A comprehensive course text based on the lecture notes for Health Psychology Part 2 by von Leupoldt Andreas. This document includes all the information from the slides, as well as additional notes from the lectures. It is highly organized with a clear table of contents (which you can find for free ...
HEALTH PSYCHOLOGY
INTRODUCTION
Aims:
1. Thorough knowledge and insight into the basic processes of psychological stress. These imply:
Homeostatic regulation& the autonomic nervous system
Central integration of stress response
Inhibition of stress responses
Endocrine stress reactions
Psychoneuroimmunology
Genes, stress and behavior
Individual differences in stress reactivity
2. Knowledge ofcontemporary research topics regarding health effects of stress, with a special focus on the
(presumed) explaining mechanisms.
Furthermore, students are able to relate these research topics with the basic processes of psychological
stress. The selected topics can change from year to year.
Examples are: psychological factors in the progression of cancer, chronic stress and the metabolic syndrome,
influence of prenatal stress from mother on child, psychoneuroimmunology and wound healing, medical
unexplained complaints, mental representation of pain, psychosocial factors in cardiovascular,
gastrointestinal and respiratory disease.
3. Situating and critically evaluating research on effects of stress on health
4. Developing an attitude to consult also scientific literature outside the field of Psychology(e.g., general
scientific or medical journals) and to relate these to psychological literature and models.
5. Insight into the relevance of research findings for the setup or evaluation of clinical health psychology
interventions.
Disciplines
Psychology: Models on Behaviour & Mental processes (learning, reasoning, perception)
Neuroscience: How does the brain function
Medicine: How does the body function
Exam
Written, closed book exam during exam period
Multiple choice questions in English (with guess correction)
The basis of the exam are:
- the slides
- 1 book chapter from Lovallo (Stress and the endocrine system, p. 115-136)
additional literature on ULTRA/Toledo helps you to better understand the topics (so you should read it), but
it is not required for the exam (You don’t have to learn the videos)
1
,content
1. psychophysiology of stress
homeostatic regulation
central integration of the psychological stress response
endocrine stress response (self-study)
psychoneuroimmunology
2. biopsychological interactions relevant to health
emotional and cognitive modulation of pain
biopsychosocial aspects of asthma
biopsychosocial aspects of COPD
positive psychology
biopsychosocial aspects of dyspnea
physical activity
gastrointestinal disorders
PSYCHOPHYSIOLOGY OF STRESS
HOMOSTATIC REGULATION
Chapter 3: Stress & Health. Biological and psychological interactions – Lovallo
1. INTRODUCTION
Organism’s ability to keep its internal environment stable, despite changes in the external environment
- e.g., temperature, blood pH, oxygen pressure, blood glucose
Central nervous system = Interface for interaction with external environment
‘Stress’ = threat to homeostasis, the power to bring
this balance out of balance
- Stressor: something of outside
o Physical (e.g. cold)
o Psychological (e.g. anticipation of pain like
seeing a knife, exam)
- Compensatory stress response: to get the
balance back
Physical vs Psychological Stress?
- They are both posing the homeostatic threat,.
Both stressor act at the same systems.
2
,2. HOMEOSTASIS
2.1. feedback control
Temperature
When it is hot outside the
body temperature rises a little
bit. Our nervous system detect
that and signal that to our
blood vessels in the skin, that
they should dilate: to have
more blood flow and give a
signal to sweat. So the body
can give away heat to his
environment. The same
happens when it is could
outside. Our body will stop
sweating and our blood
vessels will constrict so we
have less blood flow. Here we
will conserve our body
temperature. If that shouldn’t
be enough our body can let
our muscle to contract, that is
when you shivers.
Blood pressure
High blood pressure isn’t good. We have baroreceptor that can
detect changes in the pressure of our blood of the arteria. That
is send by the glossopharyngeal nerve to the medulla of the
brain stem. From their signals are send to the heart to adjust
the heart rate and also the blood pressure.
Blood pH levels/ arterial carbon dioxide pressure (PaCO2)
When we breath in a normal sitting
condition the levels are in a normal
range. When some starts to
hyperventilate, you breath faster and
you breath more CO2 out of your body.
The blood pH levels increase, that signal
sends to our brain stems that leads as an
answer to decrease stimulating of the
respiratory centres. That reduces the
stimulating of our breathing muscles and
as a result ventilating reduces and blood
levels of CO2 increase. The blood pH level
will be back his normal range. In the
other way it would give the same
homeostatic result, the opposite will
happen.
3
,2.2. feedforward control
Perturbations are being anticipated & corrected before they occur . The body has learned that something is
going to happen and does already something to prevent.
Classical conditioning as a viable mechanism
e.g., “Exercise Hyperpnea” Increases in ventilation and heart rate occur at the onset of physical exercise,
even before an increase in PaCO2. When you start to jog, your body notice and before you have big changes
in your blood level, your body will already start to breath faster and so on.
3. HIERARCHY OF HOMEOSTATIC CONTROLS
3.1. intrinsic control mechanisms
Vital organs and local reflexes
don’t need a lot of extra input of higher systems
Organ adapts its functioning on its own in response to slow, local changes
Example: Frank Starling Mechanism
- If returning (venous) blood volume increases then atrium chambers fill more before next beat
- more effective filling of atria creates more wall stretch and more muscle fiber tension
- more vigorous contraction on next beat
- left ventricle empties more completely
- more effective blood flow into aorta
Heart responses to flow demands caused by systemic circulation
Only possible when conditions are relatively stable: if you just start to stand up, this mechanism will not be
enough, only for small changes.
3.2. autonomic control mechanisms
Brainstem controls autonomic messages
We have a neuron with a cell body, nucleus,
long axon with a synapse and short
dendrites to connect to the next neuron.
This is the way how signals are transported
in out nervous system.
3.2.1. Autonomic nervous system (ANS)
Viscera (inner organs, heart stomach
longs …): limited awareness &
voluntary control ‘AUTONOMIC’
Negative feedback
ANS have different components
- Sensory pathways (afferent)
upwards
- Motor pathways (efferent)
downwards
- Divisions: sympathetic (SNS), parasympathetic (PNS), (enteric)
- Reciprocal regulation of organic function: decrease/increase is different by the parasympa/sympa
4
, Each division had
- Sensory pathways from organs via ganglia to brainstem (afferent)
- 4 response components (efferent):
a) descending autonomic and pre-ganglionic fibers
(hypothalamus/brainstem intermediolateral cell column of spinal cord
b) ganglion
(relay station for as-/descending signals, also part of local regulation system/reflexes)
c) postganglionic fibers
(messages more elaborated than in preganglionic fibers)
d) neuroeffector junctions
(postganglionic fiber/receptor at target tissue, nerve impuls motor action)
difference by the PNS: the origin is different more cranial position and more sacral position. Secondly the
preganglion is typically very long.
5
,Sympathetic division ANS
1:10 pre-vs postganglionic nerves
- General, broad influence on viscera: one pre ganglionic nerves serves 10 post ganglion nerves
- Extensive linkages across widely distributed ganglia
- Closely integrated actions across different organs (‘in sympathy’)
Neurotransmission:
- Acetylcholine (preganglionic)
- Norepinephrine (postganglionic): smooth muscle cells, cardiac muscles and pace maker: activating
function
- except: (a) sympathetic preganglionic nerves release acetylcholine at adrenal medulla
release of catecholamines (Nor-/Epinephrine) into blood
(b) sympathetic nerves release acetylcholine at sweat glands (hands, feet)
More active during stress
- Crucial for Fight/flight responses: pupil dilate, mouth gets dry, necks and shoulder muscles tense,
epinephrine release, blood pressure rises, …
Parasympathetic (vagal) division ANS
Ganglia more specific and nearer to target organ
1:3 pre-vs postganglionic nerves (lower ratio)
- localized, specific actions directed at one organ
Neurotransmission
- Acetylcholine preganglionic
- Acetylcholine (postganglionic): smooth muscle cells & cardiac muscle and pace maker: inhibitory
influence
Less active during stress
Supporting energy conservation, reproduction, digestion
Vagal division: vagal nerve it is the biggest part of the parasympathetic system
Overview
6
,3.2.2. Autonomic control of heart rate
Interaction occurs by both branches of ANS
(para)sympathetic outflows to SA-node: heart rate increase/ decrease
Electrocardiogram (ECG/EKG)
Registration of electrical activity of the
heart
Willem Einthoven (1860 –1927) Nobel prize
medicine 1924
PQRST wave in a certain path. P wave atria
activate, QRS ventricle activate, T wave
recovery
Heart rate (HR)
- Expressed in ‘beats per minute’ (bpm)
- Count number of R-peaks per minute: that is the
most visible component for each heartbeat
Heart period (HP)
- Interbeat interval (IBI) in msec, time distance
- Time between R-peaks (R-R interval)
How can we use such a measure in relation to stress:
before, during and after exam. Before the exam about
70 bpm, during exam higher activity, after exam it is a
lot lower.
7
,Heart rate variability (HRV)
Variability in time between to heart beats. It means that the time difference between to heart beats are
sometimes a bit longer or shorter.
Vagal influences on SA-node occur at respiratory rhythm
- Respiratory ‘gating’ of autonomic outflow (Eckberg, 2003)
- Only vagal influences allow for such rapid fluctuations in heart rate
Respiratory Sinus Arrhythmia (RSA)= variations in heart rate at respiratory rhythm
- inspiration: less vagal outflow, heart accelerates
- expiration: more vagal outflow, heart decelerates
8
, Time Domain Measures:
- Root Mean Square of Successive Differences (rMSSD)
- represents short term variation of heart rhythm
- rMSSD ↑ = ↑ vagal input; rMSSD ↓ = ↓ vagal input
Frequency Domain Measures:
- Ultra low frequency (ULF): < 0.00335 Hz
(circadian rhythms, other long term changes in heart rhythm)
- Very low frequency (VLF): 0.00336-0.04 Hz
(sympathetic + vagal effects, thermo regulation, vasomotoric, …)
- Low frequency (LF): 0.041-0.15 Hz
(tonic sympathetic + vagal effects, blood pressure regulation, …)
- High frequency (HF): 0.151-0.40 Hz
(vagal input; but not exclusively: also moderated by respiration)
General significance of HRV: Indicates the individual flexibility of the heart activity to fit endogenous and
exogenous demands. It can better adapt. Greater HRV is associated with better mental and physical health.
HRV is a certain range, we don’t speak about extreme orders are good like in a panic attack.
HRV (RSA) correlates with: e.g.
- Stress, depression & anxiety, Cardiac mortality, Emotional regulation, Executive functioning
HRV and mental disorders
Groups matched on: age., sex, BMI, alcohol use
similar level of depression across MDD groups
no medicated patients, no individuals with comorbid physical illness
2min resting state ECG measurement
Reduced HRV in MDD major depressive disorder (time and frequency domain)
Reduced HRV most pronounced in MDD + GAD with the highest psychological compatibility
HRV and cardiac disease
Patients with cardiac disease often show comorbid major depression
Depression associated with increased cardiac mortality via HRV? Related?
9
, 65 CAD (coronary artery disease) patients with depression vs. 54 CAD patients without depression
24h-ambulatory ECG monitoring
comparable in several risk factors (eg: age, sex, echocardiographic and inflammatory parameters)
Reduced HRV in CAD patients with major depression
Greater autonomic dysfunction plausible mechanism linking depression to increased cardiac mortality
311 MI (myocardial infarction) patients with depression vs. 367 MI patients without depression
24h-ambulatory ECG monitoring after hospital discharge followed up for 3 years
Low HRV partially mediates the effect of depression on survival after acute MI, low survival change
HRV Biofeedback training
HRV is changeable (but more/long-term studies required)
Usually via slow deep breathing (approx. 6 breaths/minute)
Potential mechanisms not fully clear, but may include:
(1)phase relationships btw. HR oscillations and breathing at specific frequencies
(2)phase relationships btw. HR and blood pressure oscillations at specific frequencies
(3) activity of the baroreflex
(4) resonance characteristics of the cardiovascular system
(5) vagal afferent signals
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