged stress response --> pathogenic state --> organic state. 

- What causes the occurrence of a prolonged stress response? The perseverative cognition hypothesis states that this has to deal with worry and rumination.

- A specialization of the human brain compared to other species is that we can make representations of past and possible feature scenarios. A disadvantage to this is that we can unlimitedly prolong stressors. Our bodies respond to stressful events that may not even occur in reality.

- So, whatever makes a stressor stressful, if you do not worry about it, it will not influence your health in the long term.

 

- A night of sleep has the function of restoring the body’s energy. If stress responses are prolonged during sleep, it can mediate the relationship of stress leading to organic disease.

- Worry can occur even though you’re asleep. Stressors and worry have prolonged cardiac effects of two hours.

- Slow physiological recovery from anger-recall is not caused by conscious anger-related thought (anger rumination). 

- Showing threatening pictures subliminally (meaning ‘without conscious awareness’) can already increase physiological activity.

- Subliminal primes of negative stereotypes of aging can increase blood pressure.

- It is likely that a major part of our emotional cognitive regulations is unconscious.

 

- A repressive personality represses anxiety. Alexithymia refers to the inability to understand and communicate emotions. It increases the disease risk.

- Repressive personalities have overactive stress responses (high increases in blood pressure, perspiration, muscle tonus), are chronically stressed (high levels of cortisol, a high autonomic activity and poor immune function) and have a higher risk of illness or complications during illnesses.


Lecture 7: Work-related stress

- Work-related stress is related to a higher risk on heart attacks, diabetes, depression and death and it accelerates aging, decreases emotional well-being, can lead to a burnout, can strain relationships and leads to higher stress levels outside of work.

- However, being unemployed is associated with a lower mental and physical health status. Possible benefits of being employed are the presence of financial resources, a social group, daily structure, a sense of accomplishment, learning and development and a sense of purpose in life.

 

Early symptoms of occupational stress are...

> Physical symptoms such as an increased blood pressure, headaches, muscle aches & pains, stomach problems and sleep disturbances; 

> Psychological symptoms are anxiety, worrying, irritation, anger and decreased concentration;

> Behavioral symptoms and unhealthy lifestyles and accidents.

 

Long-term consequences of occupational stress are...

> Physical symptoms are persistent high blood pressure, musculoskeletal disorders and cardiovascular diseases;

> Psychological symptoms are concentration problems, depression and burnouts;

> Behavioral symptoms are absenteeism of work, turnover and alcohol abuse.

 

- According to Maslach (1993), a burnout develops through the stages of 1) emotional exhaustion (stress arousal), characterized by irritation, anxiety, forgetfulness, problems concentrating, sleep problems, heart palpitations and headaches. 

In the second stage; 2) depersonalization (energy conservation), the person will get a non-involved and detached attitude towards work and colleagues. 

In stage 3) reduced personal accomplishment (exhaustion) the person will suffer from chronic mental and physical exhaustion, chronic headaches, gastro-intestinal complaints, social isolation and a loss of self-confidence.

- The incidence of burnouts has increased shockingly over the past decade.

- Apparently, health care and teaching professions are at the most risk for it.

 

- Coronary heart disease (CHD) has also been found to be clearly associated with work-related stress.

- Absenteeism of work due to work-related health problems occurs very often as well. Physical but also stress-, depressive and anxiety complaints are the most common health complaints.

 

- Occupational stress has negative consequences for...

> Individual employees: They suffer from physical and psychological complaints and often have an unhealthy lifestyle.

> Employers and organizations: They have to deal with higher turnover rates, absenteeism, lower performance, lower productivity, counterproductive behaviors and accidents at work.

> Society: The costs of absenteeism are high.

 

- The NIOSH model of Job Stress states that stressful job conditions can lead to an increased risk of injury and illness if this relationship is mediated by individual and situational factors.

- Factors that influence the intensity of the stress response are the intensity of the stressors, the extent of time of exposure to them and the recurrence of these exposures. Age, gender, physical and psychological status and available coping mechanisms are also important factors.

 

- There are different work-related stressors. Think of physical stressors, task-related stressors, role stressors, social stressors, work schedule-related stressors, career-related stressors, stressful change processes and traumatic events.

 

- Acute stress is described as sudden and typically short-lived stress, particularly experienced at a threatening event.

- Chronic stress occurs during ongoing environmental demands.

Main message 1: Brief stress functions as an emergency alert, and is typically okay. Chronic, prolonged or frequent stress is bad for health. ‘Chronic stress is a recent invention of mankind’.

 

- Important aspects of critical incidents, which are related to acute stress responses are:

> Unpredictability

> Uncontrollability

> Confrontation with suffering or death

> (Life)threatening situation

> Recurrence

- Consequences of such critical incidents can be the development of an acute stress disorder. This usually happens within a period of four weeks. Exposure to the situation and an intense emotional reaction can lead to dissociative symptoms, the event will be consistently re-experienced; the person will avoid stimuli and will have anxiety.

- Another possible consequence is the development of a post-traumatic stress disorder (PTSD). It still occurs after a period of four weeks.

- Substance abuse is another common consequence of being exposed to a critical incident.

 

- Challenge stressors are for example high workload, responsibility and complexity. Hindrance stressors are for example role ambiguity, role conflict and social conflict.

- The assumption is that both can have a negative influence on health and well-being, but they have different effects on performance.

 

- Job stressors can lead to adverse health impact, via or not via the way of worsening health behaviors first.

 

- We cannot be sure that high workload leads to fatigue, or fatigue leads to high workload or that both influence each other. 

- The drift hypothesis states that individuals with bad health drift to worse jobs.

- The true strain-stressor hypothesis states that for example depressive symptoms lead to reduced social support.

 

- Theories about occupational stress:

--> The vitamin model states that job characteristics can either lead to a constant effect on affective well-being or to additional decrement. Job characteristics are e.g. job autonomy, job demand, social support, et cetera.

--> The job demand-control model states that on X axis are job demand, and on the Y axis is control:

 

Job demand

low

high

Control

low

passive

high strain

high

low strain

active

 

 

 

 

 

 

 

High strain leads to an increased risk of psychological strain and physical illness. ‘Active’ is associated with learning and motivation to develop new behavior patterns.

Main message 3: The psychological core of any stressor is either uncontrollability or unpredictability, or both.

 

--> The job demand-resources (JDR) model states that job demands can lead to reduced health/energy. Job resources can lead to motivation. These results lead to positive or negative organizational outcomes.

- Job demands are the physical, social or organizational aspects of the job that require sustained physical/psychological effort of the employee. 

- Job resources are the physical, psychological, social or organizational aspects of the job that reduce job demands and the associated costs, are functional in achieving work goals and stimulate personal growth, learning and development.

- Resources occur at the organizational, interpersonal, work organization and task level.

- The JDR model distinguished two processes:

> Energy-draining process: The demanding aspect of work lead to constant overtaxing, and in the long run to exhaustion.

> Motivational process: Job resources lead to engagement and positive outcomes.

- Job resources thus buffer the impact of job demands on physical/psychological strain.

 

--> The Demand-Induced Strain Compensation (DISC) model includes the job’s demands, resources and outcomes.

 

--> The Effort-Reward Imbalance (ERI) model claims that there is a principle of balance between the job’s effort and the rewards. If there is an imbalance, strain reactions may occur.

- The ERI model predicts that if an imbalance between extrinsic effort and rewards occurs, there will be an increased risk on poor health (extrinsic ERI hypothesis). A high level of overcommitment increases the risk of poor health (intrinsic overcommitment hypothesis). Also, an extrinsic ERI in combination with high overcommitment leads to the highest risk of poor health (interaction hypothesis).

 

--> The Person – Environment Fit model focuses on the degree of fit between the person and the working environment. A high degree of misfit can lead to physiological, psychological, behavioral and medical strain.

- The model distinguishes the fit between supplies and values as well, just as the fit between demands and abilities.

- Research towards this model focuses more on the needs-supply fit than on the ability-demands fit. Needs-supply misfit is related to various indices of strain; like dissatisfaction, fatigue, anxiety, depression, somatic complaints and absenteeism. Demands-ability misfits are related to dissatisfaction, anxiety and exhaustion.

 

--> The transactional model (Lazarus) states that a potential stressor results in a primary and secondary appraisal. The primary appraisal is related to the first interpretation of the stressor; the secondary appraisal to the coping abilities of the person and the presence of sufficient resources. After the appraisal stages, coping may or may not occur. This may or may not lead to stress.

 

- So, all these different occupational stress theories differ in their focus. They also have different implications for interventions.

 

- Primary prevention of occupational stress is done by eliminating the source of stress. In practice, job re-design, more flexible working hours, introducing self-managing teams and changing the leadership style are possible solutions.

- The participative action research (PAR) intervention has as its aim to increase the possibilities to exert control by re-designing jobs. Research has found that PAR has positive effects on mental health, absenteeism and performance.

 


Lecture 8: Stress management

- Chronic stress can be detrimental to somatic health. This lecture will cover the topic of how this can be reversed.

- We can change our behavioral stress response by intervention programs.

- Behavioral change is difficult. Prolonged stress is a learned response to threat. Learned and hard-wired responses are hard to change.

- The success of changing behavior depends on the individual’s motivation.

 

- (1) Recognize the problem. 

(2) Reverse the problem by different stress management techniques; cognitive behavioral therapy, returning to work, time management, work-related interventions, conflict management, a healthy lifestyle (relaxation and exercise) and positive psychology.

(3) Resilience: being prepared for a relapse.

 

- Cognitive behavioral therapy:

> Changing appraisal and coping strategies is a very important part of stress management.

> The ABC of stress: Activating events + beliefs --> consequence.

> Cognitive interventions are focused on the content of thought (Rational Emotive Therapy) and the duration of the thoughts (mindfulness, limiting your worry time).

 

- With all the interventions it is important that they are voluntary.

 

- Biological interventions can also be effective in stress intervention.

- The vagus nerve is important in stress; the deactivation of the parasympathetic nervous system and activation of the sympathetic nervous system. Vagus nerve stimulation is a form of stress intervention.

- Deep brain stimulation is another method to treat depressive symptoms.

- A type of intervention that is used for patients with PTSS is prolonged exposure.

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