Lectures 2, and 3 Are Risk factors Causal? Biological Plausibility: cardiovascular Reactivity.

Post on 01-Apr-2015

212 views 1 download

Transcript of Lectures 2, and 3 Are Risk factors Causal? Biological Plausibility: cardiovascular Reactivity.

Lectures 2, and 3

Are Risk factors Causal?

Biological Plausibility: cardiovascular Reactivity

General reading in Health Psychology

To make the most of this course you should read the relevant sections in one of the recommended introductory texts, either Taylor or Sarafino.

In Taylor you should read Chapter 2 “Systems of the body” Pages 17-31 (nervous, endocrine and Cardiovascular systems). Chapter 6 “Stress” Complete Chapter (pages 152-182). Chapter 7 “Moderators of the stress experience” (pages 183-211) (Combined as “Stress & Coping” in earlier editions.

In Sarafino the equivalent chapters are essentially Chapter 2 pages 31-40, 49-51, and Chapters 3, 4 & 5 (pages 61-138).

More Reading

Another good general book is Baum, Gatchel and Krantz An introduction to Health Psychology, Chapters 2, 3 and 5.

For those who wish to find out more about of Obrist and Brod (mentioned in Lecture 2) the references are below. Not required reading.

Obrist,PA,Gaebelein,CJ,Teller,ES,Langer,AW,Grignolo,A,Light,KC,McCubbin,JA,(1978) The relationship among heart rate, carotid dp/dt and blood pressure in humans as a function of the type of stress

Psychophysiology,15,102-115 Brod J Fencl, V, Hejl, Z, Jirka, J (1959). Circulatory changes underlying blood pressure elevation during acute emotion stress (Mental arithmetic) in normotensive and hypertensive subjects. Clin Sci, 18, 269-279.

Cardiovascular Reactivity: Some reading

The most cited reference on the topic of CV reactivity is Krantz DS & Manuck SB (1984). Acute psychophysiologic reactivity and risk of cardiovascular disease: a review and methodological critique. Psychol. Bull., 96, 435-464. While old it is an important paper. It is demanding reading. The sections on CV disease will be relevant to later lectures. It can be found on PsycArticles in library Metalab

There was special section of Psychosomatic Medicine devoted to Cardiovascular Reactivity in 2003. Read

Linden WL, Gerin & Davidson K (2003) Cardiovascular reactivity: Status Quo and a research agenda for the New Millennium. Psychosomatic Medicine, 65, 5-8

CV Reactivity

Kamarck TW & Lovallo WR (2003) Cardiovascular reactivity to psychological challenge: conceptual and measurement issues. Psychosomatic Medicine, 65, 9-21.

When discussing appraisal I shall lean heavily on the studies reported in:

Tomaka, Blascovich, Kelsey & Leitten (1993) Subjective, physiological and behavioral effects of threat and challenge appraisal. J. Per. Soc. Psychol., 65, 248-260.

Tomaka, Blaskovich, Kibler & Ernst (1997). Cognitive and physiological antecedents of threat and challenge appraisal J. Per. Soc. Psychol, 73, 63-72

Blascovich & Tomaka present a fuller account of their views in Blascovich & Tomaka (1996) The biopsychosocial model of arousal regulation. Adv. Exp. Soc. Psychol., 28, 1-51.

References on social support and cardiovascular reactivity

Kamarck T (1992) Recent developments in the the study of cardiovascular reactivity: contributions from psychometric theory and social psychology. Psychophysiology, 29, 491-503.

Lapore SJ et al, (1993) Social support lowers cardiovascular reactivity to an acute stressor. Psychosomatic Medicine, 55, 518-524.

Lapore SJ (1995). Cynicism, social support and cardiovascular reactivity. Health Psychology, 14, 210-216.

When is a risk factor casual

Temporality Strength of relationship

Consistency Biological gradient

Biological Plausibility Coherence

Outcome Specificity Intervention evidence

Causality (cont)

Temporality: are there prospective studies demonstrating that x precedes development of disease?

Strength of relationship: How much of the variance in disease incidence explained by x?

Consistency: Are studies consistent in their findings?

Biological gradient: is severity and/or frequency of x associated with increasing risk of disease?

Biological plausibility: what pathogenic mechanisms link x to disease?

Causality 3

Coherence: Does evidence for the relation between x and disease come from different samples (population, patient, animal models)?

Outcome specificity: Is the risk associated with x exclusive to one disease?

Intervention Effects: Is the disease prevented if x is treated early enough?

Basic Model

The Reactivity Hypothesis: excessive cardiovascular response to stress is a risk factor for cardiovascular disease.

Simplified model of the cardiovascular (i.e., heart and blood vessels) system

CV system

Cardiovascular measures

Heart Rate (HR): Number of cardiac cycles per minute

Systolic Blood Pressure (SBP): Maximum blood pressure in a cardiac cycle

Diasystolic Blood Pressure (DBP): Minimum blood pressure in a cardiac cycle

Mean Arterial Pressure (MAP): Average blood pressure over a cardiac cycle

Cardiovascular measures (cont.)

Stroke Volume (SV): Amount of blood pumped in a cardiac cycle

Cardiac Output (CO): Amount of blood pumped in unit of time

CO = SV x HR

Total Peripheral Resistance (TPR): The total resistance in circulatory system to the flow of blood.

MAP= CO x TPR

One participant from Brod 1959

Participants from Brod 1958 split into cardiac and vascular responders

Obrist et al, 1978. Hard but not impossible produces Active Copying

Obsrist et al 1978. Active Coping (RT, Reaction time task) has larger cardiac effect than Passive Coping (CP – cold pressor) or watching pornographic film. NB. Effect of Active Coping much reduced by Beta Blocking drug which largely removes effect of sympathetic nervous system on the heart.

Obrist et al 1978. Carotid dp/dt measure of force of heart contracting. Large effect of Active Coping.

Manuck. Comparison of Cardiac & Vascular Reactors on Mental arithmetic (active coping task, cf Brod)

Manuck. All subgroups similar on mirror tracing task

Autonomic Nervous System- seriously simplified

Sympathetic Nervous System - quite diffuse

Neurotransmitter Noradrenaline

Receptors Adrenoreceptors

Beta - Heart - Increase HR & Contractility

Alpha - Smooth Muscle (e.g, vasculature) -

contract small blood vessels

Parasympathetic Nervous System- quite specific

Neurotransmitter acetylcholine

Receptors cholinergic

Heart- slows heart rate, minor effect on Contractility

Lazarus: Transactional Model of Stress & Coping. Most influential model of stress that underpins Tomaka & Blascovich studies

Tomaka & Blascovich, following Lazarus & Folkman: 2 common stress related appraisals

Threat : perception of danger greater than perception of coping abilities

Challenge: perception of danger less than perception of coping

Threat associated with negative emotions - However challenge associated with more CV activation (Obrist Active passive distinction)

Tomaka & Blascovich attempt to clarify this.

Task: Mental arithmetic (Active Coping)

Threat: rating of threat greater than rating of ability to cope (Primary/Secondary).

Challenge: rating of coping greater than rating of threat.

After task ratings of experienced stress obtained.

3 studies, Study 1 preliminary.

Study 2.

Mental arithmetic. Subjects classified into threatened or challenged.

Results

Subjective & Behavioural

Threat group More Stress 3.85 v 2.85 on 7 point scales

Threat group performed less well 2.19 v 2.85 (self ratings) and produced less correct answers, 10.5 v 14.00

NB results most clear cut first time tasks carried out.

Physiological ….

Challenge has cardiac effects, threat vascular. NB Pre-ejection period relates to force that heart contracts. It shortens with challenge and more usual to show changes as negative

Tomaka et al (1997) Cont.

They attempted to test causality of appraisal by

1. Manipulating appraisal.

Threat: emphasis on speed, accuracy.

Challenge: See task as challenge and yourself as someone who can do it. (see next slide)

2. Manipulating physiological response (reverse causality)

1. Exp 2. Alter CO with exercise- no effect on appraisal

2. Exp 3. Alter TPR with cold pressor- no effect on appraisal

-20

-10

0

mse

c

Pre-ejection PeriodTomaka 1997 Manipulating Appraisal

Threat Challenge

0

1

2

l\min

Cardiac OutputTomaka 1997 Manipulating Appraisal

Threat Challenge

9.00

10.40

11.80

13.20

14.60

16.00

bpm

Heart RateTomaka 1997 Manipulating Appraisal

Threat Challenge

.-80

-48

-16

16

48

80

dyne

s

Total Peripheral ResistanceTomaka 1997 Manipulating Appraisal

Threat Challenge

Experimental manipulation of threat and challenge has predicted effects

Social Support reduces risk of heart disease.

Does it affect reactivity?

Is effect of social support a main effect or does it buffer effect of stress?

SBP DBP HR

0

10

20

30

BP a

nd

HR

Kamarck, Manuck & Jennings 1990Social support and CV reactivity

Alone

Friend

Presence of friend reduces CV response.

Low Threat High Threat

0

10

20

SB

P

Kamarck et al 1995Affiliation, social threat & CV responses

Alone

Accompanied

Effect of social support only clear under high threat. Buffering?

Lepore (1993) study of Social Support. Presence of non-supportive person increases BP

Effects of Social support may depend on personality of recipient

Study by Kamarck of social support (or a related process?) in real life.

Cardiovascular Reactivity (CR).

Things that should be true if CR is a risk factor

•Is it an individual difference variable?

•Is it reliable?

•Is it one factor?

•Does it generalise?

Steptoe & Vogele 1991 Reliability of CV response to mental stress testing

Test-retest correlations

HR .62

SBP .52

DBP .30

Cardiovascular Reactivity. Issues.

•Is it an individual difference variable?

•Is it reliable?

•Is it one factor?

•Does it generalise?

Kamarck 1992 again. Most corr. large and positive

Cardiovascular Reactivity. Issues.

•Is it an individual difference variable?

•Is it reliable?

•Is it one factor?

•Does it generalise?

Anastasiades & Johnston (1991)

0

40

80

120

160

200

Hea

rt R

ate

(bpm

), A

ctiv

ity

& P

ostu

rePhysicalActivity

Posture Heart Rate

Median split on laboratory reactivity

HR Control HR Tutorial

Low Reactors 81.4 88.6

High Reactors 78.7 96.6

Johnston D.W., Tuomisto M.T., & Patching, G.R. (2008) The Relationship between Cardiac Reactivity in the Laboratory and in Real Life. Health Psychology. 27, 34-42

0.00 3.00 6.00 9.00 12.00 15.00

Tense Arousal

81.2

83.3

85.4

87.5

89.6

91.7

93.8

95.9

98.0

100.1

102.2

HR

REACTRES = -4.102065

REACTRES = 5.457194

High Reactors

Low Reactors

Johnston, 2004, Relationship between subjective arousal & HR in HI and LO cardiac reactors

Does CR to stress generalise.

Appears to generalise to a range of stressful situations

Suggests that people who are vulnerable and produce large CV response may be at risk if exposed to stress, i.e., Stress and diathesis (or vulnerability) model

Mechanisms? Zanstra