low-m, of Ps~choromrrc Rmearch, Vol. 35. No. 6. PP. 633-644, 1991 0022L3999/91 E3.00+ .

OCI
Prmtd in Great Britain. 0 1991 Pergamon Pres5 plc

INVITED REVIEW

THE LINKS BETWEEN STRESS AND ILLNESS

ANDREW STEPTOE

Abstract-Evidence relating stress with illness has emerged from a variety of experimental, clinical and
epidemiological research strategies. Psychobiological stress responses emerge through an imbalance
between demands and psychosocial resources, and many factors relevant to this transaction have been
identified, including the chronicity and predictability of stimulation, opportunities for control, psychological
coping responses and the availability of social supports. By contrast, the mechanisms through which
stress responses may increase risk of illness are poorly understood, and investigators are frequently
obliged to fall back upon a poorly defined biological predisposition to account for individual differences
in susceptibility to disease or variations in clinical course. It is argued in this review that several distinct
cognitive-behavioural and psychophysiological mediating processes may be postulated, and that these
are relevant to different types of influence on health (acute and chronic effects, causal and facilitatory
processes, impact on aetiology, maintenance, relapse or recurrence). It is through the recognition and
identification of separate processes that questions concerning the specificity of illness outcome, personal
resilience, the limits of the impact of psychosocial factors, and the appropriate forms of therapeutic
intervention, may be resolved.

INTRODUCTION

THE NOTION that stress influences the aetiology and maintenance of illness has
generated a vast literature. The spectrum of studies has been wide, ranging from
investigations of cellular phenomena relevant to autonomic-endocrine-immunological
integration, to epidemiological studies of psychosocial factors and health. There are
many controversial issues and empirical findings, and the role of stress processes in
many clinical conditions is not widely accepted. One limitation of research in this
field is that while there has been considerable progress in understanding the way in
which interactions between demands and resources generate psychobiological stress
responses, the pathways through which these responses affect disease remain poorly
articulated. The most influential theoretical developments of recent years have con-
cerned factors such as social support, personal resources and the coping process
11-31, while models of the mechanisms linking stress with illness have not kept pace
with experimental and clinical observations. The aim of this paper is therefore to
provide a framework within which current research can be understood. It is argued
that in terms of aetiology and maintenance of illness, the traditional distinctions
between psychiatric disorders, physical disorders in which a psychological com-
ponent can be identified (psychosomatic disorders), and physical disorder without
psychological involvement, is outmoded. Rather, psychosocial factors may influence
the entire spectrum of health disorders. In some circumstances, stress-related pro-
cesses may be involved in the initiation of disease, but more commonly they affect
the course, severity and prognosis of the condition, to an extent that varies between

Department of Psychology, St. Georges Hospital Medical School, University of London, U.K.
Address correspondence to: Dr Andrew Steptoe, Department of Psychology, St. Georges Hospital
Medical School, Cranmer Terrace, London SW17 ORE. U.K.

633
634 Invited Review

patients. The problem of individual differences in susceptibility is a central concern

which can be better elucidated when the full repertoire of behavioural and physio-
logical pathways is delineated.

MODELS OF STRESS AND COPING

The term stress is used with notorious vagueness in the experimental and clinical
literature [41. I have argued elsewhere 151 that it is fruitless to employ stress as more
than a general term defining a broad range of phenomena. In this review, it will refer
to the complex of emotional and behavioural reactions and their physiological
correlates described in more detail below, while the conditions potentially giving rise
to these responses are described as psychosocial stressors or demands. It is widely
recognized that stress cannot be defined simply as the response to aversive environ-
mental stimulation or disturbing events. The same event may produce quite different
responses in two people or in the same person on different occasions. Despite
reservations from some investigators 161. most contemporary theories of stress are
therefore transactional in nature, arguing that the conditions giving rise to stress
responses involve encounters in which there is an imbalance between stimuli and
psychosocial resources [ 1, 71. This interaction is illustrated in Fig. 1 as Stages I and
II. Many factors have been shown to influence the intensity of psychobiological
stress responses. These will not be described in detail, since they have been reviewed
extensively in recent texts. However, in terms of psychosocial demands, important
factors include the intensity, chronicity and complexity of stimulation [81, and its
novelty, predictability and potential controllability [9, 101. The resources that people
bring to bear in stress transactions include their prior experience with threatening
encounters [ 111, personal qualities such as optimism and hardiness [ 121, together
with external factors such as social networks and support [21. These factors are
modulated through psychological coping responses. Several types of coping response
have been identified, and one of the most exciting issues currently under investi-
gation is trying to understand which coping responses are most adaptive in particular
situations [131. Progress is also being made towards the classification of coping
responses into clusters that are relevant to salient patterns of behaviour [ 141. It
should be emphasized that although demands and resources are viewed as distinct
entities, they are of course difficult to disentangle in practice. For instance, social
isolation can be conceived both as the absence of a resource or as a factor con-
tributing to psychosocial demand, while parameters of stimulation such as control-
lability depend on the persons appraisal of the situation together with outcome and
efficacy expectations.
The psychobiological stress response itself (Stage II) is a loosely coupled system
involving adjustments at the affective, cognitive and behavioural levels, together
with associated changes in neuroendocrine, autonomic and immune function [ 151.
The original research on stress inspired by Hans Selye focused on the neuroendocrine
features. visualizing the stress response as a nonspecific pattern of activation adapted
to protect the organism from environmental hazard. Modern research has challenged
this view in a number of respects. Firstly, the notion of nonspecificity cannot be
maintained in the light of studies indicating that the pattern of neuroendocrine and
autonomic response varies according to the emotional demands elicited I1 61. This is
 Invited Review 635

II

1 DISEASE 1 IV

FIG. I. Conventional stress-vulnerability model.

not simply an intensity effect. but a consequence of the coping behaviours engaged
in the situation. Patterning becomes even more important when cognitive responses
are taken into consideration, since selective changes in information processing
capability with different types of exposure have been identified 1171. Secondly, the
hypothesis that the physiological stress response is adapted to bolstering the organisms
biological defences is hard to reconcile with features such as the anti-inflammatory
and immunosuppressive effects of glucocorticoids. Instead, it has been argued that
several components of the activation profile may have a regulatory rather than a
direct resistance function [ 18, 191. They may protect against the overshoot of other
defence responses, but in doing so can render the organism more rather than less
vulnerable. Thirdly, the conventional view that peripheral physiological changes are
secondary to central nervous system activation in the stress process is misleading in
the light of evidence concerning the bidirectional traffic between the two [201. In
view of these reservations, it becomes facile to discuss stress as if it involves a
generalized response profile. Rather, greater attention must be paid to the particular
demands on people, and the resources that they have at their disposal.

INDIVIDUAL DIFFERENCES IN ILLNESS SUSCEPTIBILITY

Models linking psychobiological stress responses with illness must account for two
major problems 1211. The first, which can be termed the intensity issue, is the
problem of why some people become ill when exposed to adverse circumstances and
life experiences while others do not. The second, termed the variability issue, is why
susceptible people who have similar life experience develop different types of illness.
These individual differences are conventionally explained by invoking the biological
and genetic predisposition of the person 122, 231. This is shown as Stage III of Fig.
1. The argument is that the extent to which psychobiological stress responses
dissipate without causing damage, or else contribute to increased risk of disease,
depends on the constitutional vulnerability and the locus minoris resistentiae of the
636 Invited Review

individual. Among factors thought to determine biological predispositions are genetic

make-up, health status, nutritional state, physical fitness and pre-existing pathology.
In relation to the intensity issue, it can therefore be inferred that some people are
more susceptible to adverse life experience than others because of differences in
these predisposing factors. The variability of disease outcomes may be explained by
hereditary factors (such as a genetic predisposition to coronary heart disease), or by
the presence of pre-existing pathology.
These factors are certainly important, and go some way towards explaining indi-
vidual differences in response. In studies related to hypertension, for example, it has
been demonstrated in animal models that hereditary predisposition and nutritional
status (salt intake) interact with aversive environmental stimulation in producing
renal changes and elevated blood pressure [24, 251. Normotensive humans with
family histories of hypertension have a tendency towards heightened cardiovascular
responses to actively challenging tasks [261, a pattern that may be representative of
the more general psychophysiological notion of individual-response specificity [271.
Cardiovascular responses to mental stress tests are also modulated by such factors
as physical fitness and age [281. Yet there are limits to the usefulness of biological
predisposition and vulnerability factors in accounting for individual variations in
susceptibility. The first is that most of the vulnerability factors that have been iden-
tified are non-specific, increasing or decreasing risk in a general way. For example,
a sedentary lifestyle, poor nutrition and old age increase vulnerability to a range of
stress-related complaints, and not to specific problems. These factors are therefore
more relevant to the intensity than the variability issues. Of course, this may not be
seen as problematic, and there is an epidemiological tradition that explicitly espouses
a nonspecific role for psychosocial factors, suggesting that they increase or decrease
host resistance without having an influence on the nature of health outcomes I29, 301.
Such a position is not appealing from the psychophysiological and clinical perspec-
tives since it places the more interesting issues of disease aetiology outside the orbit
of emotional and behavioural factors. The second difficulty is that predisposing
factors and genetic markers are obscure for all but a handful of conditions [311. In
most cases therefore, predisposing factors are inferred retrospectively, following
illness onset. This limits the ability of biological vulnerability and predisposition to
explain individual differences across a range of illnesses.
Another possible explanation for at least some of the individual differences in
susceptibility may lie in the specific patterns of psychobiological response to par-
ticular experiences. As noted earlier, characteristic profiles of autonomic and
endocrine response may be associated with particular patterns of coping behaviour,
which may in turn be determined by situational factors and perceived resources. In
animal studies. for example, it has been suggested that effective control over threat
is coupled with increased noradrenaline and testosterone output, while active
behavioural coping or effortful striving are associated with raised adrenaline and
O-endorphin levels and with mobilization of stored energy supplies, and loss of
control and withdrawal are correlated with parasympathetic discharge and release of
corticosteroids [321. In terms of pathology, the active coping responses of sub-
dominant rats may promote high blood pressure, while subordinates who withdraw
behaviourally display marks of immunosuppression [331. These findings may provide
the basis for specific event-illness associations. Harris and Brown [341 have argued
 Invited Review 637

from life event research that particular classes of events combined with specific
vulnerabilities may lead to specific illnesses. Thus loss events occurring in people
with low self-esteem may trigger depression, while goal frustration in striving
individuals who display stubbornness may lead to gastrointestinal disorder.
It is as yet too early to know how far specific event-vulnerability associations can
predict the nature of resulting disease. Research on the psychophysiological substrate
has only identified broad categories of autonomic and endocrine discharge related to
patterns of coping, rather than precise associations with disease endpoints 1351. In
order to understand individual differences more fully, it is necessary to consider the
pathways through which psychobiological stress effects are mediated.

COGNITIVE-BEHAVIOURAL PATHWAYS

Two major pathways can be distinguished through which psychobiological stress

responses may influence health 1361. These are cognitive-behavioural and psycho-
physiological pathways, and are illustrated in Fig. 2. Much of the research in
psychosomatics is concentrated on the psychophysiological pathway, so it is easy to
overlook the importance of cognitive-behavioural mechanisms.
The involvement of cognitive-behavioural pathways implies that the cognitive,
affective and behavioural components of the psychobiological response can influence
health independently of any direct action of stress on physiological systems. Within
this framework, several mediating processes can be distinguished. The most important
possibility is that psychosocial stressors influence health through alterations in
health-related behaviours and practices. These include such activities as drinking
alcohol, cigarette smoking, regular exercise, sexual behaviour, and the use of seat
belts. The importance of risk behaviours and positive health practices was recog-
nized in the Alameda study more than two decades ago, and has since been exten-
sively corroborated 137, 381. The relevance of these practices to the present
argument is not merely that they influence health; nor is it assumed that psychosocial
stressors are the main determinants of such behaviours 139-4 1I. Rather, it is that the
pattern or frequency of health-related practices may be affected by psychosocial
stressors. Although some of the associations are controversial 1421, a number of
studies have shown that increases in substance abuse 1431, alcohol consumption 1441,
and dietary fat consumption 1451, together with changes in smoking frequency and
the likelihood of relapse following smoking cessation 146, 471, may coincide with
stressful life episodes. The extent to which this mechanism is responsible for changes
in disease incidence or severity is largely unknown. However, modifications of
health-related behaviour may on occasion by a great deal more important than
physiological stress responses. A study that illustrates this point in relation to hyper-
tension in air traffic controllers was reported by DeFrank et ul. 1481. The high
prevalence and incidence of hypertension and other conditions in air traffic con-
trollers has been for many years amongst the most striking examples of stress-related
occupational health risk 1491, and it has been widely assumed that heightened cardio-
vascular and neuroendocrine responses to the work might be responsible. DeFrank
et (11. studied the mediating role of alcohol in data collected longitudinally from air
traffic controllers over a three year period. During this time, a number of previously
normotensive controllers became hypertensive, with psychosocial factors such as
638 Invited Review

work anxiety, life events and investment in the job being correlated with blood
pressure. However, it was found that increased alcohol intake was a consistent
predictor of blood pressure elevation and mediated the influence of stress on hyper-
tension. In this case, therefore, there was no need to postulate a direct effect 01
psychosocial demands on psychophysiological pathways.
Other cognitive-behavioural processes that may be relevant include attention to
bodily symptoms, ranging from extreme preoccupation to avoidance or even denial
of physical signs, and these variations influence medical consultation behaviour 150,
5 11. These processes may be affected by concurrent adverse life experience, leading
some people to complain of physical symptoms that are out of proportion to objective
health status. while others ignore potentially life-threatening symptoms 152, 531. Yet
another process that can account for associations between psychobiological stress
and illness is the occurrence of emotionally expressive behaviours. A good example
of this mechanism is crying-induced asthma, where bronchospasm is precipitated
by crying 1541. This response is mediated through nonspecific pathophysiological
mechanisms such as bronchial hyperreactivity, rather than through specific psycho-
physiological links. Studies of family interaction suggest that persistent crying-
induced asthma is triggered during stress-related episodes of emotional disturbance
and may be maintained by parental responses 1551. Finally, adverse life experience
may affect illness progression through disrupting adherence to medication regimens
or medical advice 156, 571. The point underlying all these examples is that cognitive-
behavioural elements of psychobiological stress responses can influence health status
irrespective of psychophysiological connections.

PSYCHOPHYSIOLOGICAL PATHWAYS

The cognitive-behavioural processes outlined in the last section are unlikely to

account for all associations between stress and illness. Many investigations have
shown correlations between stressors, resources and disease that remain robust after
controlling for health-related behaviours and other factors [371. The second set of
pathways linking stress with illness in Fig. 2 involves psychophysiological processes.
The role of these responses in promoting illness is becoming better understood. with
longstanding evidence about autonomic and endocrine reactions being supplemented
in recent years by work on psychoneuroimmunology I5Sl. Systematic studies in
animals and humans have revealed modifications in cellular and humorally-mediated
immune competence with psychosocial stress. leading to the exciting possibility that
a physiological mechanism may be found for the involvement of emotional and
behavioural factors in susceptibility to infection and the progression of cancer. At
the same time, this research has exposed the limitations of current theoretical models
of psychophysiological mediation [591. Effects may be acute or chronic, and have
an influence on aetiology, maintenance or recurrence, depending on the illness under
investigation.
The situation may be clarified by recognizing that there are at least three types of
physiological process relevant to connections between stress and illness L361. The
one that has received the greatest attention can be termed the psychophysiological
hyperreactivity process. Psychophysiological hyperreactivity is the tendency to
respond to behavioural stress with abnormally large autonomic or neuroendocrine
 __----_ -.
/-
1
\
\
. \
\
DEMANDS
1PSYCHOSOCIAL.

Health practices and behaviours

Affective
Cognitive
Behavioural
Autonomic
Endocrine 1 PSYCHOPPW;;;OGICAL ,
Immunological
COPING RESOURCES
I 1
, I I I
Appraisal I I
Prior experience
Personality - behaviour /
I
;; I
I
1 Ho~~$tijk?&z~ses t
Social support / \
// \\
--. -_
I .
// \
---_____-- \ i

\
\

Pre-existing Pathology,Health Status

FIG. 2. Elaborated model, detailing the cognitive-behavroral and psychophysiological processes mediating strcs>-ilIne+ relationships.
reactions, or to display delayed recovery followin, ~7 termination of the stressful
encounter. Hyperreactivity may arise from constitutional factors or previously learned
response patterns, and may be restricted to specific organ systems. Support for the
relevance of this process to disease comes from studies in which people with par-
ticular disorders show hyperreactivity in their vulnerable systems. Thus hypcr-
tensives tend to produce exaggerated pressor responses to tasks involving active,
effortful behavioural coping in comparison with normotensives [26]. People suffering
from tension headache may show greater EMG responses from facial or neck
musculature during mental stress than do controls. or else delayed return to baseline
[601. Similarly. paraspinal EMG may be disturbed during stress in patients with
chronic back pain. Some insulin-dependent diabetics show disturbances in glucose
metabolism during challenging tasks [6 I I. while bronchoconstrictive responses are
characteristic to asthmatics 1621. Another interesting observation of recent years has
been that patients with coronary artery disease may display asymptomatic transient
myocardial ischacmia or other cardiac disturbances during mental stress [631.
The hypothesis relating these phenomena to disease is that repeated or prolonged
exposure to the psychosocial demands that provoke hyperreactivity may be pathogenic.
Here the evidence is weaker, for the simple reason that studies on people with pre-
existing disorders cannot disentangle the causal sequence - does hypcrrcactivity
precede disease onset. or is it a consequence of the pathology that is already present?
Few studies have yet been conducted that have identified psychophysiological
hyperreactivity in healthy people, then assessed susceptibility to disease prospec-
tively. Perhaps the best evidence has emerged from the study of hypertension. It has
been found not only that hyperreactivity is present in normotensives at high risk for
the disorder, but also that at least in some investigations, hyperreactivity predicts
future blood pressure level [64, 651.
Prospective data are not available for many clinical conditions, leaving open
the role of psychophysiological hyperreactivity in the aetiology of other disorders.
Nevertheless. intense physiological responses to psychosocial stressors may be
important to health by acting through a second mechanism which can be called the
disease stability process. The principal hypothesis underlying this process is that in
the presence of an established disorder, physiological stress responses will affect the
stability or progression of a clinical condition. Exaggerated reactivity may not in
these cases be directly implicated in aetiology, but in the maintenance of clinical
stability in those with a pre-existing health problem.
Many of the studies cited above showing hyperreactivity in patients with diagnosed
illnesses are consistent with the disease stability process. Other investigations have
addressed the mechanism more directly. For instance, changes in mood and pcr-
ceived stress levels have been shown to precede headache activity or the exacerbation
of phantom limb pain in some patients 166, 671. Associations between daily stress
and blood glucose concentration have been observed in adolescent diabetics, even
after allowing for the effects of caloric consumption, insulin use and exercise 1681.
One study of rheumatoid arthritis patients found that life events were correlated with
fluctuations in immune competence that might promote infammation 1691. Poor
control over hypertension has been associated with life events and chronic life
stressors by Caldwell PI nl. 1.561.
In addition to these influences over chronic conditions, psychophysiological
 Invited Review 641

processes may lead to acute clinical crises in some circumstances. One example is
the provocation of myocardial ischaemia or cardiac arrhythmia in patients with
coronary heart disease 170, 711. Experimental studies indicate that the threshold for
dangerous ventricular arrhythmias can be lowered in susceptible animals by behavioural
stress, and this process may underlie cases in which sudden cardiac death has
occurred during periods of acute psychological trauma [721. Alternatively, myocardial
ischaemia may arise through stress-induced coronary spasm or enhanced thrombus
formation in the coronary vasculature, leading to acute myocardial infarction.
The two mechanisms discussed thus far - the psychophysiological hyperreactivity
and disease stability processes - do not account for all the stress-induced physio-
logical influences on health. Many investigators have argued that health may be
compromised not only by the direct influence of physiological responses, but also
by reducing the organisms vulnerability and resistance to external challenge [291.
This third physiological mediator (the host vulnerability process) implies that stress-
induced alterations in endocrine and immunological parameters may render the
person more susceptible to invasive organisms. In these cases, the psychobiological
stress responses do not cause illness, but lower resistance to pathogens.
The action of this process may frequently involve the immune system, since stress-
induced immunosuppression may increase likelihood of infections becoming established.
Studies of respiratory tract infection suggest that minor stressors may increase
susceptibility provided that they coincide with acquisition of the pathogen, while
recurrences of persistent infections such as genital herpes may be associated with life
stress 173, 741. It is possible that this process underlies links between stress and
cancer, by reducing the persons intrinsic resistance to tumour proliferation [751.
The partition of physiological mediators into three distinct processes is not a purely
taxonomic exercise, since predictions vary for these processes, as do the types of
study relevant to their investigation [761. Documentation of psychophysiological
hyperreactivity processes requires prospective study of healthy individuals, in which
links can be tested between predispositions to hyperreactivity, persistent exposure to
stress-provoking environments, and the development of disease. Disease stability
processes on the other hand would benefit from longitudinal studies of the covariation
between disease perturbation, life stress and intervening neuroendocrine and im-
munological mechanisms, analysed using time series techniques. Finally, host
vulnerability processes may best be investigated with studies in which the presence
of infective agents at a sub-clinical level is monitored together with immune and
endocrine parameters, and associated with prior or concurrent adverse life experi-
ence. In each case, the causal sequence will ultimately be confirmed only with
experimental studies in which the putative chain of events is disrupted, with
appropriate consequences in terms of disease incidence or clinical course.

CONCLUSIONS

The main conclusion to be drawn from this summary is that the pathways mediating
stress influences on health are more complex than is sometimes appreciated. Never-
theless, this is no excuse for vagueness in postulating links, since careful analysis
can distinguish processes with characteristic properties. Moreover, specific hypotheses
related to the various cognitive-behavioural and physiological processes may be
642 Invited Review

generated, so that the relevance of each to mental and physical wellbeing can be
assessed.
There are important implications of this framework of understanding for psycho-
logical and other behavioural interventions. It cannot be assumed that the reiation-
ship between psychobiological stress responses and ill health will be the same in
different clinical conditions, so a range of treatment options may be warranted.
Interventions can be mounted at several stages of the model outlined in Fig. 2 from
cognitive-behavioural techniques designed to alter appraisals or the mobilization of
social supports, through psychophysiological techniques intended to modify psycho-
biological stress responses directly, to efforts at toughening biological resistance
through exercise and nutritional interventions 1771. The most appropriate strategies
for individual conditions may vary across the life span and according to socio-
cultural factors. Future research must establish these connections more precisely. At
present, however, it is essential to ensure that theoretical constructs relating life
experience and coping responses with health and illness do not remain static, but
develop in the light of the empirical findings continually emerging from this exciting
field of scientific and medical research.

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