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Theory and data in the study of ‘coronary proneness’ (type a behaviour pattern)
Sot. Sri. & Med. Printed in Great
Vol. 16. Britain
pp
107
10 114.
1982
0277.9536/82/010107-08103.00~ Pcreamon
Press Ltd
THEORY AND DATA IN THE STUDY OF ‘CORONARY PRONENESS’ (TYPE A BEHAVIOUR PATTERN) A. R. Department
RADLEY
of Social Sciences, Loughborough
University. England
Abstract-Current research into ‘coronary proneness’ is considered particularly in relation to attempts to extend the idea of the Type A Behaviour Pattern. A generalised critique is made of research aiming at an explanation of ‘coronary-proneness’ through the association of empirical categories or through predictive investigations, which lead in the one case to a plethora of conceptually indistinct findings and in the other away from the elaboration of theory. By reference to the cross-disciplinary nature of work on this problem it is argued that the designation of people as ‘Type A’ is a categorial description rather than an explanation in terms of conceptually integrated theory. The assumptions underlying this issue are sought in the relation between medical and social scientific approaches to CHD, and a summary
statement offered on this problem
INTRODUCHON
Over recent years there have been a number of in the literature presenting findings relating either behaviour patterns or social contexts to the incidence of coronary heart disease (CHD) [la]. This research effort has included the perspectives of cardiologists, psychologists, epidemiologists and social scientists, each addressing a wide range of questions-some apparently overlapping. and some falling more securely within the boundaries of these specific fields. Summary papers have now become a regular feature of the literature, drawing work together, directing attention to promising questions and often suggesting areas which merit further empirical investigation. Reviewers often conclude that substantial progress has been made arid that more research is now required in order to tackle outstanding questions [S. 63. There is evidence of a clear sense of progress in some areas, particularly in that of the Type A Behaviour Pattern (TABP). of which Rosenman has been able to state: reports
The concept of TABP and its relevance for CHD are shown to have cross-cultural validity and to have specificity for CHD in a relationship that has a biological gradient of pathogenecity. TABP can be assessed with substantial replicability and probably can be quantified [4]. Claims for the theoretical validity and the therapeutic promise of the TABP have grown alongside the em-
pirical woik associated with it. At the time of writing, the authors of a current review paper on the Coronary Pkone Behaviour Pattern conclude by saying: Unquestionably. future CPBP research will continue to enhance our knowledge so that we may better understand its role in cardiovascular. and perhaps other. diseases [5]. While not putting the issue beyond question. other writers have expressed their belief that the relationship between social and individual behaviour patterns and CHD will yield to additional research .[6]. and that what is required is the refinement of working concepts together with the use of more elegant metho-
dologies to examine further interactions between the variables under study [7]. There are relatively few dissenting voices to these recommendations, although Cassel [8] has urged that the premise that specific etiological processes are related to single clinical manifestations be examined (as it may be false), while attention has also been drawn to the tendency to treat the TABP as a personality characteristic thus confounding Type A classification with occupational and other variables [3]. These reservations about the general direction which research into coronary-proneness has taken reflect something of the assumptions on which the work is based. First, that a study of psychological or social characteristics associated with the occurrence of CHD will be instrumental in providing explanation of its cause, inasmuch as these factors are implicated; and second, that a separation of individual from situational factors in research will lead to advances in the explication of the explanatory concepts employed. At first sight. both premises may appear satisfactory inasmuch as a comprehensive survey of the social and psychological variables associated with CHD should reveal both where further research is warranted and, no less important, where observations of association can be discounted as spurious. If pursued thoroughly, such a course of action should indicate with increasing precision the characteristics of individuals and situations to be regarded as pathogenic and should also be the vehicle for the elaboration of theory which accounts for these findings. The body of this paper will examine this claim which is implicit in much of the research on TABP to date. To do this it is not necessary (nor possible here) to review the whole field of work, though we shall be required to show the kind of research which this assumption supports and the form of explanation to which it has led so far. Reference will be made to studies which exemplify this approach and to critical papers which offer, through their summaries and recommendations, a direction in which the development of the theory of coronary-proneness might take. In particular. a critical view will be taken of the assumption (again. impli107
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tit in the body of work, but often stated in review papers) that the considerable effort being made to explain proneness to CHD through empirical studies will yield an elaborated theory of the problem. The work on the characteristics of individuals related to the occurrence of CHD has not proceeded without reference to the findings of researchers in associated fields, particularly in psychophysiology and in epidemiology. Whatever the ‘causative’ role may be of individual characteristics in the onset of heart disease it has been deemed necessary to relate them in some way to the ‘mechanisms’ of (bodily) change, and to the social context presumed either to engender or to elicit the behaviours constituting proneness. The form of this integration is to some extent determined bjr the assumption of disease specificity, which is an expression of a particular relationship between the research orientations of medical and social scientists. Put simply, to search only for features of societies and individuals associated with a single disease entity is not merely to ignore other features (designated, perhaps, insignificant), but is to adopt a particular orientation towards or understanding of the way in which social events and bodily changes can influence one another. This, in turn, forms the basis for how the very problem of coronary-proneness is itself conceptual&d, and therefore for the kinds of research which tend to be carried out. Based upon these considerations the rationale of this paper is a reappraisal of this problem area, not restricted to a review of its methodological strengths or shortcomings per se but to the terms in which such empirical advances might be judged. It is to the relations between data, theory and discipline that we must look if we are to attain this critical advantage. though restricting our discussion only to the field of coronary-proneness which it seeks to illuminate. In summary, the paper examines three aspects of this issue : (a) the adequacy of certain kinds of empirical’ research for providing answers to questions asked about the social and psychological context of CHD; (b) the forms of conceptualisation of coronary-proneness arising from such research; and (c) the way in which coronary-proneness is investigated as a result of the relationship of medical and social Science researchers to the problem of CHD. EMPIRICAL EXPLANATION
RESEARCH AND THE
OF CORONARY
PRONENESS
Early research comparing individuals who had suffered heart attacks with those who had not was critic&d for the shortcomings of its methodology, although the validity of exploring proneness through the study of individuals as such was not put in question [9]. Since then, prospective investigations have demonstrated the significance of psychological and social study for an understanding of the etiology of CHD [lo. 11). Apart from this work there has been epidemiological and sociological research indicating relationships between the incidence of CHD and differences between. and within. different cultures. Both kinds of study have laboured to show that their findings cannot be reduced to the effects of the traditional
risk factors alone [12], and thereby claimed validity for the problems which they pose. This initial work has been followed by a large number of investigations using various populations. designs and methods of analysis purporting to refine. extend or otherwise elaborate upon the original formulation of the problem. Among these the research on Type A Behaviour Pattern has perhaps been most prominent in the literature. many studies being carried out with the purpose of clarifying the possible ‘links’ in the supposed chain of events leading up to CHD [13], or else with the aim of elaborating the original categorisation (Type A) in terms of the concepts of psychology [lC16]. There is a distinct belief that both types of research will lead to progress in our understanding of the problem : Only when all variables that mediate and,or condition the relationship between objective social conditions and health outcomes are explicitly conceptualised and measured can we have an adequate understanding of the effect of social stress on heart disease [17]. It should be noted that in this area of personality variables there is probably more room for question asking and formation of hypothesis than in any other area. The possibilities for usine. the breadth and concentual models of the personality tlheorists are virtually unending [S]. There are two points to be made here. One concerns
the argument that adequate understanding will follow from measuring all of the mediating variables: the other that central concepts (in this case TABP) can be elaborated by relating the operational category to a variety of other variables in the relevant discipline. While it is possible to discover associations between measures derived from concepts drawn from different disciplines-or even different aspects of the problem-the status ascribed to these relations remains in question for so long as they are considered only as operational definitions. The problem of pinpointing causal relations within cross-sectional designs is wellknown, for not only is it not possible within the framework of the research design to say which is cause and which is effect, but the influence of other mediating variables is an unknown factor. Indeed, the selection of variables for study is all-important if the designation of significant differences between populations studied is the aim of the research. However, even if one is able to select what are believed to be the appropriate characteristics for inclusion in the study there still remains the problem of how their statistical associations should be explained. For without a detailed discussion of the relation between chosen concepts and their operational definition no explanation of theoretical significance can be given of measures whose claim to significance is through statistical association only 1181. For example, Lehr et al. [19]. in what they call a “sociobiological approach” to the study of CHD, use stepwise discriminant analysis in the correlation of twelve “social variables” and 12 “biological variables”. The outcome of the study is the isolation of certain “key social and biological variables” which include systolic blood pressure, the parental religious difference factor. age. serum cholesterol, cigarette smoking, father’s occupation and Type A behaviour. We list these in full to illustrate that, in the end. such multivariate research produces only a
Theory and data in the study of ‘coronary proneness’
re-sortment of categories, associated certainly within the logic of the statistical design but providing no clear indication as to the theoretical status and form of integration of the concepts employed. It is conceptual integration which is the requisite outcome if one is to satisfy the claim that sociology and biology meet in such a study. This confusion betwe& abstract concepts and empirical categories was pointed out long ago by Kurt Lewin [20] in his discussion of problems in psychological research, and has been the subject of more recent discussion in a review of social science methodology 1213. What are generally referred to as factors or variables in current research on TABP are empirical categories formed by generalising on the basis of similar objects. such as Type A or Type B people. These are then related to other empirical categories, be it serum cholesterol level or the individuals’ patterns of work. This leads to the attribution of the generalised class as being the essential nature of the object-whatever is common to men of a particular type (e.g. Type A) is set up as a fundamental character of individuals of that class. Even though it will have exceptions in statistical research designs such attributes are taken, in this context. as the basis for the explanation of some aspect of CHD. It is this form of thinking which underlies the use of large samples in cross-sectional research designs which typically make assessment once rather than repeatedly on the assumption that they are measuring stable psychological characteristics and/or chronic situational conditions [22]. That is to say, the establishment of such categories as variables and their operational definition in the methodology employed will tend towards a perseveration of their existence as separate ‘factors’ which enter, conceptually unchanged, into further studies. This latter outcome can be seen more clearly when considered in’the context of the growing literature relating Type A behaviour to a variety of psychological measures. While the linking of TABP into an implicative network of psychological concepts does raise a number of interesting questions about the genesis of this style of coping. it does so by replacing the general term with more specific concepts which still rely upon it entirely for their relevance to the problem. That is to say. ‘psychological’ terms such as “hyperactivity” and “learned helplessness” can be applied systematically in place of “overworking” and “dependence”, but they cannot replace the category “TABP” because they offer little further insight into the genesis of the condition than the original term already implies [23]. It is for this reason that such studies do not yield an internal elaboration of the concept TABP, but an ever-increasing bundle of psychological terms and categories which have been found to be associated with people designated as Type A.‘B. The extent to which this refines the idea of TABP is limited, albeit that we may now use a greater variety of terms to indicate the essential thing which still remains a categorial description. Added to this. one may see the truth in the statement of Matteson and Ivancevich (quoted above) that the possibilities for using models of the personality theorists in research on TABP are virtually unending: they are. for without the guidance of abstract. rationally-integrated concepts (theory) the
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plethora of independent bits of knowledge wi]] con_ tinue to grow and grow. Much of the empirical work associated with the TABP has been concerned with predicting coronary_ proneness; that is, in developing a meth&o]ogy by which such designation can be made with accuracy. Jenkins, who perhaps more than any other worker has been responsible for developing this line of enquiry, has related this to the question of expianation by saying: It is possible for a variable to be a good predictor and still give little insight into the processes involved. Yet it is hardly possible that a variable can really assist in explanation it if is impotent as a predictor. The ability of a variable to be used in explanation is directly associated with the multiplicity of its connections into a nomothetic network of already known relationships [24, p. 733.
We have already dealt with the logical error arising from confusing variables (empirical categories) with explanations (conceptual systems), as implied in Jenkins’ second sentence. The reverse-logic embedded in his initial proposition and subsequent deduction can be seen also to emerge from a concern only with variables and empirical relationships. While it is likely that a variable giving weak prediction will not by itself assist in explanation there is no reason (given the preceding arguments) to subordinate explanation to the search for good prediction. The important distinction to be made is that where theory may be used for prediction on the basis of its explanation (e.g. the laws of motion), empiricism (the association of variables) can claim explanation only if it controls or can manage events. If no association is determined between events then it is often taken that there is nothing to explain, for little has been discovered. With particular reference to the postulated psychological and social factors associated with the incidence of CHD, this means that successful predictions made today concerning ‘links’ and ‘mechanisms’ depend upon the replication of these same events in the future if the relationship is to stand the test of experience. Given that the social world-at a cultural, societal or interpersonal level-is in a state of change, then some of the variables which medical and social scientists will need to study in the future will be different from those currently of interest. The oft-used preamble to papers concerning the “modern problem of CHD in Western society” presumes such change. The attempt to isolate and then to relate particular variables selected from our society (e.g. achievement
motive [lS]; job tension [13]) with coronary-proneness or its incidence begs the issue posed in the assumption of social change. Not only is the researcher who relies on empirical categories in a position of carrying out seemingly endless cross-sectional comparisons within the context of present day knowledge, but future workers will be committed to continuing this exercise should theoretical developments not be forthcoming. The counter-argument might be made to the above that “surely theory will build on all this data”. The response to this is twofold. A theory embracing physical health and disease and events in the social world might use selected data, but it is unlikely to begin from any attempt to summarise it all because con‘%)-
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tualisation and categorisation are distinct activities in scientific thinking. And furthermore, the argument that “more research is required” is a continuation Of the emphasis that data collection of this kind must come first, a view sometimes forthcoming from attempts to take stock of research progress to date. One way in which research findings on coronaryproneness have been brought together is in review papers presenting work in the form of a ‘model’ of the process in qutstion. This is interesting if only to reveal the extent to which the concepts in use remain separate eten as they are placed together, in spite of attempts to present diagrammatically the interrelation of concepts such as “psychosocial stimuli” “mechanism”, and “disease” [25] ; “conditioning variables”. “perceived stress” and “responses to stress” [17]; “psychosocial risk factor”. “information processing” and “psychological reactions and behaviours” [26]. These models illustrate that far from integrating these ideas the writers are merely juxtaposing concepts abstracted from different areas of research in the attempt to indicate possible “lines of connection”. Such juxtaposition is unlikely to lead to advances in the theory of how CHD develops in a social world if, as happens, it besets itself with confusions. Firstly, by separating out the aspects of the problem into essential units (social environment, features of individuals, physiological processes) such thinking tends to attribute to those units properties which may better describe transactions or relations between them [22.27]. There is also what may be called a confusion of levels of conceptual thinking, in which concepts which overlap in terms of their referents are presented as if they were exclusive. To take an example, Dembroski derives the following question, among others, from his model: “Is the manner in which they (high Type A. low Type B) process information differentially affecting and/or affected by particular psychological reactions (e.g. anger, impatience. etc.) and behaviours (e.g. aggression, avoidance, etc.)?’ [26]. Within this statement labels are attached to one state which might very well have appeared in the other (is “anger” a reaction or a behaviour?), while one aspect of the way in which people might “process information” (avoidance) is itself set out as a potential variable. In another presentation Kagan and Levi [ZS] suggest that stimuli arising from a social situation “may or may not produce an emotional or other physiological response”. Here there is an attempt at reduction of a psychological concept (emotion) to one of physiological status, while Hinkle [28] has spoken of people’s “exposure to a certain kind of interpersonal relationship or social condition” as if people existed apart from their social relationships. The purpose of making these critical points is not to deny the problem area the attention it merits, nor to play down the contributions which have been made by researchers in establishing the validity of investigating physical ill-health within a social perspective. What is at issue is the progress which is now to be made on the basis of constructs which were first used to grasp the phenomena under study. Where these constructs are drawn from different disciplines-or from different sub-systems of thought in a Particular discipline-then their presentation as if they formed a unitary system is quite misleading.
It is misleading because it invites us to investigate ‘relationships’ or ‘interactions’ between ‘variables’. the logical status of which is often only to be found in their operational definitions. By abstracting ideas from their conceptual systems in order to “get the variables together”, the distinct and fundamental issues pertaining to them are either lost or confused. This can be seen in the treatment of cause and effect relations between variables under study. While some [29,30] have questioned the validity of current hypotheses on the grounds that this makes the unwarranted assumption of a chain of events with ‘original’ event and ‘final’ cause, others have speculated in this vein. On the one hand there is a search for ‘mechanisms’ [6.7,23] by which is usually meant the physiological events which immediately precede the onset of CHD. On the other, there are efforts to discover the kinds of social context which either give rise to the behaviour pattern associated with coronary-proneness or in which such behaviour tends to be elicited. There is an implied sequence in these arguments which suggests that the social context ‘causes’ people to behave in certain ways, which in turn ‘causes’ them to suffer pathogenic changes in their physiological systems. This is the assumption of a “final common pathway” suggesting that the individual is the recipient of something from outside. However, this begs the question of how individuals adapt and cope with life’s demands. Insofar as an individual is regarded as striving for achievement and as “confidently advancing to grapple with his challenges” [4] then his style of behaviour (his embodied actions) can just as well be regarded as initial as final. More accurately, this question of the direction of causality only arises if one separates out person from environment and proceeds to ask how one affects the other, overlooking entirely that individuals might be constituted by their social relations and yet can place their own interpretations on events. It might be objected that these criticisms constitute an impertinent demand to make at this stage of the investigation, and that the elucidation of these links ‘must proceed experimentally’ [31]. Indeed, demand for explanation seems at odds with the recent statement of Matteson and Ivancevich that: much of the current thinking regarding mechanisms is theoretical in nature rather than empirical. There is no direct evidence which clearly identifies a particular mechanism as being implicated in the proposed link [S].
This appraisal depends, however, upon the assumption that particular mechanisms will be revealed directly in the search for links between variables. For, following Herd [32] Matteson and Ivancevich identify the explanation of the association between “behavioural phenomena” and “alterations in physiological processes” with the designation of “mechanisms”--by which they mean cause and effect links. This is a further illustration of the belief that empirical categories can attain an explanatory status through demonstrating that a particular set of circumstances obtains, without having to make clear the conceptual ‘linkage’ which it implies. It. is not apparent from this whether the identification of mechanisms will demand a physiological reduction of the “behavioural patterns” under study. If so, such a reduction would be
Theory and data in the study of ‘coronary proneness’ Table 1. Conceptualisation
111
of psychological and social precursors to CHD used by different research perspectives-a schematic outline Level of conceptualisation
Working perspective Cardiologist
Culture, social environment
Individual person
Physiological systems
Illustrative authors
Little, if any statement in these terms.
Either use of simple categorial constructs or reference to specific concepts (‘conditioning’, ‘stimuli’)
Problem defined and elaborated in these terms (dependent variables)
Rosenman [lo. 381 Nixon [33] Selye [34] Obrist [36]
Some elaboration of problem in terms of cultural and structural differences.
No formal statement in these terms
Problem initially defined here in terms of incidence of categories of disease
Cassel [8] Marmot [12] Syme et al. [29] Wardwell et al. [37]
Little, if any statement in these terms.
Problem articulated in terms of associated concepts applied to individual behaviour and/or personality
Problem located here, but in categorial terms (independent variable).
Jenkins [24] Glass [23] Dembroski [7]
Psychophysiologist
Epidemiologist
Sociologist Psychologist
inadmissable (voiding the phenomerion of individual experience) as would be a “psychologism” which attempted to attribute to individuals characteristics which actually derive from people’s relationships in a social world. However, these problems of relating sep arate concepts in theory is one which is implicit ratlier than extant in the literature on the association of social and psychological variables to CHD. There is a recognition that the juxtaposition of variables currently only implies causal linkages and does not yet reveal them, but the problem is then designated “multifactorial” [2] and this becomes the basis for further recommendations that more empirical research is required. The circularity of this argument and, indeed, of the research endeavour only becomes apparent when the need for conceptual analysis as well as the collecting of data can be admitted C21.223. THE CONCEPTUALISATION OF CHD BY MEDICAL AND SOCIAL SCIENTISTS
The question of why some of the work into coronary-proneness has taken the form critic&d in this paper can be illuminated by reference to the relationships of medical and of social science researchers to the problem of CHD. Their approaches differ both in the conceptual systems which are employed (the languages of physiology, psychology, or social science), in their preferred methods and in their location of the problem to be solved. It is this last aspect which can be exemplified by reference to Table 1 which shows three broad approaches to the problem. While the Table is meant to be schematic rather than definitive, it does allow comparisons to be made between perspectives with regard to their use in CHD research. As originally stated by some cardiologists who have noted the types of individuals consulting them in their capacity as medical practitioners, the problem is defined by a thorough description of its clinical manifestation using regular clinical indices (e.g. B.P., serum
.
lipids, E.C.G.). This is then related to individuals described either in what one might call “lay psychological language”, or else in terms of concepts which have a certain face validity in relation to the physiological definition of CHD. For example, Rosenman. et al. refer to a “certain emotional complex in the pathogenesis of CHD” [lo] (lay language), while concluding their argument with reference to “the pathogenetic relevance of the central nervous system to the occurrence of manifest CHD” (face-valid concept). Similarly, Nixon talks of exhaustion leading to CHD as resulting from “‘emotional responses” and then describes it more formally as a “morbid level of arousal” c331. In comparison, the approach of psychophysiologists is similar in their use of physiology, but different in their emphasis upon particular facets of heart function. In addition, they often rely very strongly on concepts drawn from conditioning theory in psychology such as endogenous or exogenous conditioning factors when describing the physiology of cell necrosis [34], or the relation of classical conditioning and shock avoidance to heart rate and cardial force [35,36-J. This perspective grounds the problems of CHD firmly in physiology, using selected psychological concepts to express the conditions under which physiological changes might occur. The problem field is delineated, as it were, ‘by the skin of the individuals under study’, with little or no consideration of the social context in which it occurs. In contrast to this, epidemiologists have attempted to show that the incidence of CHD varies with culture, and that this is not to be explained by the “traditional risk factors alone” [g, 123. In studies of large groupings defined by culture or by particular indices of socio-economic status or mobility [29] there have beeri attempts to relate the relative incidence of CHD to factors which presuppose a relationship between health and social integration. These studies, however, do not make clear just how particular individuals
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mlgnt oevelop CHD, so that they trust, like Wardwell er al. to “these more distant factors (serving) as indices or clues to significant factors in the etiology of this prevalent and puzzling disease” [37]. Finally, the third perspective is that offered by researchers who have emphasized the features of particular individuals who have suffered, or who might develop CHD [ll, 383. The growing literature on TABP [4] is now evidence to the attempt to relate the occurrence of CHD to aspects of persons which can be explained in terms of psychological concepts. While it is argued that the TABP does not stem solely from an individual’s personality but emerges only when certain challenges or conditions of the milieu arise, the actual work on TABP has tended to treat it as a stable personality characteristic. This is shown by its repeated use as an independent variable in studies which seek to relate it to other factors proposed to be pertinent to the problem [23]. The point is not that the choice of TABP as an independent variable is in itself a wholly limiting condition, but that it is necessary to consider the study of coronary-proneness in the context of the multidisciplinary research carried out in order to gain a perspective on‘the use of this typology. Table 1 presents a schematie outline of the way in which research on the social and psychological aspects of CHD varies in its conceptual foci, in its choice of dependent and independent variables and in those aspects which, being assumed as constants, are selectively ignored by the researchers concerned. This variation in cross-disciplinary investigations means that within each main conceptual system the problems are articulated so as to achieve a limited but effective basis of understanding and communication among researchers. It also has the effect of setting out the significant differences in the investigator’s chosen subsidiary system in a more circumscribed manner, in which they take on the appearance of either ‘independent variables’ or ‘factors’. These various research efforts define a multifaceted problem field in which concepts explicated from the working perspective of a given discipline are differentiated through the use of more simple categories drawn from another discipline. So with work on TABP, a typology having simple status in psychological terms has been used to make articulated points about the physiology of the individuals concerned. This perspective is the one used by Friedman and Rosenman, as caidiologists, and is also that taken by psychologists working with the group on the development of a predictive tool which could be used in their research. Such methodology essentially involves a refinement of the operational definition of TABP rather than a conceptual elaboration of the categorisation. (Jenkins has been quoted earlier in this paper on his belief in the primacy of predictive utility in scientific explanation.) In fact, much subsequent work has been justified in terms of its potential contribution towards the aim of predicting who is prone to develop CHD C38-413. Inasmuch as this aim has been sought by the use of psychological testing (either directly of TABP or by its association with other tests of personality), this has meant that the category itself has remained largely unelaborated. TWO reasons for this have been anticipated in the previous discussion. The standpoint of
the cardiologist is in the discipline of physiology in which terms the problem of CHD is initially defined. The category ‘Type A behaviour’ is a description at the level of psychological explanation, serving as an independent variable, the significance of which is given by differences observed in terms of measures such as serum cholesterol level, angiography, E.C.G. and blood pressure. To maintain this perspective. even as a social scientist, is to preserve the opacity of the phenomenon (‘Type A behaviour pattern’) in its role as an index of differences accounted for in terms of physiology. Predictive research into social and psychological aspects of CHD is also related to the need for therapeutic intervention by medical practitioners. If one can designate who is likely to suffer a heart attack then one can do something in order to prevent it. But do what, exactly? This depends upon one’s conceptualisation of the problem, and in particular the theory of its etiology. Inasmuch as our knowledge is restricted to the likelihood of associations between empirical categories, then the ‘risk’ of suffering a coronary attack or the ‘causes’ of CHD will be attributed to various parts of the problem field. Either the individual himself is seen to be the repository of the problem (in which case he might be given either behaviour therapy or psychotherapy [42]), or else some aspect of his working environment is selected as the locus of the stress involved. In spite of its predictive utility a focus on empirical categories treated as variables is of limited help in guiding therapeutic intervention at those levels, for it has eschewed the articulation of abstract concepts in which observables can be comprehended in terms of an integrated system. Not surprisingly, the issue of the modification of TABP has certain contradictory features. One mentioned above is the question of whether therapy is aimed at Type A individuals, at environments believed to engender Type A behaviour. or at both. Rosenman and Chesney [4] believe that modification of Type A behaviour should be aimed at individuals (rather than environments), particularly at post-infarction patients who are able to gain some insight into their way of life. Cooper and Maishall [2] have called (rather optimistically) for more fundamental structural changes in organisations to encourage participation of people in their jobs, although TABP appears to be so embedded in the modern occupational career that intervention, observed one investigator, “might meet with resistance from the subject population” [43]. These difficulties and uncertainties, while not following from a concern with prediction, illustrate the limitations of this approach in the sphere of medical and social science. Even if one can designate with great accuracy who, among healthy individuals, is ‘coronary prone’ one is still left with all the questions about what to do about it and how to proceed. Indeed, there is a deeper contradiction within empiricist approaches to TABP which is not always apparent in the research literature, but of significance nonetheless. If CHD develops in greater or lesser part from certain cultural, organisational and individual styles of living then no technical intervention by medical practitioners is likely to affect it greatly, in spite of considerable efforts to define the problem in a technical way. (By ‘technical’ is meant the specification of
Theory
and data
in the study
mechanisms, social or psychological, which by association are inferred to cause or to predispose an individual to suffer CHD). This is. firstly, because such an approach is geared towards intervention with individuals. as is much of modern medicine [44]. While this curative approach has, arguably, been successful in the struggle against disease it has not been so in the fight against ill-health due to maladaptation. In defining a set of precursors of CHD within the social field the researchers whose work is under discussion here have often been at pains to indicate the limitations of an ‘engineering’ approach to the problem of heart disease. And yet, in pursuing a line of research premised upon prediction (management) it would seem that these same principles have guided much of their work. Laudable as this is in the attempt to help post-infarction patients, the problems which arise when applied to otherwise healthy individuals are difficult indeed, being in part due to a failure to transcend, conceptually, the observables under study. Finally, we should note that one likely effect of successful prediction of coronary-proneness would be redoubled effort to specify the physiological mechanisms in such a way that intervention by chemo-therapy would be attempted. While this runs counter to the expressed concerns of Rosenman and his colleagues, such a reductionist approach is not only a current part of the wider research field but is latent in their early work implicating the ‘role of the CNS’ in the etiology of CHD. By comparison, there was once a brief literature on the psychological features which might predispose people to pulmonary tuberculosis [45]. The discovery of the tuberculosis bacillus and the effective use of vaccination meant that this approach was promptly rendered sterile for the purposes of curing TB. What is of interest here is that the cery idea of asking about predisposition to tuberculosis in terms other than those of physiology has recently been ridiculed in the light of the demonstrated effectiveness of microbiological methods in that field [46]. Although far more extensive and sophisticated in its methodology, inasmuch as current literature treats the TABP and other social/psychological variables as just one more index of disease occurrence, then their de facto displacement due to advances in other fields of research is always possible. This is particularly so while we lack a conceptual framework in social science within which these problems can be grasped. and equally important, can be Seen by a wider audience to be a basis for asking valid questions. CONCLUDING
REMARKS
The burden of this paper has been to draw attention to some of the issues and problems which beset the field of research into social and psychological aspects of CHD. Most attention has been paid to the concept of TABP first put forward by Friedman and Rosenman because their efforts at establishing the relevance of this approach are now the basis for a considerable enthusiasm among researchers wanting to extend the original work. It has been argued that while some categorial thinking may be necessary in early research employing disciplines at two ‘levels’ of conceptualisation. the retention of such categories S.SM16I -H
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‘coronary proneness’
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(mis)taken as explanatory concepts, their cross-relation in empirical investigations and their refinement as indices for prediction leads away from the con_ struction of a system of abstract, Jogicaffy_related con_ cepts (theory). In saying this the intention is neither to draw attention away from research nor to brand ah studies in the field as being without merit. Rather, criticism is aimed at research which either confuses empiricism with explanation or does not attempt to relate its methods to existing concepts or to the elaboration of new ones. Associated with this are review papers which, summarising all the evidence, offer only an aggregation of material with the recommendation that “more research” be carried out on the assumption that only more empirical work can make for explanation. One symptom of this attitude in evidence is the flight from case material and example, apart from almost ritual references to the description of typical’ CHD patients made long ago by Osler. And yet case study, alongside other methods, may yield fruitful descriptions if only because it can give the “minute-byminute” detail required if we are to see how the various areas of a person’s life, separated by current foci of conceptuahsation. function together over time C3.223. This might result in the realisation that the properties which we ascribe to one level (e.g. the Type A individual) are more fittingly described as a function of the relationships within a particular field or situation. To take this view is to relinquish the felt necessity of beginning with a particular disease entity defined in terms of physiological changes, and then seeking out those psychological and cultural variables that play a possible causal role in the chain of events leading up to coronary heart disease. Arguably, the sequencing of such variables (e.g. social conditionspsychological responses-physiological adaptation) derives its rationale not from a close inspection of the problem itself, but from assumptions engendered upon the relationships obtaining between disciplinary approaches employed in empirical research (see Table 1). It is within the context of these assumptions that questions as to the part played by psychological and social conditions can arise-that is, how much do these factors count in the etiology of CHD? This is not merely a difficult question on the (empirical) grounds that the genesis of CHD is ‘multidetermined’, but is an unanswerable one on the (logical) grounds that the parts to be considered are products of conceptual analysis, not of the real world. However, there is no a priori reason why a theory of CHD considered as a ‘stress-related illness’ must confine itself to accounting for findings obtained on the basis of assumptions criticised in this paper, except that we overlook the relationship between medical and social scientific research on this problem and continue to seek for explanation in empirical endeavour. REFERENCES
1. Jenkins C. D. Psychologic and social precursors of coronary disease (in two parts). N. Engl. .I. Med. 284, 244. 307. 1971. 2. Cooper C. L. and Marshall J. Occupational sources of stress: a review of the literature relating to coronary
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heart disease and mental ill health. J. occupot. Psychol. 49, 11. 1976. 3. Kasl S. V. Epidemiological contributions to the study of work stress. In Stress a? Work (Edited by Cooper. C. L. and Payne R.). pp. 3-48. Wiley. New York. 1978. 4. Rosenman R. H. and Chesney M. The relationship of Type A behaviour pattern to coronary heart disease. Act. Nerc. Sup. 22, 1. 1980. 5. Matteson M. T. and lvancevich J. M. The coronaryprone behaviour pattern: a review and appraisal. Sot. Sci. Med. 14A. 337. 1980. 6. Sparacino J. The Type A Behaviour pattern: a critical assessment. J. Hum. Stress 5. 37. 1979. 7. Dembroski T. M.. Weiss S. M.. Shields J. L.. Haynes S. G. and Feinleib M. (Eds) Coronary-Prone Behaviour. Springer. New York. 1978. 8. Cassel J. The contribution of the social environment to host resistance. Am. J. Epidem. 104, 107. 1976. 9. Mordkoff A. M. and Parsons 0. A. The coronary personality: a critique. Psychosom. Med. 29, 1. 1967. 10. Rosenman R. H.. Friedman M., Straus R.. Wurm R., Jenkins C. D. and Messinger H. B. Coronary heart disease in the Western collaborative group study: a follow up experience of two years. J. Am med. Ass. 195, 130, 1966. 11. Rosenman R. H., Friedman M.. Straus R.. Wurm M., Kositcheck R., Hahn W. and Werthessen N. A predictive study of coronary hearts disease: the Western collaborative group study. J. Am. med. Ass. 189, 103, 1964. 12. Marmot M. and Syme S. L. Acculturation and coronary heart disease in Japanese-Americans, J. Epidem. 104, 225. 1976.
13. Howard J. H.. Cunningham D. A. and Rechnitzer P. A. Work patterns associated with Type A behaviour: a managerial population. Hum. Relar. 30, 825. 1977. 14. Glass D. C.. Snyder M. C. and Hollis J. F. Time urgency and the Type A coronary-prone behaviour pattern. J. appl. Sot. Psycho/. 4, 125, 1974. 15. Matthews K. A. and Saal F. E. Relationship of the Type A coronary-prone behaviour pattern to achievement. power, and affiliation motives. Psychosom. Med. 40, 631, 1978. 16. van Egeren L. F. Social interactions, communications. and the coronary-prone behaviour pattern: a psychophysiological study. Psychosom. Med. 41, 2, 1979. 17. House J. S. Occupational stress and coronary heart disease: a review and theoretical integration. J. Hlrh sot. Behar.
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19. Lehr 1.. Messinger H. B. and Rosenman R. H. A sociobiological approach to the study of coronary heart disease. J. chron. Dis. 26, 13, 1973. 20. Lewin K. The conflict between Aristotelian and Galilean modes of thought in contemporary psychology. 1. gen. Psgchol. 5. 141. 1931. 21. Willer D. and Wilier J. Sysremaric Empiricism: Critique of a Pseudoscience. Prentice-Hall. Englewood Cliffs. NJ, 1973. 22. Lazarus R. S. A strategy for research on psychological and social factors in hypertension. J. Hum. Stress 4, 35.
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23. Glass D. C. Behaciour Parterns. Stress and Coronary Disease. Lawrence Erlbaum Associates, Hillsdale. NJ, 1977. 24. Jenkins C. D. A comparative review of the interview and questionnaire methods in the assessment of the coronary-prone behaviour pattern. In Coronary-Prone Behat?our (Edited by Dembroski T. M. er al.). pp. 71-88. Springer. New York, 1978.
A. R. and Levi L. Health and environment psychosocial stimuli: a review. Sot. Sci. Med. 8. 225. 1974. Dembroski T. M. Reliability and validity of methods used to assess coronary-prone behaviour. In CoronaryProne Behaciour (Edited by Dembroski T. M. er al.). pp. 95-106. Springer. New York. 1978. Lazarus R. S. and Launier Stress-related transactions between person and environment. In Perspectives in Internutional Psychology (Edited by Pervin L. A. and Lewis M.). pp. 287-327. Plenum, New York. 1978. Hinkle L. E. The concept of stress in the biological and social sciences. Sci. Med. Man. 1. 31. 1973. Syme S. L.. Hyman M. M. and Enterline P. E. Some social and cultural factors associated with the occurrence of coronary heart disease. J. chron. Dis. 17, 277.
30. Haney C. A. Life events as precursors of coronary heart disease. Sot. Sci. Med. 14A. 119. 1980. 31. Williams R. B., Friedman M.. Glass D. C.. Herd J. A. and Schneiderman N. Mechanisms linking behavioural and pathophysiological processes. In Coronary-Prone Behariour (Edited by Dembroski T. M. et al.). pp. 120-128. Springer. New York. 1978. 32. Herd J. A. Physiological correlates of coronary-prone behaviour. In Coronary-Prone Behaciour (Edited by Dembroski T. M. et al.). Springer. New York. 1978. 33. Nixon P. G. F. The human function curve: with special reference to cardio-vascular disorders. Practitioner 217, 765 and 935. 1976. 34. Selye H. The evolution of the stress concept* Am. J. Cardiol. 26, 289. 1970. interac3.5 Obrist P. A. The cardiovascular-behavioural tion-as it appears today. Psychophysiology 13, 95.
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Wardwell W. I., Hyman M. and Bahnson C. B. Stress and coronary heart disease in three field studies. J. chron. Dis. 17, 73. 1964. Friedman M. and Rosenman R. H. T.vpe A @ehoriour and Your Heart. Knopf, New York. 1974. Jenkins C. D.. Rosenman R. H. and Friedman M. Development of an objective psychological test for the determination of the coronary-prone behaviour pattern in employed men. J. chron. Dis. 20, 371. 1967. Schuker B. and Jacobs D. R. Assessment of behavioural risk for coronary disease by voice characteristics. Psychosom. Med. 39. 219. 1977. Dimsdale J. E.. Hackett T. P.. Catanzano D. M. and White P. J. The relationship between diverse measures for Type A personality and coronary angiographic findings. J. Psychosom. Res. 23, 289. 1979. Roskies E.. Spevack M.. Surkis A.. Cohen C. and Gilman S. Changing the coronary-prone (Type A) behaviour pattern in a non-clinical population. J. behar. Med. 1. 201. 1978. Mettlin C. Occupational careers and the prevention of coronary-prone behaviour. Sot. Sci. Med. 10, 367. 1976. Powles J. On the limitations of modern medicine. Sci. Med. Man 1. 1. 1973. Wittkower E. A Psychiatrist Looks at Tuberculosis. The National Association for the Prevention of Tuberculosis, London, 1949. Sontag S. Illness as Metaphor. Allen Lane. Harmondsworth, 1979.
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1982
0277.9536/82/010107-08103.00~ Pcreamon
Press Ltd
THEORY AND DATA IN THE STUDY OF ‘CORONARY PRONENESS’ (TYPE A BEHAVIOUR PATTERN) A. R. Department
RADLEY
of Social Sciences, Loughborough
University. England
Abstract-Current research into ‘coronary proneness’ is considered particularly in relation to attempts to extend the idea of the Type A Behaviour Pattern. A generalised critique is made of research aiming at an explanation of ‘coronary-proneness’ through the association of empirical categories or through predictive investigations, which lead in the one case to a plethora of conceptually indistinct findings and in the other away from the elaboration of theory. By reference to the cross-disciplinary nature of work on this problem it is argued that the designation of people as ‘Type A’ is a categorial description rather than an explanation in terms of conceptually integrated theory. The assumptions underlying this issue are sought in the relation between medical and social scientific approaches to CHD, and a summary
statement offered on this problem
INTRODUCHON
Over recent years there have been a number of in the literature presenting findings relating either behaviour patterns or social contexts to the incidence of coronary heart disease (CHD) [la]. This research effort has included the perspectives of cardiologists, psychologists, epidemiologists and social scientists, each addressing a wide range of questions-some apparently overlapping. and some falling more securely within the boundaries of these specific fields. Summary papers have now become a regular feature of the literature, drawing work together, directing attention to promising questions and often suggesting areas which merit further empirical investigation. Reviewers often conclude that substantial progress has been made arid that more research is now required in order to tackle outstanding questions [S. 63. There is evidence of a clear sense of progress in some areas, particularly in that of the Type A Behaviour Pattern (TABP). of which Rosenman has been able to state: reports
The concept of TABP and its relevance for CHD are shown to have cross-cultural validity and to have specificity for CHD in a relationship that has a biological gradient of pathogenecity. TABP can be assessed with substantial replicability and probably can be quantified [4]. Claims for the theoretical validity and the therapeutic promise of the TABP have grown alongside the em-
pirical woik associated with it. At the time of writing, the authors of a current review paper on the Coronary Pkone Behaviour Pattern conclude by saying: Unquestionably. future CPBP research will continue to enhance our knowledge so that we may better understand its role in cardiovascular. and perhaps other. diseases [5]. While not putting the issue beyond question. other writers have expressed their belief that the relationship between social and individual behaviour patterns and CHD will yield to additional research .[6]. and that what is required is the refinement of working concepts together with the use of more elegant metho-
dologies to examine further interactions between the variables under study [7]. There are relatively few dissenting voices to these recommendations, although Cassel [8] has urged that the premise that specific etiological processes are related to single clinical manifestations be examined (as it may be false), while attention has also been drawn to the tendency to treat the TABP as a personality characteristic thus confounding Type A classification with occupational and other variables [3]. These reservations about the general direction which research into coronary-proneness has taken reflect something of the assumptions on which the work is based. First, that a study of psychological or social characteristics associated with the occurrence of CHD will be instrumental in providing explanation of its cause, inasmuch as these factors are implicated; and second, that a separation of individual from situational factors in research will lead to advances in the explication of the explanatory concepts employed. At first sight. both premises may appear satisfactory inasmuch as a comprehensive survey of the social and psychological variables associated with CHD should reveal both where further research is warranted and, no less important, where observations of association can be discounted as spurious. If pursued thoroughly, such a course of action should indicate with increasing precision the characteristics of individuals and situations to be regarded as pathogenic and should also be the vehicle for the elaboration of theory which accounts for these findings. The body of this paper will examine this claim which is implicit in much of the research on TABP to date. To do this it is not necessary (nor possible here) to review the whole field of work, though we shall be required to show the kind of research which this assumption supports and the form of explanation to which it has led so far. Reference will be made to studies which exemplify this approach and to critical papers which offer, through their summaries and recommendations, a direction in which the development of the theory of coronary-proneness might take. In particular. a critical view will be taken of the assumption (again. impli107
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tit in the body of work, but often stated in review papers) that the considerable effort being made to explain proneness to CHD through empirical studies will yield an elaborated theory of the problem. The work on the characteristics of individuals related to the occurrence of CHD has not proceeded without reference to the findings of researchers in associated fields, particularly in psychophysiology and in epidemiology. Whatever the ‘causative’ role may be of individual characteristics in the onset of heart disease it has been deemed necessary to relate them in some way to the ‘mechanisms’ of (bodily) change, and to the social context presumed either to engender or to elicit the behaviours constituting proneness. The form of this integration is to some extent determined bjr the assumption of disease specificity, which is an expression of a particular relationship between the research orientations of medical and social scientists. Put simply, to search only for features of societies and individuals associated with a single disease entity is not merely to ignore other features (designated, perhaps, insignificant), but is to adopt a particular orientation towards or understanding of the way in which social events and bodily changes can influence one another. This, in turn, forms the basis for how the very problem of coronary-proneness is itself conceptual&d, and therefore for the kinds of research which tend to be carried out. Based upon these considerations the rationale of this paper is a reappraisal of this problem area, not restricted to a review of its methodological strengths or shortcomings per se but to the terms in which such empirical advances might be judged. It is to the relations between data, theory and discipline that we must look if we are to attain this critical advantage. though restricting our discussion only to the field of coronary-proneness which it seeks to illuminate. In summary, the paper examines three aspects of this issue : (a) the adequacy of certain kinds of empirical’ research for providing answers to questions asked about the social and psychological context of CHD; (b) the forms of conceptualisation of coronary-proneness arising from such research; and (c) the way in which coronary-proneness is investigated as a result of the relationship of medical and social Science researchers to the problem of CHD. EMPIRICAL EXPLANATION
RESEARCH AND THE
OF CORONARY
PRONENESS
Early research comparing individuals who had suffered heart attacks with those who had not was critic&d for the shortcomings of its methodology, although the validity of exploring proneness through the study of individuals as such was not put in question [9]. Since then, prospective investigations have demonstrated the significance of psychological and social study for an understanding of the etiology of CHD [lo. 11). Apart from this work there has been epidemiological and sociological research indicating relationships between the incidence of CHD and differences between. and within. different cultures. Both kinds of study have laboured to show that their findings cannot be reduced to the effects of the traditional
risk factors alone [12], and thereby claimed validity for the problems which they pose. This initial work has been followed by a large number of investigations using various populations. designs and methods of analysis purporting to refine. extend or otherwise elaborate upon the original formulation of the problem. Among these the research on Type A Behaviour Pattern has perhaps been most prominent in the literature. many studies being carried out with the purpose of clarifying the possible ‘links’ in the supposed chain of events leading up to CHD [13], or else with the aim of elaborating the original categorisation (Type A) in terms of the concepts of psychology [lC16]. There is a distinct belief that both types of research will lead to progress in our understanding of the problem : Only when all variables that mediate and,or condition the relationship between objective social conditions and health outcomes are explicitly conceptualised and measured can we have an adequate understanding of the effect of social stress on heart disease [17]. It should be noted that in this area of personality variables there is probably more room for question asking and formation of hypothesis than in any other area. The possibilities for usine. the breadth and concentual models of the personality tlheorists are virtually unending [S]. There are two points to be made here. One concerns
the argument that adequate understanding will follow from measuring all of the mediating variables: the other that central concepts (in this case TABP) can be elaborated by relating the operational category to a variety of other variables in the relevant discipline. While it is possible to discover associations between measures derived from concepts drawn from different disciplines-or even different aspects of the problem-the status ascribed to these relations remains in question for so long as they are considered only as operational definitions. The problem of pinpointing causal relations within cross-sectional designs is wellknown, for not only is it not possible within the framework of the research design to say which is cause and which is effect, but the influence of other mediating variables is an unknown factor. Indeed, the selection of variables for study is all-important if the designation of significant differences between populations studied is the aim of the research. However, even if one is able to select what are believed to be the appropriate characteristics for inclusion in the study there still remains the problem of how their statistical associations should be explained. For without a detailed discussion of the relation between chosen concepts and their operational definition no explanation of theoretical significance can be given of measures whose claim to significance is through statistical association only 1181. For example, Lehr et al. [19]. in what they call a “sociobiological approach” to the study of CHD, use stepwise discriminant analysis in the correlation of twelve “social variables” and 12 “biological variables”. The outcome of the study is the isolation of certain “key social and biological variables” which include systolic blood pressure, the parental religious difference factor. age. serum cholesterol, cigarette smoking, father’s occupation and Type A behaviour. We list these in full to illustrate that, in the end. such multivariate research produces only a
Theory and data in the study of ‘coronary proneness’
re-sortment of categories, associated certainly within the logic of the statistical design but providing no clear indication as to the theoretical status and form of integration of the concepts employed. It is conceptual integration which is the requisite outcome if one is to satisfy the claim that sociology and biology meet in such a study. This confusion betwe& abstract concepts and empirical categories was pointed out long ago by Kurt Lewin [20] in his discussion of problems in psychological research, and has been the subject of more recent discussion in a review of social science methodology 1213. What are generally referred to as factors or variables in current research on TABP are empirical categories formed by generalising on the basis of similar objects. such as Type A or Type B people. These are then related to other empirical categories, be it serum cholesterol level or the individuals’ patterns of work. This leads to the attribution of the generalised class as being the essential nature of the object-whatever is common to men of a particular type (e.g. Type A) is set up as a fundamental character of individuals of that class. Even though it will have exceptions in statistical research designs such attributes are taken, in this context. as the basis for the explanation of some aspect of CHD. It is this form of thinking which underlies the use of large samples in cross-sectional research designs which typically make assessment once rather than repeatedly on the assumption that they are measuring stable psychological characteristics and/or chronic situational conditions [22]. That is to say, the establishment of such categories as variables and their operational definition in the methodology employed will tend towards a perseveration of their existence as separate ‘factors’ which enter, conceptually unchanged, into further studies. This latter outcome can be seen more clearly when considered in’the context of the growing literature relating Type A behaviour to a variety of psychological measures. While the linking of TABP into an implicative network of psychological concepts does raise a number of interesting questions about the genesis of this style of coping. it does so by replacing the general term with more specific concepts which still rely upon it entirely for their relevance to the problem. That is to say. ‘psychological’ terms such as “hyperactivity” and “learned helplessness” can be applied systematically in place of “overworking” and “dependence”, but they cannot replace the category “TABP” because they offer little further insight into the genesis of the condition than the original term already implies [23]. It is for this reason that such studies do not yield an internal elaboration of the concept TABP, but an ever-increasing bundle of psychological terms and categories which have been found to be associated with people designated as Type A.‘B. The extent to which this refines the idea of TABP is limited, albeit that we may now use a greater variety of terms to indicate the essential thing which still remains a categorial description. Added to this. one may see the truth in the statement of Matteson and Ivancevich (quoted above) that the possibilities for using models of the personality theorists in research on TABP are virtually unending: they are. for without the guidance of abstract. rationally-integrated concepts (theory) the
109
plethora of independent bits of knowledge wi]] con_ tinue to grow and grow. Much of the empirical work associated with the TABP has been concerned with predicting coronary_ proneness; that is, in developing a meth&o]ogy by which such designation can be made with accuracy. Jenkins, who perhaps more than any other worker has been responsible for developing this line of enquiry, has related this to the question of expianation by saying: It is possible for a variable to be a good predictor and still give little insight into the processes involved. Yet it is hardly possible that a variable can really assist in explanation it if is impotent as a predictor. The ability of a variable to be used in explanation is directly associated with the multiplicity of its connections into a nomothetic network of already known relationships [24, p. 733.
We have already dealt with the logical error arising from confusing variables (empirical categories) with explanations (conceptual systems), as implied in Jenkins’ second sentence. The reverse-logic embedded in his initial proposition and subsequent deduction can be seen also to emerge from a concern only with variables and empirical relationships. While it is likely that a variable giving weak prediction will not by itself assist in explanation there is no reason (given the preceding arguments) to subordinate explanation to the search for good prediction. The important distinction to be made is that where theory may be used for prediction on the basis of its explanation (e.g. the laws of motion), empiricism (the association of variables) can claim explanation only if it controls or can manage events. If no association is determined between events then it is often taken that there is nothing to explain, for little has been discovered. With particular reference to the postulated psychological and social factors associated with the incidence of CHD, this means that successful predictions made today concerning ‘links’ and ‘mechanisms’ depend upon the replication of these same events in the future if the relationship is to stand the test of experience. Given that the social world-at a cultural, societal or interpersonal level-is in a state of change, then some of the variables which medical and social scientists will need to study in the future will be different from those currently of interest. The oft-used preamble to papers concerning the “modern problem of CHD in Western society” presumes such change. The attempt to isolate and then to relate particular variables selected from our society (e.g. achievement
motive [lS]; job tension [13]) with coronary-proneness or its incidence begs the issue posed in the assumption of social change. Not only is the researcher who relies on empirical categories in a position of carrying out seemingly endless cross-sectional comparisons within the context of present day knowledge, but future workers will be committed to continuing this exercise should theoretical developments not be forthcoming. The counter-argument might be made to the above that “surely theory will build on all this data”. The response to this is twofold. A theory embracing physical health and disease and events in the social world might use selected data, but it is unlikely to begin from any attempt to summarise it all because con‘%)-
110
A. R. RADLEY
tualisation and categorisation are distinct activities in scientific thinking. And furthermore, the argument that “more research is required” is a continuation Of the emphasis that data collection of this kind must come first, a view sometimes forthcoming from attempts to take stock of research progress to date. One way in which research findings on coronaryproneness have been brought together is in review papers presenting work in the form of a ‘model’ of the process in qutstion. This is interesting if only to reveal the extent to which the concepts in use remain separate eten as they are placed together, in spite of attempts to present diagrammatically the interrelation of concepts such as “psychosocial stimuli” “mechanism”, and “disease” [25] ; “conditioning variables”. “perceived stress” and “responses to stress” [17]; “psychosocial risk factor”. “information processing” and “psychological reactions and behaviours” [26]. These models illustrate that far from integrating these ideas the writers are merely juxtaposing concepts abstracted from different areas of research in the attempt to indicate possible “lines of connection”. Such juxtaposition is unlikely to lead to advances in the theory of how CHD develops in a social world if, as happens, it besets itself with confusions. Firstly, by separating out the aspects of the problem into essential units (social environment, features of individuals, physiological processes) such thinking tends to attribute to those units properties which may better describe transactions or relations between them [22.27]. There is also what may be called a confusion of levels of conceptual thinking, in which concepts which overlap in terms of their referents are presented as if they were exclusive. To take an example, Dembroski derives the following question, among others, from his model: “Is the manner in which they (high Type A. low Type B) process information differentially affecting and/or affected by particular psychological reactions (e.g. anger, impatience. etc.) and behaviours (e.g. aggression, avoidance, etc.)?’ [26]. Within this statement labels are attached to one state which might very well have appeared in the other (is “anger” a reaction or a behaviour?), while one aspect of the way in which people might “process information” (avoidance) is itself set out as a potential variable. In another presentation Kagan and Levi [ZS] suggest that stimuli arising from a social situation “may or may not produce an emotional or other physiological response”. Here there is an attempt at reduction of a psychological concept (emotion) to one of physiological status, while Hinkle [28] has spoken of people’s “exposure to a certain kind of interpersonal relationship or social condition” as if people existed apart from their social relationships. The purpose of making these critical points is not to deny the problem area the attention it merits, nor to play down the contributions which have been made by researchers in establishing the validity of investigating physical ill-health within a social perspective. What is at issue is the progress which is now to be made on the basis of constructs which were first used to grasp the phenomena under study. Where these constructs are drawn from different disciplines-or from different sub-systems of thought in a Particular discipline-then their presentation as if they formed a unitary system is quite misleading.
It is misleading because it invites us to investigate ‘relationships’ or ‘interactions’ between ‘variables’. the logical status of which is often only to be found in their operational definitions. By abstracting ideas from their conceptual systems in order to “get the variables together”, the distinct and fundamental issues pertaining to them are either lost or confused. This can be seen in the treatment of cause and effect relations between variables under study. While some [29,30] have questioned the validity of current hypotheses on the grounds that this makes the unwarranted assumption of a chain of events with ‘original’ event and ‘final’ cause, others have speculated in this vein. On the one hand there is a search for ‘mechanisms’ [6.7,23] by which is usually meant the physiological events which immediately precede the onset of CHD. On the other, there are efforts to discover the kinds of social context which either give rise to the behaviour pattern associated with coronary-proneness or in which such behaviour tends to be elicited. There is an implied sequence in these arguments which suggests that the social context ‘causes’ people to behave in certain ways, which in turn ‘causes’ them to suffer pathogenic changes in their physiological systems. This is the assumption of a “final common pathway” suggesting that the individual is the recipient of something from outside. However, this begs the question of how individuals adapt and cope with life’s demands. Insofar as an individual is regarded as striving for achievement and as “confidently advancing to grapple with his challenges” [4] then his style of behaviour (his embodied actions) can just as well be regarded as initial as final. More accurately, this question of the direction of causality only arises if one separates out person from environment and proceeds to ask how one affects the other, overlooking entirely that individuals might be constituted by their social relations and yet can place their own interpretations on events. It might be objected that these criticisms constitute an impertinent demand to make at this stage of the investigation, and that the elucidation of these links ‘must proceed experimentally’ [31]. Indeed, demand for explanation seems at odds with the recent statement of Matteson and Ivancevich that: much of the current thinking regarding mechanisms is theoretical in nature rather than empirical. There is no direct evidence which clearly identifies a particular mechanism as being implicated in the proposed link [S].
This appraisal depends, however, upon the assumption that particular mechanisms will be revealed directly in the search for links between variables. For, following Herd [32] Matteson and Ivancevich identify the explanation of the association between “behavioural phenomena” and “alterations in physiological processes” with the designation of “mechanisms”--by which they mean cause and effect links. This is a further illustration of the belief that empirical categories can attain an explanatory status through demonstrating that a particular set of circumstances obtains, without having to make clear the conceptual ‘linkage’ which it implies. It. is not apparent from this whether the identification of mechanisms will demand a physiological reduction of the “behavioural patterns” under study. If so, such a reduction would be
Theory and data in the study of ‘coronary proneness’ Table 1. Conceptualisation
111
of psychological and social precursors to CHD used by different research perspectives-a schematic outline Level of conceptualisation
Working perspective Cardiologist
Culture, social environment
Individual person
Physiological systems
Illustrative authors
Little, if any statement in these terms.
Either use of simple categorial constructs or reference to specific concepts (‘conditioning’, ‘stimuli’)
Problem defined and elaborated in these terms (dependent variables)
Rosenman [lo. 381 Nixon [33] Selye [34] Obrist [36]
Some elaboration of problem in terms of cultural and structural differences.
No formal statement in these terms
Problem initially defined here in terms of incidence of categories of disease
Cassel [8] Marmot [12] Syme et al. [29] Wardwell et al. [37]
Little, if any statement in these terms.
Problem articulated in terms of associated concepts applied to individual behaviour and/or personality
Problem located here, but in categorial terms (independent variable).
Jenkins [24] Glass [23] Dembroski [7]
Psychophysiologist
Epidemiologist
Sociologist Psychologist
inadmissable (voiding the phenomerion of individual experience) as would be a “psychologism” which attempted to attribute to individuals characteristics which actually derive from people’s relationships in a social world. However, these problems of relating sep arate concepts in theory is one which is implicit ratlier than extant in the literature on the association of social and psychological variables to CHD. There is a recognition that the juxtaposition of variables currently only implies causal linkages and does not yet reveal them, but the problem is then designated “multifactorial” [2] and this becomes the basis for further recommendations that more empirical research is required. The circularity of this argument and, indeed, of the research endeavour only becomes apparent when the need for conceptual analysis as well as the collecting of data can be admitted C21.223. THE CONCEPTUALISATION OF CHD BY MEDICAL AND SOCIAL SCIENTISTS
The question of why some of the work into coronary-proneness has taken the form critic&d in this paper can be illuminated by reference to the relationships of medical and of social science researchers to the problem of CHD. Their approaches differ both in the conceptual systems which are employed (the languages of physiology, psychology, or social science), in their preferred methods and in their location of the problem to be solved. It is this last aspect which can be exemplified by reference to Table 1 which shows three broad approaches to the problem. While the Table is meant to be schematic rather than definitive, it does allow comparisons to be made between perspectives with regard to their use in CHD research. As originally stated by some cardiologists who have noted the types of individuals consulting them in their capacity as medical practitioners, the problem is defined by a thorough description of its clinical manifestation using regular clinical indices (e.g. B.P., serum
.
lipids, E.C.G.). This is then related to individuals described either in what one might call “lay psychological language”, or else in terms of concepts which have a certain face validity in relation to the physiological definition of CHD. For example, Rosenman. et al. refer to a “certain emotional complex in the pathogenesis of CHD” [lo] (lay language), while concluding their argument with reference to “the pathogenetic relevance of the central nervous system to the occurrence of manifest CHD” (face-valid concept). Similarly, Nixon talks of exhaustion leading to CHD as resulting from “‘emotional responses” and then describes it more formally as a “morbid level of arousal” c331. In comparison, the approach of psychophysiologists is similar in their use of physiology, but different in their emphasis upon particular facets of heart function. In addition, they often rely very strongly on concepts drawn from conditioning theory in psychology such as endogenous or exogenous conditioning factors when describing the physiology of cell necrosis [34], or the relation of classical conditioning and shock avoidance to heart rate and cardial force [35,36-J. This perspective grounds the problems of CHD firmly in physiology, using selected psychological concepts to express the conditions under which physiological changes might occur. The problem field is delineated, as it were, ‘by the skin of the individuals under study’, with little or no consideration of the social context in which it occurs. In contrast to this, epidemiologists have attempted to show that the incidence of CHD varies with culture, and that this is not to be explained by the “traditional risk factors alone” [g, 123. In studies of large groupings defined by culture or by particular indices of socio-economic status or mobility [29] there have beeri attempts to relate the relative incidence of CHD to factors which presuppose a relationship between health and social integration. These studies, however, do not make clear just how particular individuals
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mlgnt oevelop CHD, so that they trust, like Wardwell er al. to “these more distant factors (serving) as indices or clues to significant factors in the etiology of this prevalent and puzzling disease” [37]. Finally, the third perspective is that offered by researchers who have emphasized the features of particular individuals who have suffered, or who might develop CHD [ll, 383. The growing literature on TABP [4] is now evidence to the attempt to relate the occurrence of CHD to aspects of persons which can be explained in terms of psychological concepts. While it is argued that the TABP does not stem solely from an individual’s personality but emerges only when certain challenges or conditions of the milieu arise, the actual work on TABP has tended to treat it as a stable personality characteristic. This is shown by its repeated use as an independent variable in studies which seek to relate it to other factors proposed to be pertinent to the problem [23]. The point is not that the choice of TABP as an independent variable is in itself a wholly limiting condition, but that it is necessary to consider the study of coronary-proneness in the context of the multidisciplinary research carried out in order to gain a perspective on‘the use of this typology. Table 1 presents a schematie outline of the way in which research on the social and psychological aspects of CHD varies in its conceptual foci, in its choice of dependent and independent variables and in those aspects which, being assumed as constants, are selectively ignored by the researchers concerned. This variation in cross-disciplinary investigations means that within each main conceptual system the problems are articulated so as to achieve a limited but effective basis of understanding and communication among researchers. It also has the effect of setting out the significant differences in the investigator’s chosen subsidiary system in a more circumscribed manner, in which they take on the appearance of either ‘independent variables’ or ‘factors’. These various research efforts define a multifaceted problem field in which concepts explicated from the working perspective of a given discipline are differentiated through the use of more simple categories drawn from another discipline. So with work on TABP, a typology having simple status in psychological terms has been used to make articulated points about the physiology of the individuals concerned. This perspective is the one used by Friedman and Rosenman, as caidiologists, and is also that taken by psychologists working with the group on the development of a predictive tool which could be used in their research. Such methodology essentially involves a refinement of the operational definition of TABP rather than a conceptual elaboration of the categorisation. (Jenkins has been quoted earlier in this paper on his belief in the primacy of predictive utility in scientific explanation.) In fact, much subsequent work has been justified in terms of its potential contribution towards the aim of predicting who is prone to develop CHD C38-413. Inasmuch as this aim has been sought by the use of psychological testing (either directly of TABP or by its association with other tests of personality), this has meant that the category itself has remained largely unelaborated. TWO reasons for this have been anticipated in the previous discussion. The standpoint of
the cardiologist is in the discipline of physiology in which terms the problem of CHD is initially defined. The category ‘Type A behaviour’ is a description at the level of psychological explanation, serving as an independent variable, the significance of which is given by differences observed in terms of measures such as serum cholesterol level, angiography, E.C.G. and blood pressure. To maintain this perspective. even as a social scientist, is to preserve the opacity of the phenomenon (‘Type A behaviour pattern’) in its role as an index of differences accounted for in terms of physiology. Predictive research into social and psychological aspects of CHD is also related to the need for therapeutic intervention by medical practitioners. If one can designate who is likely to suffer a heart attack then one can do something in order to prevent it. But do what, exactly? This depends upon one’s conceptualisation of the problem, and in particular the theory of its etiology. Inasmuch as our knowledge is restricted to the likelihood of associations between empirical categories, then the ‘risk’ of suffering a coronary attack or the ‘causes’ of CHD will be attributed to various parts of the problem field. Either the individual himself is seen to be the repository of the problem (in which case he might be given either behaviour therapy or psychotherapy [42]), or else some aspect of his working environment is selected as the locus of the stress involved. In spite of its predictive utility a focus on empirical categories treated as variables is of limited help in guiding therapeutic intervention at those levels, for it has eschewed the articulation of abstract concepts in which observables can be comprehended in terms of an integrated system. Not surprisingly, the issue of the modification of TABP has certain contradictory features. One mentioned above is the question of whether therapy is aimed at Type A individuals, at environments believed to engender Type A behaviour. or at both. Rosenman and Chesney [4] believe that modification of Type A behaviour should be aimed at individuals (rather than environments), particularly at post-infarction patients who are able to gain some insight into their way of life. Cooper and Maishall [2] have called (rather optimistically) for more fundamental structural changes in organisations to encourage participation of people in their jobs, although TABP appears to be so embedded in the modern occupational career that intervention, observed one investigator, “might meet with resistance from the subject population” [43]. These difficulties and uncertainties, while not following from a concern with prediction, illustrate the limitations of this approach in the sphere of medical and social science. Even if one can designate with great accuracy who, among healthy individuals, is ‘coronary prone’ one is still left with all the questions about what to do about it and how to proceed. Indeed, there is a deeper contradiction within empiricist approaches to TABP which is not always apparent in the research literature, but of significance nonetheless. If CHD develops in greater or lesser part from certain cultural, organisational and individual styles of living then no technical intervention by medical practitioners is likely to affect it greatly, in spite of considerable efforts to define the problem in a technical way. (By ‘technical’ is meant the specification of
Theory
and data
in the study
mechanisms, social or psychological, which by association are inferred to cause or to predispose an individual to suffer CHD). This is. firstly, because such an approach is geared towards intervention with individuals. as is much of modern medicine [44]. While this curative approach has, arguably, been successful in the struggle against disease it has not been so in the fight against ill-health due to maladaptation. In defining a set of precursors of CHD within the social field the researchers whose work is under discussion here have often been at pains to indicate the limitations of an ‘engineering’ approach to the problem of heart disease. And yet, in pursuing a line of research premised upon prediction (management) it would seem that these same principles have guided much of their work. Laudable as this is in the attempt to help post-infarction patients, the problems which arise when applied to otherwise healthy individuals are difficult indeed, being in part due to a failure to transcend, conceptually, the observables under study. Finally, we should note that one likely effect of successful prediction of coronary-proneness would be redoubled effort to specify the physiological mechanisms in such a way that intervention by chemo-therapy would be attempted. While this runs counter to the expressed concerns of Rosenman and his colleagues, such a reductionist approach is not only a current part of the wider research field but is latent in their early work implicating the ‘role of the CNS’ in the etiology of CHD. By comparison, there was once a brief literature on the psychological features which might predispose people to pulmonary tuberculosis [45]. The discovery of the tuberculosis bacillus and the effective use of vaccination meant that this approach was promptly rendered sterile for the purposes of curing TB. What is of interest here is that the cery idea of asking about predisposition to tuberculosis in terms other than those of physiology has recently been ridiculed in the light of the demonstrated effectiveness of microbiological methods in that field [46]. Although far more extensive and sophisticated in its methodology, inasmuch as current literature treats the TABP and other social/psychological variables as just one more index of disease occurrence, then their de facto displacement due to advances in other fields of research is always possible. This is particularly so while we lack a conceptual framework in social science within which these problems can be grasped. and equally important, can be Seen by a wider audience to be a basis for asking valid questions. CONCLUDING
REMARKS
The burden of this paper has been to draw attention to some of the issues and problems which beset the field of research into social and psychological aspects of CHD. Most attention has been paid to the concept of TABP first put forward by Friedman and Rosenman because their efforts at establishing the relevance of this approach are now the basis for a considerable enthusiasm among researchers wanting to extend the original work. It has been argued that while some categorial thinking may be necessary in early research employing disciplines at two ‘levels’ of conceptualisation. the retention of such categories S.SM16I -H
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(mis)taken as explanatory concepts, their cross-relation in empirical investigations and their refinement as indices for prediction leads away from the con_ struction of a system of abstract, Jogicaffy_related con_ cepts (theory). In saying this the intention is neither to draw attention away from research nor to brand ah studies in the field as being without merit. Rather, criticism is aimed at research which either confuses empiricism with explanation or does not attempt to relate its methods to existing concepts or to the elaboration of new ones. Associated with this are review papers which, summarising all the evidence, offer only an aggregation of material with the recommendation that “more research” be carried out on the assumption that only more empirical work can make for explanation. One symptom of this attitude in evidence is the flight from case material and example, apart from almost ritual references to the description of typical’ CHD patients made long ago by Osler. And yet case study, alongside other methods, may yield fruitful descriptions if only because it can give the “minute-byminute” detail required if we are to see how the various areas of a person’s life, separated by current foci of conceptuahsation. function together over time C3.223. This might result in the realisation that the properties which we ascribe to one level (e.g. the Type A individual) are more fittingly described as a function of the relationships within a particular field or situation. To take this view is to relinquish the felt necessity of beginning with a particular disease entity defined in terms of physiological changes, and then seeking out those psychological and cultural variables that play a possible causal role in the chain of events leading up to coronary heart disease. Arguably, the sequencing of such variables (e.g. social conditionspsychological responses-physiological adaptation) derives its rationale not from a close inspection of the problem itself, but from assumptions engendered upon the relationships obtaining between disciplinary approaches employed in empirical research (see Table 1). It is within the context of these assumptions that questions as to the part played by psychological and social conditions can arise-that is, how much do these factors count in the etiology of CHD? This is not merely a difficult question on the (empirical) grounds that the genesis of CHD is ‘multidetermined’, but is an unanswerable one on the (logical) grounds that the parts to be considered are products of conceptual analysis, not of the real world. However, there is no a priori reason why a theory of CHD considered as a ‘stress-related illness’ must confine itself to accounting for findings obtained on the basis of assumptions criticised in this paper, except that we overlook the relationship between medical and social scientific research on this problem and continue to seek for explanation in empirical endeavour. REFERENCES
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