Stress and Health Flashcards
1
Q
What are some important stress related terms/concepts?
A
- stressor: the perceived threat to an organism
- stress response: the response to that stressor
- situational stereotypy: the degree to which a situation evokes different patterns of biologic responses
- e.g. vigilance response; involving sympethatic nervous system (SNS) and activive inhibition, or fight or flight response with increased autonomic and hormonal activities
- response stereotypy: individual difference in stress response to same situation (pattern)
2
Q
Why may adverse effects of chronic stress be particularly common in humans?
A
- possibly, via high capacity for symbolic thinking which may elicit persistent stress response
3
Q
What are some psychologically relevant stressors with adverse effects in childhood. What are its effects?
A
- maltreatment/abuse: leads to dysregulation of affect, provocative behaviours, avoidance of intimacy, disturbances in attachment
- childhood sexual abuse survivors: increased general stress, personality disorders more prevalent, associated with negative views toward learning
- children of divorced parents: increased antisocial behaviour, anxiety, depression.
- exposure to non-responsive environments: leading to learned helplessness
- exposure to war/terrorism: PTSD, depression. (70% of childreen in Kuwait reported ptsd-symptoms after Gulf War. In lebanon 40% of children had PTSD like symptoms symptoms 10 years after the war
4
Q
What role do neo-natal experiences play in the development of response stereotypy?
A
neonatal experiences in rats were shown to have long-term effects in cognitive-emotional responses:
- rats with nurturing mothers have increased levels of serotonine activity compared with rats raised by less nurturing mothers
- increased serotonine activity lead to increased expression of glucocorticoid receptor gene (e.g. receptor for cortisol)
- this lead to improved glucocorticoid feedback into the SNS. These rats (if female) became themselves highly nurturing mothers and low-anxiety adults
- those rats that were seperated from their moms a few hour a day had highly active HPA-axes and elevated SNS arousal
5
Q
Please explain the variability of stress responses
A
- Due to differences in situations (situational stereotypy):
- intensity or severity of stressor
- controllability
- features that influence appraisals and cognitive responses
- usually, multiple stressors have more sever health consequences (e.g. work stress in combination with threat or high demand with low control)
- due to personal differences
- rsik factors:
- having prior psychiatric history
- neuroticism
- being female etc.
- levels of neuroticism and reactivity correlates with event proneness
- protective factors:
- coping resources
- social support (fare better after natural disaster, infarcts)
- self-esteem, (lower cortisol responses to acute stressors)
- optimism
- finding meaning (e.g. political activists were better able to handle torture in Turkey than those that were noot)
- coping resources
- rsik factors:
6
Q
What are particularly harmful stressors for major depression and generlaised and anxiety?
And for PTSD?
A
- depression and GAD:
- dimensions of loss
- humiliation
- and danger
- for PTSD:
- injury
- damage to property
- loss of resources
- bereavement
- perceived life threat
7
Q
What makes a stress response adaptive?
A
If its short term (selye, 1956)
- stress hormones make energy stores available for immediate use
- new pattern of energy distribution emerges
- energy is diverted to tissues i.p skeletaal muscles and brain
- immune cells are activate; sent to battle stations
- less important activities are suspended (e.g. digestion and production of growth and gonadal hormones
- eating growth and sexual activity may be destructive in life or death situations
8
Q
How does the stress response work hormonally?
A
- Stress hormones are produced by the SNS
- (SNS stimulates adrenal medulla to produce catecholamines (epineprine).
- and (simultaneously) by the hypothalamic-pituitary adreno-cortical axis (HPA-Axis) -
- paraventricular nucleus of hypothalamus produces corticotrophin releasing factor
- which stimulates the pituitary to produce adrenocorticotropin
- which stimulates adrenal cortex to secrete cortisol
- catecholamines and cortisol increase available sources of energy by promoting lipolysis and conversion of glycogen into glucose (i.e. blood sugar)
- Lipolysis is the process of breaking down fats into usable sources of energy (e.g. fatty acids, glycerol)
9
Q
How does the cardiovascular and immunal stress response look like?
A
- energy is distributed to the organs that need it by increasing blood pressre and conrtacting certain blood vessels while dilating others
- There are two hemodynamic mechanism to increase blood pressure:
- myocardial mechanism: increase blood pressure through enhanced cardiac output (increase in HR and stroke volume output)
- vascular mechanism: constrict vasculature, hence increasing blood pressure
- specific stressors tend to elicit one of the two mechanisms:
- stressors that require active coping (e.g. giviing a speech) elicit myocardial response
- stressors that require vigilant coping mechanism (keeping food in bucket of ice water) tend to elicit vascular response
- these mechanisms seems to be evolutionarily adaptive:
- cardiac response facilitates active coping by shunting blood to skeletal muscles - fight-flight response
- situations that do not require decisive action but instead need skeletal muscle inhibition and vigilance (freeze-response) vascular mechanism is adaptive
- shunts away blood from periphery to internal orans in case one ecxperiences a wound
- also immune system is responing by macrophages and natural killer cells depart from lymphatic tissue and spleen to bloodstream (temorarily raising number of immune cells in blood; leukocytosis)
- then wander to battle stations e.g. skin where wounds are likely
10
Q
What are the cardial consequences of Chronic Stress?
A
- acture stress response becomes maladaptive if it is continuously activated (Selye 1956)
- chronic SNS activation leads to:
- sustained blood pressure elevation
- forces heart to work harder causing hypertrophy of left ventricle, over time elevated BP, damaged arteries, plaque
- vascular hypertrophy; i.e. muscles that constrict the vasculature thicken leading to
- elevated RBP and
- response stereotypy
- or a tendency to respond to all stressors with a vascular response
- sustained blood pressure elevation
11
Q
What are hormonal consequences of a Chronic Stress Response?
A
- immunity is suppressed through elevated basal levels of stress hormones directly affecting ccytokine profiles
- cytokines are communicatory molecules produced by immune cells.
- there are three types of cytokines:
- Proinflammatory cytokines that mediate acute inflammatory reactions
- Th 1 cytokines mediate cellular immunity by stimulating jatural killer cells and cytotoxic T cells
- Th 2 cytokines mediate humoral immunity by stimulating B cells to produce antibodies (they “tag” extracellular cells, e.g. bacteria)
- stressors such as examination can lead to a Th2 shift (increase in Th2 cells relative to Th1 cells) which suppresses cellular immunity in favor of humoral immunity.
- more chronic stressors can lead to suppression of humora (Th2) and cellular (Th1) immunity
- intermediate and chronic stressors are realted to slower wound healing, recovery from surgery, antibody responsesantiviral deficits
- particularly problematic for the elderly who may have immunoscenescence (gradual loss of immune function due to age)
12
Q
Stress and Cardiovascular disease.
A
- Occupational gradient in Coronary Heart Disease (CHD): men with lowest socioeconomic status have poorest health outcomes
- variance can be accounted for with lack of perceived job control, also smoking, alcohol use and sedentary lifestyle, behaviours that may be facilitated via stress
- for men: work stress seems to predict CHD and hypertension
- among women with existing CHD marital stress seems to be predicting poor prognosis
- atherosclerotic CHD (Kaplan et al., 1982): studied male cynomolgus monkeys:
- stressor: reorganising group every three months so they have new companions and moderate atherogenic diet for all monkeys
- were assessed for their relative dominance
- socially dominant monkey iin unstable groups had more atherosclerosis than socially less dominant monkeys
- socially dominant males in unstable groups had more atherosclerosis than their counterparts in stable, unchanging groups
- heart-rate reactivity to threat of capture predicted atherosclerosis
- SNS blocking agent decreased progression of atherosclerosis
- findings that affiliative social behaviour decreased progresseion of atheroclerosis even if the rabits had a genetic predisposition and stable groups exhibited koore such behaviour compared to changing groups
13
Q
Stress and Upper Respiratory Disease (Cold).
A
- stress predicts scusceptibility to common cold
- maybe they just spend more time outside?
- people that were quarantined and exposed to Rhinovirus and had been exposed to life-stress were more likely to catch a cold (events lasting longer than a month), those that had shorter stress did not catch it more often
14
Q
Human Immunodeficiency Virus and Stress
A
- faster HIV progression to AIDS associated with cumulative stressors, use of denial as coping, lower satisfaction with social support and elevated cortisol levels.
15
Q
Stress and Inflammation, The Immune System and Physiscal Health.
A
- despite its immunosuppressive effects, stress is also associated with exacerbatioons of autoimmune disease and CHD
- acute stress response includes activation of cells to innate immune system (effect mediated by pro-inflammatory cytokines)
- in chronic stress cortisol eventually suppresses proinflammatory cytokine production, in people with autoimmune disease or CHD stress lead to a chronic activation of the proinflammatory cytokine production
- Miller et al. (2002) glucocorticoid-resistance model argues thatimmune-cells become resistent to effects of cortisol through reduction of cortisol receptors.
- so cortisol cannot suppress inflammation, stress will promote proinflammatory cytokine production indefinetly
- implications for rheumatoid arthritis were excessive inflammation leads to joint damage, swellimg pain and reduced morbidity
- in multiple sclerosis (MS) overactive immune system targets myeline surround nerves eventually leading to blindness and paralysis
- in CHD. immune system responds to vascular injury just like any other wound: immune cells infiltrate artery wall which can eventually lead to thrombosis (i.e. clot)
- elevated inflammatory markers as C-reactivity protein (CRP) predicts heart attack
- CRP has been associated with major depressive episodes in men
