Invited Commentary: Structure and Context Matters The Need to Emphasize Social in Psychosocial Epidemiology

Transcription

1 American Journal of Epidemiology ª The Author Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please Vol. 175, No. 7 DOI: /aje/kws033 Advance Access publication: March 5, 2012 Invited Commentary Invited Commentary: Structure and Context Matters The Need to Emphasize Social in Psychosocial Epidemiology Reiner Rugulies* * Correspondence to Dr. Reiner Rugulies, National Research Centre for the Working Environment, Lersø Parkallé 105, DK-2100 Copenhagen, Denmark ( rer@nrcwe.dk). Initially submitted November 24, 2011; accepted for publication December 8, A high level of influence on core aspects of life in general and at the workplace in particular is believed to reduce the risk of ill health. In this issue of the Journal, Joensuu et al. (Am J Epidemiol. 2012;175(7): ) shake this belief by presenting prospective associations between high decision authority at work and increased all-cause, cardiovascular, and alcohol-related mortality among Finnish forest company employees followed through In this invited commentary, the author welcomes these findings as a much needed inspiration for reflections on the current state of psychosocial epidemiology and how it can be advanced in the future. Although it is important to investigate possible harmful effects of too high decision authority, the author argues that it is even more important to be aware that psychosocial factors originate from societal structures and social contexts. Understanding these structures and contexts, their changes over time, and their relation to psychosocial factors is key for understanding the effect of psychosocial factors on health and illness. Joensuu et al. have presented thought-provoking findings. It is the hope of the author that this will push the research community to emphasize the social in psychosocial epidemiology. epidemiologic methods; epidemiologic studies; mortality; occupational health; psychology; social class; social environment; stress, psychological The level of influence a person has on core aspects of his or her life is thought to be a powerful determinant of health and illness (1). Regarding working life, the demand-control model proposes that the mismatch between high psychological demands at work and low job control leads to a state of job strain that subsequently increases the risk of psychological and physical ill health (2). The model has generated a wealth of epidemiologic research over the last 30 years, in particular with regard to cardiovascular disease (3, 4). The results, however, are mixed, with several studies supporting and not supporting a prospective association between job strain and/or its components with morbidity and mortality (3, 4). Methodological limitations of the studies might explain overand underestimation to some extent (4), but concerns about conceptual problems of the model have also been raised (5). One concern has been whether there is a joint effect of high psychological demands and low job control or whether only one of the components is affecting health (3, 5). It is often overlooked, though, that job control itself consists of 2 factors: skill discretion and decision authority. Whether both or only one of the factors predicts health endpoints is usually not reported in the empirical literature (3, 4). In this issue of the Journal, Joensuu et al. (6) present results on the separate associations of skill discretion and decision authority with all-cause and cause-specific mortality in a cohort of Finnish forest company employees. The study was well conducted, and the findings are both interesting and disturbing. Low skill discretion measured as monotonous and repetitive work, low use of knowledge and skills, low requirement of deliberation and decision making, and few learning possibilities showed inconsistent patterns of associations with all-cause mortality across the different statistical models. Surprisingly, high decision authority measured as a high level of influence on work pace, work methods, planning of work, objectives of work, and as the possibility to leave the work station for a short while was not a protective factor but, instead, predicted all-cause, cardiovascular, and alcohol-related mortality. Moreover, in a previous article from the same cohort, high decision authority predicted hospitalization for mental disorders (7). 620

2 Structure and Context Matters 621 CAN DECISION AUTHORITY BE TOO HIGH? Assuming that the unexpected findings on decision authority are not due to chance, how can they be explained? In the literature, 2 major methodological concerns with psychosocial research in general and research on the demandcontrol model in particular have been intensively discussed: 1) overreliance on self-reported exposure measurements and 2) potential confounding by socioeconomic position (8 12). Measuring exposure by self-report means that the participants responses are driven partly by the work environment itself (i.e., the entity that is intended to be measured) and partly by individual differences (e.g., personality, mood, previous experiences, preclinical disorders entities that are not intended to be measured) (8, 13, 14). This causes misclassification, which could be differential when, for example, a preclinical disorder influences both the perception/appraisal of the exposure at baseline and the onset of the clinical disorder during follow-up. However, in the present study, it seems difficult to understand why a preclinical disorder should have caused participants to overestimate their decision authority. Confounding with socioeconomic position is also an unlikely explanation, because high decision authority was associated with high socioeconomic position (white-collar work), which was, as usual (15), protective against mortality. Because these 2 major methodological concerns from the literature do not seem to explain the results, might high decision authority indeed be health hazardous? Joensuu et al. (6, p. 0000) seem to favor this explanation as they point out that there might be a possible downside of high decision authority, maybe in the form of burden arising from too high responsibility and freedom of choice. This is a reasonable consideration, especially in the light of contemporary work life that seems to put increasing demands on employees for self-optimizing, self-organization, and high flexibility, at least in some areas of the labor market (16, 17). Against this background, it is understandable that Joensuu et al. are skeptical that more decision authority is always beneficial and that they argue for investigating the optimal level of decision authority. However, because there was a graded relation between increasing decision authority and mortality, the results by Joensuu et al. suggest that the optimal level of decision authority is very low. Does this mean that we should advocate that employees should have almost no influence at work, for example, on work pace and objectives of work, as Web Table 4 seems to indicate? A THEORETICAL FRAMEWORK FOR PSYCHOSOCIAL EPIDEMIOLOGIC RESEARCH Before considering the possible downside of high decision authority, we might find it worthwhile to reflect on the role of macro-level structures and social contexts in psychosocial epidemiology. To my knowledge, no authoritative definition of psychosocial epidemiology exists, but I suggest distinguishing between social epidemiology (18) as a discipline focusing primarily on the direct effectofsocialstructures on health and psychosocial epidemiology as a discipline explicitly considering psychological phenomena, that is, cognitions, emotions, behaviors, and psychophysiologic processes, as a step between social structures and health outcomes. In this reasoning, I follow the thoughts outlined by Martikainen et al. who wrote as follows:... psychosocial factors, at least in the context of health research, can be seen as: (1) mediating the effects of social structural factors on individual health outcomes, or (2) conditioned and modified by the social structures and contexts in which they exist. The definition thus raises the question of what the relevant broader social structural forces are, and how such forces might influence health through their effects on individual characteristics (19, p. 1091). Figure 1 shows a simple hierarchical framework for psychosocial epidemiology. It is based on an adaptation and modification of 2 earlier figures published by Martikainen et al. (19, p. 1092, Figure 1) and Rugulies et al. (15, p. 40, Figure 2.4). The starting point in this hierarchical framework, the prima causa or the spider in the web of causation (20), if one will, is the macro-level economic, social, and political structures of the society. These societal structures produce the meso-level social contexts, that is, specific social structures and relations, in the communities, families, and workplaces (15, 19). From this social context, the psychosocial factors originate, such as control over core aspects of life (1), social cohesion (21, 22), social reciprocity (23), interpersonal conflicts (24, 25), or availability of socioemotional support (26), to name just a few. The psychosocial factors are experienced and cognitively and emotionally processed by the individual (13). At this point, personality, previous experiences, and other individual psychological differences play an important role (13, 14), but note that it is presumed that these individual differences in their substance are shaped by societal structures and social contexts (27). As a result of the processing, the individual shows certain reactions on the behavioral and the psychophysiologic levels. It is assumed that exposure to adverse psychosocial factors will increase risk of problematic Material pathway: effect of social contexts on health behaviors and health independent of psychosocial factors Macro-level economic, social, and political structure Health behaviors Meso-level social context Meso-level psychosocial factors Individual-level psychologic states and processes Psychophysiologic processes Population and Individual Health Figure 1. A simple hierarchical framework for psychosocial epidemiology. (Adaption and modification of 2 figures published earlier by Martikainen et al. (19, p. 1092, Figure 1) and Rugulies et al. (15, p. 40, Figure 2.4).)

3 622 Rugulies health behaviors (28) and of health-hazardous psychophysiologic processes (29, 30). The framework also includes a material pathway connecting the social context directly with health behaviors and health. Hence, although the framework emphasizes the role of psychosocial factors, it is not ignorant of the role of material factors. This is important, because of the passionate controversy on the relative contribution of material and psychosocial pathways to health (31, 32). The framework is both oversimplified and too complex. It is oversimplified because it proposes a hierarchical causal pathway from societal structures via social contexts and psychosocial factors to health, while deliberately not considering bidirectional associations (e.g., an effect of poor health on the onset of adverse psychosocial factors). On the other hand, the framework is too complex to be tested in a single empirical study. At the current stage, the main value of the framework probably is to remind researchers that psychosocial exposures are complex phenomena that do not exist independently of macro-level societal structures and meso-level social contexts. THE NEED TO UNDERSTAND THE ROLE OF STRUCTURES, CONTEXTS, AND PSYCHOSOCIAL EXPOSURES If it is correct that psychosocial factors are conditioned and modified by the social structures and contexts in which they exist (19, p. 1091), then it is key to understand these structures and contexts. This includes the understanding that the effect of psychosocial exposures on health is not ubiquitous, that is, not necessarily always the same, irrespective of time and place (33, 34), which emphasizes the value of an age cohort (33) and a life-course perspective (35) in psychosocial epidemiology. There are indications that, in the study by Joensuu et al. (6), context might have modified the effect of the psychosocial factors. Whereas, in the unadjusted analyses, high skill discretion came close to predicting all-cause mortality, it became almost a protective factor when adjusted for the covariates in model 2 (Table 3). This is difficult to understand. One explanation could be that some covariates, such as occupational status, supervisor status, and workplace social support, were not confounders but contextual factors that have acted as effect modifiers. Both skill discretion (e.g., usage of knowledge and skills) and decision authority (e.g., influence on the objectives of work) might have very different meanings, and subsequently different health effects, for white versus blue collar workers or for supervisors versus nonsupervisors. Macro-level societal changes might also have affected the results. When reading the article by Joensuu et al. (6), I was reminded of another Finnish study, the Valmet Study (36). In this study, exposure to job strain and effort-reward imbalance measured in 1973 predicted cardiovascular mortality over a 27-year follow-up. When I first read the study, I had the same reaction as I had when reading the article by Joensuu et al.: amazement and disbelief. Can it really be that psychosocial work exposures, measured at one point in time, have such a strong effect on mortality over such a long follow-up period? Others wondered as well, and Macleod and Davey Smith (37) suggested that the results were due to confounding with low socioeconomic position. However, when in a follow-up article several indicators of socioeconomic position were taken into account, hazard ratios changed only marginally (38). Why are the results in the Valmet Study and in the forest worker study so different? Besides important methodological differences (e.g., job strain and not decision authority being the main predictor in Valmet), macro-level societal structures might have played a role. In the early 1990s, Finland underwent a major recession, causing downsizing, unemployment, and changes in the work environment (39 41). For the Valmet Study, this recession was probably not of great importance, because most of the middle-aged participants surveyed in 1973 were likely either retired or close to retirement in the early 1990s. Indeed, job stability was high in the Valmet Study, and therefore exposure to psychosocial workplace factors might have been rather stable over time (36, 38). In the forest worker study, however, the baseline survey was only a few years before the onset of the recession. Joensuu et al. (6) reported that those participants scoring high on decision authority had an increased likelihood to leave the company during follow-up. This could indicate that employees with high prerecession levels of decision authority might have been more negatively affected by the recession, for example, in terms of downward social mobility, than those with low levels. CONCLUSIONS Joensuu et al. (6) have presented thought-provoking findings. It is now up to the research community how to use this. It is my hope that the results will not initiate a search for the toxic component of job control, in a fashion similar to the unfortunate search for the toxic component of type A behavior in the 1980s (33). Instead, I hope that the findings will push researchers to emphasize the social in psychosocial epidemiology to motivate investigators considering information on societal structures and social contexts over time when studying the associations between psychosocial exposures and health endpoints. ACKNOWLEDGMENTS Author affiliations: National Research Centre for the Working Environment, Copenhagen, Denmark; Department of Public Health, University of Copenhagen, Copenhagen, Denmark; and Department of Psychology, University of Copenhagen, Copenhagen, Denmark. The author thanks Dr. Birgit Aust, Ida E. H. Madsen, and Dr. Tage Søndergård Kristensen for thoughtful comments on earlier versions of this invited commentary. The author does not feel a conflict of interest. However, he wishes to disclose that he collaborates with several of the authors of the commented article in a European Research Consortium on work-related psychosocial factors and health in subgroups, The IPD-Work ( individual-participant-data meta-analysis of working populations ) Consortium.

4 Structure and Context Matters 623 REFERENCES 1. Syme SL. Control and health: an epidemiological perspective. In: Rodin J, Schooler C, Schaie K, eds. Self-Directedness: Cause and Effects Throughout the Life Course. Hillsdale, NJ: Lawrence Erlbaum Associates, Inc; 1990: Karasek R, Theorell T. Healthy Work: Stress, Productivity, and the Reconstruction of Working Life. New York, NY: Basic Books; de Lange AH, Taris TW, Kompier MA, et al. The very best of the millennium : longitudinal research and the demandcontrol-(support) model. J Occup Health Psychol. 2003;8(4): Belkic KL, Landsbergis PA, Schnall PL, et al. Is job strain a major source of cardiovascular disease risk? Scand J Work Environ Health. 2004;30(2): de Jonge J, Kompier MAJ. A critical examination of the demand-control-support model from a work psychological perspective. Int J Stress Manag. 1997;4(4): Joensuu M, Kivimäki M, Koskinen A, et al. Differential associations of job control components with mortality: a cohort study, Am J Epidemiol. 2012;175(7): Joensuu M, Väänänen A, Koskinen A, et al. Psychosocial work environment and hospital admissions due to mental disorders: a 15-year prospective study of industrial employees. J Affect Disord. 2010;124(1-2): Kasl SV, Jones BA. An epidemiological perspective on research design, measurement, and surveillance strategies. In: Quick JC, Tetrick LE, eds. Occupational Health Psychology. Washington, DC: American Psychological Association; 2003: Macleod J, Smith GD, Heslop P, et al. Are the effects of psychosocial exposures attributable to confounding? Evidence from a prospective observational study on psychological stress and mortality. J Epidemiol Community Health. 2001;55(12): Macleod J, Davey Smith G. Psychosocial factors and public health: a suitable case for treatment? J Epidemiol Community Health. 2003;57(8): Singh-Manoux A. Psychosocial factors and public health. J Epidemiol Community Health. 2003;57(8): Macleod J, Davey Smith G. Authors reply. J Epidemiol Community Health. 2003;57(8): Frese M, Zapf D. Methodological issues in the study of work stress: objective vs subjective measurement of work stress and the question of longitudinal studies. In: Cooper CL, Payne R, eds. Causes, Coping and Consequences of Stress at Work. Wiley Series on Studies in Occupational Stress. Chichester, United Kingdom: John Wiley & Sons; 1988: Ursin H, Eriksen HR. The cognitive activation theory of stress. Psychoneuroendocrinology. 2004;29(5): Rugulies R, Aust B, Syme SL. Epidemiology of health and illness. A socio-psycho-physiological perspective. In: Sutton S, Baum A, Johnston M, eds. The Sage Handbook of Health Psychology. London, United Kingdom: Sage Publications; 2004: Sennett R. The Corrosion of Character. The Personal Consequences of Work in the New Capitalism. New York, NY: Norton; Kompier MA. New systems of work organization and workers health. Scand J Work Environ Health. 2006;32(6): Berkman LF, Kawachi I, eds. Social Epidemiology. New York, NY: Oxford University Press; Martikainen P, Bartley M, Lahelma E. Psychosocial determinants of health in social epidemiology. Int J Epidemiol. 2002;31(6): Krieger N. Epidemiology and the web of causation: has anyone seen the spider? Soc Sci Med. 1994;39(7): Muntaner C, Lynch J. Income inequality, social cohesion, and class relations: a critique of Wilkinson s neo-durkheimian research program. Int J Health Serv. 1999;29(1): Wilkinson RG. Income inequality, social cohesion, and health: clarifying the theory a reply to Muntaner and Lynch. Int J Health Serv. 1999;29(3): Siegrist J. Social reciprocity and health: new scientific evidence and policy implications. Psychoneuroendocrinology. 2005;30(10): Zapf D, Einarsen SE. Mobbing at work. Escalated conflicts in organizations. In: Fox S, Spector PE, eds. Counterproductive Workplace Behavior: Investigations of Actors and Targets. Washington, DC: American Psychological Association; 2005: Orth-Gomér K, Wamala SP, Horsten M, et al. Marital stress worsens prognosis in women with coronary heart disease: The Stockholm Female Coronary Risk Study. JAMA. 2000; 284(23): Berkman LF, Glass T. Social integration, social networks, social support, and health. In: Berkman LF, Kawachi I, eds. Social Epidemiology. New York, NY: Oxford University Press; 2000: Horkheimer M, Adorno TW. Excursus I: Odysseus or myth and enlightenment. (In German). In: Horkheimer M, Adorno TW. Dialectic of Enlightenment: Philosophical Fragments. Frankfurt am Main, Germany: Fischer; 1969: (original 1947). 28. Sutton S. Determinants of health-related behaviours: theoretical and methodological issues. In: Sutton S, Baum A, Johnston M, eds. The Sage Handbook of Health Psychology. London, United Kingdom: Sage Publications; 2004: Henderson BN, Baum A. Biological mechanism of health and disease. In: Sutton S, Baum A, Johnston M, eds. The Sage Handbook of Health Psychology. London, United Kingdom: Sage Publications; 2004: Brunner EJ. Toward a new social biology. In: Berkman LF, Kawachi I, eds. Social Epidemiology. New York, NY: Oxford University Press; 2000: Lynch JW, Smith GD, Kaplan GA, et al. Income inequality and mortality: importance to health of individual income, psychosocial environment, or material conditions. BMJ. 2000; 320(7243): Marmot M, Wilkinson RG. Psychosocial and material pathways in the relation between income and health: a response to Lynch et al. BMJ. 2001;322(7296): Muntaner C. Commentary: social capital, social class, and the slow progress of psychosocial epidemiology. Int J Epidemiol. 2004;33(4): ; discussion Szreter S, Woolcock M. Rejoinder: crafting rigorous and relevant social theory for public health policy. Int J Epidemiol. 2004;33(4): Ben-Shlomo Y, Kuh D. A life course approach to chronic disease epidemiology: conceptual models, empirical challenges and interdisciplinary perspectives. Int J Epidemiol. 2002; 31(2): Kivimäki M, Leino-Arjas P, Luukkonen R, et al. Work stress and risk of cardiovascular mortality: prospective cohort study of industrial employees. BMJ. 2002;325(7369):857. (doi: /bmj ).

5 624 Rugulies 37. Macleod J, Davey Smith G, et al. Does work stress cause heart disease? [letter]. Rapid response to article: Kivimäki M, et al. Work stress and risk of cardiovascular mortality: prospective cohort study of industrial employees. BMJ. 2002;325(7369): 857. ( responses). (Accessed November 17, 2011). 38. Brunner EJ, Kivimäki M, Siegrist J, et al. Is the effect of work stress on cardiovascular mortality confounded by socioeconomic factors in the Valmet study? J Epidemiol Community Health. 2004;58(12): Vahtera J, Kivimäki M, Pentti J. Effect of organisational downsizing on health of employees. Lancet. 1997;350(9085): Kivimäki M, Vahtera J, Pentti J, et al. Factors underlying the effect of organisational downsizing on health of employees: longitudinal cohort study. BMJ. 2000;320(7240): Vahtera J, Kivimäki M, Pentti J, et al. Organisational downsizing, sickness absence, and mortality: 10-town prospective cohort study. BMJ. 2004;328(7439):555. (doi: /bmj D).