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- SECURING THE EVIDENCE BASE FOR PUBLIC HEALTH AND ACTING ON IT
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- Tores TheorellPublished on: 27 April 2016
- John MacleodPublished on: 27 April 2016
- Richard PeterPublished on: 27 April 2016
- John MacleodPublished on: 27 April 2016
- Published on: 27 April 2016Re: Psychosocial factors and Public Health. Authors' reply to the eLetter by John MacleodDear EditorShow More
The discussion triggered by this paper is a useful one. In general I agree with McLeod, and Davey Smith that we have to be careful when we make conclusions regarding etiology. Socioeconomic factors could certainly confound the relationships. Adjustment for socioeconomic factors could also conceal true relationships, however. In this literature (see the review by Schnall et al. 2000 which has been referred...
Dear EditorShow LessThe discussion triggered by this paper is a useful one. In general I agree with McLeod, and Davey Smith that we have to be careful when we make conclusions regarding etiology. Socioeconomic factors could certainly confound the relationships. Adjustment for socioeconomic factors could also conceal true relationships, however. In this literature (see the review by Schnall et al. 2000 which has been referred to previously in the correspondence and also Theorell et al. 1998) it has been found that the demand control model is more important in blue collar worker strata than in white collars. Adjustment for social class certainly does not solve the problem that psychosocial factors may be related to cardiovascular illness risk in different ways in different social classes. In addition, if we adjust for social class in analyses of the relationship between psychosocial factors at work and cardiovascular illness risk we are neglecting the possibility that one of the reasons why people in lower social classes have more cardiovascular disease might be that they might be humiliated due to bad working conditions (with resulting accumulating psychophysiological reactions) more often at work than those in higher classes.
Still, I agree that it is relevant to do such adjustments for social class but we have to interpret the total picture in the best possible way. Accordingly we need to do analyses that are both adjusted and non-adjusted for social class. Of course I agree that if adjustment is made it should be done in the best possible way and we should try to avoid residual confounding.
There is one passage in their letter that needs to be commented. They refer to our paper (Orth-Gomir et al. 1994) describing our intervention as a two-day course. The two-day course was only part of the total program. I quote from our own paper:
"In the third component of the stress management program, self-initiatives were solicited from workers to improve the work stress situation according to the three aspects of this theory (demand-control-support). This was stimulated by having each group of workers set up an action plan consisting of a a list of problems to attack and factors to improve."
Thus, the third component of the intervention lasted for several weeks. One of the aims of the initial course was to increase awareness in employees regarding what the relevant factors might be and to stimulate them to make suggestions for improvements. These suggestions were followed up systematically and did result in some organisational changes. In these particular work sites high work load was not the main factor but rather other structural problems. This study was not ideal because it was based upon small samples and the intervention had a mix of both structural and individual components. However, it was not primarily an effort to make the employees think that they had more say at work than they had! We certainly need more intervention research in this field.
References
(1) Hallqvist J, Diderichsen F, Theorell T, Reuterwall C, Ahlbom A.: Is the effect of job strain on myocardial infarction risk due to interaction between high psychological demands and low decision latitude? Results from Stockholm Heart Epidemiology Program (SHEEP). Soc Sci Med 1998 Jun;46(11):1405-15.
(2) Orth-Gomir K, Eriksson I, Moser V, Theorell T and Fredlund P. Lipid lowering through work stress reduction. Int J Beh Med 1994 1:204-14
(3) Schnall PL, Belkic K, Landsbergis P och Baker D. The workplace and cardiovascular disease. State of the Art Reviews. Occ Med 2000; 15(1).
(4) Theorell T, Tsutsumi A, Hallquist J, Reuterwall C, Hogstedt C, Fredlund P, Emlund N, Johnson VJ, and the SHEEP Study Group. Decision Latitude, Job Strain, and Myocardial Infarction: A Study of Working Men in Stockholm. American Journal of Public Health 1998; 88 (3):382-8.
Conflict of Interest:
None declared. - Published on: 27 April 2016Psychosocial factors and health: response by Macleod and Davey Smith to authors' reply
- John Macleod, Clinical Research Fellow
- Other Contributors:
- George Davey Smith
Show MoreDear Editor
We are grateful to Peter and colleagues for taking the trouble to respond to our e-letter. They raise several issues that we will try to address briefly.
First, they say effort-reward imbalance had no relation to socio-economic status in their study. We are unclear how they assessed this – the only SES measure they mention in their paper is a white-collar/blue- collar binary distinction. Effort–r...
Show LessDear Editor
We are grateful to Peter and colleagues for taking the trouble to respond to our e-letter. They raise several issues that we will try to address briefly.
First, they say effort-reward imbalance had no relation to socio-economic status in their study. We are unclear how they assessed this – the only SES measure they mention in their paper is a white-collar/blue- collar binary distinction. Effort–reward imbalance may well have varied with SES without such variation being apparent in relation to such a crude measure. Furthermore the fact that effects were apparent amongst “homogenous socio-economic groups” does not rule out residual confounding as a possible explanation. For confounding to be possible the exposure under assessment simply needs to be a better proxy for social position than the stratification measure by which these “homogenous” groups are defined.[1] Again, if the groups are defined as broadly as “white-collar” and “blue collar” then residual confounding seems a distinct possibility.
Second, we don’t understand the basis for their suggestion that we failed to consider experimental evidence as a criterion for causality in this context and were thus in some way guilty of bias. A substantial part of our letter related to this very point – as Peter and colleagues appear to concede in the first sentence of their fourth paragraph. The experimental evidence that we cited was that examining effects in relation to objective cardiovascular endpoints[2] – as opposed to intermediate outcomes of questionable significance or subjective outcomes that might be influenced by response bias. None of the publications cited by Peter and colleagues appear to relate to any additional evidence of this former type. For example one of the specific studies they mention described a two -day educational intervention for civil servants aimed at increasing perceptions of workplace control.[3] Perceptions of control were increased in the intervention group, but other than a marginal change in apolipoprotein B to A1 ratio, objective parameters were unaffected. The nature and magnitude of these effects (or non-effects) are typical of those seen with interventions targeting work stress.[4] We applaud the efforts of Peter and others to evaluate such interventions more rigorously. However till these evaluations demonstrate more impressive results, we stick with our original suggestions as to the current most evidence-based strategy to improve population cardiovascular health and reduce health inequalities.
References
(1) Phillips AN, Davey Smith G. How independent are independent effects? Relative risk estimation when correlated exposures are measured imprecisely. J Clin Epidemiol 1991;44:1223-31.
(2) Louis AA, Manousos IR, Coletta AP, Clark AL, Cleland JG. Clinical trials update: The Heart Protection Study, IONA, CARISA, ENRICHD, ACUTE, ALIVE, MADIT II and REMATCH. Eur J Heart Fail 2002;4:111-6.
(3) Orth-Gomer K, Eriksson L, Moser V et al. Lipid lowering through work stress reduction. Int J Behav Med 1994;1: 204-14.
(4) van der Klink JJL, Blonk RWB, Schene AH, van Dijk FJH. The benefits of interventions for work-related stress. Am J Public Health 2001;91:270-6.
Conflict of Interest:
None declared. - Published on: 27 April 2016Re: Psychosocial factors and Public Health. Authors' reply to the e-letter by John Macleod
- Richard Peter
- Other Contributors:
- Johan Hallqvist, Johannes Siegrist, Töres Theorell
Show MoreDear Editor
We agree with John Macleod concerning the importance of a better understanding of social inequalities in health. Yet, the paper to which he refers (Peter et al., 2002) [1] was not primarily intended to explain social inequalities, but rather to demonstrate an improved prediction of CHD risk by combining standardized measures of two innovative theoretical concepts of psychosocial stress at work. M...
Show LessDear Editor
We agree with John Macleod concerning the importance of a better understanding of social inequalities in health. Yet, the paper to which he refers (Peter et al., 2002) [1] was not primarily intended to explain social inequalities, but rather to demonstrate an improved prediction of CHD risk by combining standardized measures of two innovative theoretical concepts of psychosocial stress at work. Macleod’s claim that confounding may invalidate reported findings and that "the two psychosocial measures were proxies for social position" is not justified in our case.
First, the association between job stress and SES, while significant for demand-control, was non-existing for effort-reward imbalance. If there is an association between effort-reward imbalance and SES it may be analysed in terms of effect-measure modification.
Second, associations of job-stress with CHD and cardiovascular risk factors (e.g. hypertension, atherogenic lipids) were reported for different, heterogeneous as well as homogeneous socio-economic groups, thus ruling out confounding as a major explanation (see e.g. Bosma et al. 1998,[2] Theorell et al. 1998,[3] Lynch et al. 1997,[4] Peter et al. 1997, 1998.[5,6]
We agree that controlled intervention studies are needed as an additional source of evidence when drawing causal inferences in epidemiology. In fact, at least a few such studies, not cited by the author, have been conducted, partly with promising findings (e.g. Orth-Gomer et al. 1994,[7] Kristensen 2000,[8] Theorell et al. 2001[9]). It is hard not to interpret Macleod´s comments as biased as he does not consider additional criteria of causality in epidemiology, for instance experimental evidence of psychosocial stress and changes in cardiovascular parameters (for review of a substantial body of evidence e.g. Schnall et al. 2000,[10] Stansfeld & Marmot 2002[11]).
In contrast to Macleod we conclude that interventive and preventive activities to reduce social inequalities in health should not be restricted to established forms of behavioural and physiological factors. Although knowledge on exposure and resources related to specific SES groups needs to be improved psychosocial factors including job stress should be part of preventive activities more often in the future.
Richard Peter
Johan Hallvqist
Johannes Siegrist
Töres TheorellReferences
(1) Peter R, Siegrist J, Hallqvist J, Reuterwall C, Theorell T and the SHEEP Study Group. Psychosocial work environment and myocardial infarction: improving risk estimation by combining two alternative job stress models in the SHEEP Study. J Epidemiol Community Health 2002;56:294-300.
(2) Bosma H., Peter R., Siegrist J., Marmot M. Two alternative job stress models and the risk of coronary heart disease. Am J Publ Health 1998;88:68-74.
(3) Theorell T, Tsutsumi A, Hallqvist J, Reuterwall C, Hogstedt C, Fredlund P, Emlund M, Johnson JV, and SHEEP Study Group. Decision latitude job strain, and myocardial infarction: a study of working men in Stockholm. Am J Publ Health 1998;88:382-8.
(4) Lynch J, Krause N, Kaplan GA, Tuomilehto JT, Salonen JT. Workplace conditions, socio-economic status, and the risk of mortalitiy and acute myocardial infarction: The Kuopio Ischemic Heart Disease Risk Factor Study. Am J Publ Health 1997;87: 617-22.
(5)Peter R & Siegrist J. Chronic work stress, sickness absence, and hypertension in middle managers: general or specific sociological explanations? Soc Sci Med 1997;45:1111-20.
(6) Peter R, Alfredsson L, Hammar N, Siegrist J, Theorell T, Westerholm P. High effort, low reward and cardiovascular risk factors in employed Swedish men and women: baseline results from the WOLF-Study. J Epidemiol Community Health 1998;52:540-7.
(7) Orth-Gomer K, Eriksson L, Moser V et al. Lipid lowering through work stress reduction. Int J Behav Med 1994;1: 204-14.
(8) Kristensen TS. Workplace intervention studies. In The workplace and cardiovascular diseases Schnall, K. Belkic, P. Landsbergis P., D. Bakker (Eds). Occup Med State of the Art Reviews 2000;15:293-306.
(9) Theorell T, Emdad R, Arnetz B, Weingarten AM. Employee effects of an educational program for managers at an insurance company. Psychosom Med 2001;63:724-33.
(10) Schnall P, Belkic K, Landsbergis P, Bakker D (Eds) The workplace and cardiovascular disease. Occupat Med State of the Art Reviews 2000;15:1-374.
(11) Stansfeld S & Marmot M (Eds) Stress and the Heart. Psychosocial Pathways to Coronary Heart Disease. 2002. London: BMJ Books.
Conflict of Interest:
None declared. - Published on: 27 April 2016Psychosocial factors and Public Health
- John Macleod, Clinical Research Fellow
- Other Contributors:
- George Davey Smith
Show MoreDear Editor
Patterns of human health, particularly the inequalities in health associated with inequalities in social position, are not fully explicable in terms of the social distribution of established risk factors. This lack of understanding may hamper initiatives to ameliorate health inequalities – one of the most important contemporary social projects. The significance of these issues is reflected in the amount o...
Show LessDear Editor
Patterns of human health, particularly the inequalities in health associated with inequalities in social position, are not fully explicable in terms of the social distribution of established risk factors. This lack of understanding may hamper initiatives to ameliorate health inequalities – one of the most important contemporary social projects. The significance of these issues is reflected in the amount of coverage devoted to them in journals such as this one. It also means that, as we have recently argued, evaluation of evidence relating to the determinants of health inequality must be particularly critical.[1,2]
Some epidemiologists have interpreted a substantial body of observational evidence as indicating that "psychosocial" factors – in particular those related to peoples’ working lives – are important, independent determinants of physical health. We have suggested that, in reaching this conclusion, commentators may not have fully considered the role of confounding and bias.[1,2]
In short, the challenge here is first to differentiate between factors which themselves have a causal relation with health and those which are merely markers for other factors which are causally related to health.[3] As George Bernard Shaw remarked in his introduction to “The Doctor’s Dilemma”,
“It is easy to prove that the wearing of tall hats and the carrying of umbrellas enlarges the chest, prolongs life, and confers comparative immunity from disease; for the statistics show that the classes which use these articles are bigger, healthier, and live longer than the class which never dreams of possessing such things.”[4]
Shaw is, of course, talking of confounding. The association between tall hats and health is confounded by socio-economic position.
A second challenge is to overcome the problem that certain individuals may perceive and/or report, their experience of adversity to be greater and their health to be poorer than others whose experience in these domains is, objectively, no different.[5] Such common reporting tendency can generate apparent associations that are the product of bias, rather than a reflection of any true causal relation.
These issues are well illustrated in this month’s issue of the JECH. Ala-Mursula and colleagues report that workingwomen who perceive their workplace temporal autonomy to be lower, perceive that their health is worse.[6] Women with lower perceived worktime control also have greater medically certified sickness absence. The relation between worktime control and perceived health is considerably stronger than that with sickness absence. Socio-economic confounding appears an unlikely explanation for this relation as perceived worktime control in women showed no clear gradient with educational level (university educated women perceived their control to be lowest - the control perceived by women with no vocational training was slightly lower than that of those with vocational or college qualifications). The other index of social position measured was occupational class. The relation between this and perceived worktime control is not reported, nor does it appear that (despite being measured) occupational class was included as an adjustment in any models. The authors do report that within a single occupational group (teachers) these relations were similar.
Ala-Mursala and colleagues speculate on several plausible explanations for their findings. However they do not appear to consider one rather obvious, if less exciting, possibility – the influence of reporting tendency. A striking feature of their data is that the more subjective the outcome considered the greater the apparent effect of perceived control. Thus for a fully subjective outcome, such as self- perceived poor health, the odds ratio associated with low perceived control is 2.20 whereas for a partly subjective outcome, such as medically certified sickness absence, it is only 1.19. Certified sickness absence is substantially dependent on individual subjective illness perception and help-seeking behaviour though it also contains an element of physician judgement. We have empirically demonstrated, the influence of bias in this situation elsewhere.[7]
In the same issue, Peter and colleagues report a case-control study showing that a combination of two indices of “job stress” – Karasek’s job strain and Siegrist’s effort-reward imbalance – were better risk markers for myocardial infarction than either index individually.[8] Given the objectivity of the outcome, bias appears less likely in this case – what about confounding? The social distribution of “job stress” was not reported in this study – indeed, surprisingly, no measure of social position appears to have been included in the reported analyses. The authors mention in their discussion that adjustment for socio-economic group, “did not affect the results of this study”. They do not present these adjustments and concede that their index of socio-economic group, a white collar/blue collar binary classification, was somewhat crude. It would be interesting to know if job stress was higher amongst blue collar employees in this population. Others have found a consistent association between higher job stress and social disadvantage.[9] Therefore it seems highly likely that both these psychosocial measures were proxies for social position. In this situation one would predict that both together would allow better risk estimation than either singly – a phenomenon that has been demonstrated in relation to other proxies for social position on many occasions.[10,11,12] Most of the explanatory mechanisms invoked as plausible explanations for the effects of psychosocial exposures suggest a specific relation with certain outcomes, particularly cardiovascular disease.[13] The general importance of specificity of association as a criterion for a causal relation has recently been reiterated.[14] It would go some way to allay fears of residual confounding in this case if Peter and colleagues could demonstrate that job stress was particularly associated with specific endpoints. If, however, heightened job stress showed a general association with increased disease risk (for example what was the relation between job stress and accidents?) socio-economic confounding seems more likely.
Given the above, we find it difficult to agree with the suggestion by John Ashton and Carlos Alvarez-Dardet that “Work on stressors in the workplace continues to refine our understanding of job control and its effect on public health”.[15] It seems to us that the water remains distinctly muddy. Better observational studies could help clarify this situation. Insistence on experimental evidence to support policy action is not always appropriate.[16] However this appears one situation where randomised controlled trials could help. If workplace stressors are – of themselves – important determinants of public health and if intervening to reduce workplace stress can lead to objective improvements in public health then this should be demonstrable in experimental studies. Until such studies have been conducted, and their results reported, further observational evidence, that essentially replicates previous findings whilst being subject to the same methodological shortcomings has, arguably, little to add. Intervention trials in North America such as ENRICHD and SADHART have shown that there are no particular methodological or practical difficulties preventing the undertaking of experimental studies in this area. Unfortunately, they have also shown that psychosocial interventions, whilst modifying psychosocial exposure, appear to have no effect on cardiovascular outcomes. [17]
These points are neither pedantic, nor destructive. There is no more important issue in Public Health than the shameful fact of widening health inequalities.[18] If psychosocial interventions are shown to be able to help close this gap then we will be happy to endorse their widespread implementation. However, given the current state of our understanding we feel that resources should more rationally be directed at reducing established forms of behavioural and physiological risk. Furthermore, until it is convincingly demonstrated that the psychosocial correlates of material disadvantage are more health damaging than material disadvantage itself, then the reduction of material disadvantage should be the priority of healthy fiscal policy.
References
(1) Macleod J, Davey Smith G, Heslop P, Metcalfe C, Carroll D, Hart C. 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;55:878-84.
(2) Macleod J, Davey Smith G, Heslop P, Metcalfe C, Carroll D, Hart C. Limitations of adjustment for reporting tendency in observational studies of stress and self reported coronary heart disease. J Epidemiol Community Health. 2002;56:76-7.
(3) Davey Smith G, Harding S. Is control at work the key to socio-economic gradients in mortality? Lancet 1997;350:1369-70.
(4) Shaw GB. The Doctor’s Dilemma. London: Constable, 1911.
(5) Watson D, Pennebaker JW. Health complaints, stress and distress: exploring the central role of negative affectivity. Psychol Rev 1989;96:234-54.
(6) Ala-Mursula L, Vahtera J, Kivimäki M, Kevin MV, Pentti J. Employee control over working times: associations with subjective health and sickness absences. J Epidemiol Community Health 2002;56:272-278.
(7) Macleod J, Davey Smith G, Heslop P, Metcalfe C, Carroll D, Hart C. Psychological stress and cardiovascular disease: empirical demonstration of bias in a prospective observational study on Scottish men. BMJ 2002 (in press).
(8) Peter R, Siegrist J, Hallqvist J, Reuterwall C, Theorell T. Psychosocial work environment and myocardial infarction: improving risk estimation by combining two complementary job stress models in the SHEEP Study. J Epidemiol Community Health 2002;56:294-300.
(9) Hemingway H, Marmot M. Evidence based cardiology: Psychosocial factors in the aetiology and prognosis of coronary heart disease: systematic review of prospective cohort studies. BMJ 1999;318:1460-1467.
(10) Davey Smith, G., Hart, C., Blane, D. et al. Lifetime Socioeconomic Position and Mortality: prospective observational study. BMJ 1997;314:547- 552.
(11) Davey Smith, G., Hart, C., Watt G et al. Individual social class, area -based deprivation, cardiovascular disease risk factors, and mortality: the Renfrew and Paisley Study J Epidemiol Community Health 1998;52:399- 405.
(12) Marmot MG, Smith GD, Stansfeld S, Patel C, North F, Head J, White I, Brunner E, Feeney A. Health inequalities among British civil servants: the Whitehal II study. Lancet 1991;337:1387-93.
(13) Brunner E. Stress and the biology of inequality. BMJ 1997;314:1472-6.
(14) Weiss NS. Can the “specificity” of an association be rehabilitated as a basis for supporting a causal hypothesis? Epidemiology 2002;13:6-8.
(15) Ashton JR, Alvarez-Dardet C. Securing the evidence base for public health and acting on it. J Epidemiol Community Health 2002;56:241.
(16) Davey Smith G, Ebrahim S, Frankel S. How policy informs the evidence. BMJ 2001;322:184-185.
(17) Louis AA, Manousos IR, Coletta AP, Clark AL, Cleland JG. Clinical trials update: The Heart Protection Study, IONA, CARISA, ENRICHD, ACUTE, ALIVE, MADIT II and REMATCH. Eur J Heart Fail 2002;4:111-6.
(18) Shaw M, Dorling D, Gordon D, Davey Smith G. The Widening Gap. Bristol: Policy Press, 1999.
Conflict of Interest:
None declared.