Workplace environment and risk of hypertension: is obesity on the causal pathway?

Siervo, Marioa; Wells, Jonathan C.K.b; Stephan, Blossom C.M.c

Journal of Hypertension:
doi: 10.1097/HJH.0b013e3283543bb3
Editorial Commentaries
Author Information

aHuman Nutrition Research Centre, Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle on Tyne

bChildhood Nutrition Research Centre, UCL Institute of Child Health, London

cInstitute for Health and Society, Newcastle University, Baddiley-Clark, Richardson Road, Newcastle upon Tyne, UK

Correspondence to Dr Mario Siervo, Human Nutrition Research Centre, Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle on Tyne NE4 5PL, UK. E-mail:

Article Outline

In this issue of the Journal of Hypertension Oksanen et al.[1] explore the association between risk of severe hypertension and social capital in the workplace in a Finnish cohort of public sector employees. Incident hypertension was recorded during a 3.5-year follow-up through cross-linkage of personal information collected at baseline with medical records. Social capital was defined as level of support perceived by each worker from their colleagues and the work environment based on items assessing shared values, attitudes, norms of trust and reciprocity, and collective action. The sample size was substantial (>60 000 individuals after exclusion criteria and drop outs at follow-up), but women were overrepresented (>80%). The authors found that low workplace social capital was associated with an increased risk of hypertension in men even after the adjustment of covariates including, for example, age, job strain, and diagnosis of depression and diabetes. Furthermore, obesity and high alcohol consumption were found to mediate this relationship. The results have relevant physiopathological and public health implications that have been clearly outlined by the authors.

A few points regarding the methodology and analysis merit further discussion. The diagnosis of hypertension was based on very stringent criteria [blood pressure (BP) higher than 200 mmHg systolic and/or 105 mmHg diastolic or 95 mmHg diastolic with at least one cardiovascular risk factor). Although this conservative diagnostic approach may provide stronger evidence on the association between social capital and hypertension, the applicability of the findings to the population with mild or moderate hypertension may be limited. Obesity was found to mediate the association between social capital and hypertension but the variable was not entered into the Cox regression model wherein relative risk was assessed (Tables 3 and 4). Why obesity was excluded from this analysis raises questions regarding the role of obesity in the relationship. Is obesity on the causal pathway of the relationship between social capital and hypertension, or it is a confounder? Although the former assumption may be plausible – low social support may lead to a greater and more prolonged activation of the stress response which may favour weight gain through a modification of appetite and energy metabolism – this was not discussed in the study. A similar query can be raised for alcohol consumption, as this was also not entered into the Cox regression model.

Mechanistically, the authors suggested that lower social capital might also be associated with abnormally high activation of the neuroendocrine system thereby increasing risk of obesity. However, the authors have not discussed the role of the sympathetic system. The two main components of the stress system, the hypothalamic–pituitary–adrenal and the sympathetic system, have integrated metabolic and cardiovascular effects which are complex and depend significantly on insulin secretion, insulin sensitivity, and cardiovascular reactivity [2,3]. In a state of positive energy balance, fat accumulates due to the synergistic action of corticosteroids and insulin; protein turnover in the muscle is increased to an extent depending on the corticosteroid : insulin ratio [2]. BP is also increased due to an increased sympathetic drive (postload) and effects of cortisol and insulin on electrolyte and fluid balance (preload) [4]. In the Whitehall study, a large prospective cohort of British civil servants, a dose–response relationship was found between exposure to work stressors, high cortisol levels, central obesity, and risk of metabolic syndrome [5,6]. Recently, our group proposed that the neuroendocrine response to psychosocial stress is the result of evolutionary selective pressure related to survival. We have postulated how changes in social structure and in-built environment have profoundly altered the physiological homeostatic mechanisms and contributed to the epidemics of obesity, insulin resistance, and hypertension [2].

Social capital was not significantly associated with hypertension in women and the results were consistent with a sexually dimorphic relationship between job strain and increased BP reported in other studies [7–9]. Various hypotheses have been proposed to explain the lack of association in women, including lower BP variability in premenopausal women, higher social interaction and propensity to seek social support, ethnicity, and education [9]. These results may also be explained with the framework of the allostatic model [10]. In the context of the social environment, this model predicts that there is a cumulative physiological risk associated with repeated exposure to psychosocial stressors over the life course [10]. This is consistent with the idea that greater cumulative dysregulation may be associated with significantly greater risks for subsequent disease (cardiovascular disease) [11]. The allostatic model could be individualized for predicting risk of hypertension in the workplace by identifying a critical allostatic threshold, which may be derived by the interaction between resilience (i.e. the ability of an individual to effectively overcome the stressors and restore homeostasis) and vulnerability (i.e. the propensity of an individual to be negatively affected by the stressor) [12,13]. In women, greater health seeking behaviour may be related to decreased vulnerability and increased social networks (both within and outside work) may be related to resilience, both of which were suggested by the authors, resulting in greater capacity to maintain homeostasis.

In the context of obesity and chronic diseases, much attention has been directed to the issue over where ‘responsibility’ for health lies [14]. Governments and general practitioners are increasingly placing that responsibility on the individual, through programmes advising healthy lifestyles. Yet, how much responsibility should the individual actually bear for behaviour in the workplace? To a large extent, social capital is a product of workplace relationships, shaped, promoted, and restricted by a variety of factors over which the employer exerts substantial influence. Both physical and social components of the workplace environment affect the capacity of individuals to develop and maintain social capital. Office workers, whether in the private or public sectors, are under increasing pressure to work long hours, though practices vary by country. Thus, the work environment is itself a key locus in which social capital can be developed. The results of this study carry a strong message that employers bear major responsibility for the environment within which work force can acquire supportive relationships and networks. However, it would also be valuable to gain further insight into the relative benefits of social capital deriving from relationships within the workplace, compared with those from relationships outside the workplace.

With the worldwide epidemic of obesity and hypertension, identification of modifiable risk factors is a priority. Workplace environments have dramatically changed over the last 50 years especially with regard to stress level and sedentarism and unhealthy dietary habits have been extensively discussed in the context of the obesity pathogenesis [15]. These results send an important public health message for the promotion of healthy work environments and positive and supportive workplaces. The motto should be ‘work hard and live well’!

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Conflicts of interest

There are no conflicts of interest.

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1. Oksanen T, Kawachi I, Jokela M, Kouvonen A, Suzuki E, Takao S, et al. Workplace social capital and risk of chronic and severe hypertension: a cohort study. J Hypertens 2012; 30:1129–1136.
2. Siervo M, Wells JC, Cizza G. The contribution of psychosocial stress to the obesity epidemic: an evolutionary approach. Horm Metab Res 2009; 41:261–270.
3. Matthews K, Woodall K, Allen M. Cardiovascular reactivity to stress predicts future blood pressure status. Hypertension 1993; 22:479–485.
4. Ganong WF. Review of medical physiology, 19th ed. Stamford, CT: Appleton & Lange; 1999, ch. VI, pp. 489–586.
5. Brunner EJ, Chandola T, Marmot MG. Prospective effect of job strain on general and central obesity in the Whitehall II study. Am J Epidemiol 2007; 165:828–837.
6. Chandola T, Brunner E, Marmot M. Chronic stress at work and the metabolic syndrome: prospective study. BMJ 2006; 332:521–525.
7. Light KC, Brownley KA, Turner JR, Hinderliter AL, Girdler SS, Sherwood A, et al. Job status and high-effort coping influence work blood pressure in women and blacks. Hypertension 1995; 25 (4 Pt 1):554–559.
8. Schlussel YR, Schnall PL, Zimbler M, Warren K, Pickering TG. The effect of work environments on blood pressure: evidence from seven New York organizations. J Hypertens 1990; 8:679–685.
9. Rosenthal T, Alter A. Occupational stress and hypertension. J Am Soc Hypertens 2012; 6:2–22.
10. McEwen BS. Allostasis and allostatic load: implications for neuropsychopharmacology. Neuropsychopharmacology 2000; 22:108–124.
11. McEwen BS. Protection and damage from acute and chronic stress: allostasis and allostatic overload and relevance to the pathophysiology of psychiatric disorders. Ann N Y Acad Sci 2004; 1032:1–7.
12. Charney DS. Psychobiological mechanisms of resilience and vulnerability: implications for successful adaptation to extreme stress. Am J Psychiatry 2004; 161:195–216.
13. Dimsdale JE. Psychological stress and cardiovascular disease. J Am Coll Cardiol 2008; 51:1237–1246.
14. Finegood DT, Merth TDN, Rutter H. Implications of the foresight obesity system map for solutions to childhood obesity. Obesity 2010; 18:S13–S16.
15. Papas MA, Alberg AJ, Ewing R, Helzlsouer KJ, Gary TL, Klassen AC. The built environment and obesity. Epidemiol Rev 2007; 29:129–143.
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