Victimization in the Workplace: A New Target for Cardiovascular Prevention?

Christoph Herrmann-Lingen


Eur Heart J. 2019;40(14):1135-1137. 

The relevance of psychosocial cardiovascular risk factors is increasingly recognized. Depression and other mental disorders, but also subclinical depressive symptoms, vital exhaustion, anger, and personality traits such as hostility, are independent predictors of incident cardiovascular disease (CVD). Social factors associated with increased CVD risk include low socio-economic status, social isolation, low social support, and stress at work or in family life.[1,2] Psychological and social factors are strongly inter-related and tend to cluster in certain individuals.

In this issue of the European Heart Journal, Xu et al.[3] provide evidence for another psychosocial factor that may be involved in CVD risk. Analysing data from four Scandinavian cohort studies with a total of 79 201 healthy men and women, they looked at workplace bullying and violence as predictors of incident CVD, defined as first hospitalization for coronary heart disease or stroke. Over a mean follow-up period of 12.4 years, the authors observed 3229 cases of new CVD. After adjustment for confounders, CVD incidence was increased by 59% in persons reporting workplace bullying at baseline and by 25% in those who reported physical violence or threat of violence at work. On the population level, 5% of CVD cases were explained by bullying and 2.9% by workplace violence. The associations showed a dose–response pattern for workplace bullying and to a lesser extent also for workplace violence. They remained stable in sensitivity analyses with, for example, additional adjustment for length of follow-up, baseline mental disorders, or unhealthy lifestyle. The magnitude of the effects is comparable with that previously shown for other psychosocial CVD risk factors.

Workplace bullying and violence might therefore be new, potentially modifiable cardiovascular risk factors. However, despite the impressive number of almost 1 million subject-years and >3000 cases of CVD, the findings need cautious interpretation and independent replication.

When looking at possible mechanisms (see Figure 1) and their consequences for CVD prevention, it makes sense first to examine the measurement of the exposure variables. For determining workplace bullying, participants in the Swedish cohorts were asked whether they had experienced 'personal persecution in the form of unkind words or behaviour from … superiors or fellow workers' during the past 12 months, while the term 'bullying' and the time frame were not further specified in the Danish questionnaire. 'Workplace violence' covered 'violence or threats of violence' at work in the Swedish cohorts and threats of violence only in the Danish sample.[3]

Figure 1.

Hypothetical mechanisms linking environmental and individual predispositions, and workplace victimization to increase in long-term CVD risk.

This means that (i) both exposure variables entirely relied on self-report and (ii) it is hard to decide whether actual physical violence or the mere threat of violence was involved.

As the authors state, workplace bullying 'is mostly of a psychological nature', and so is threat of violence. Self-reports of psychological stressors are influenced not only by the nature and intensity of the objective stressor but also by the emotional reaction to it and the psychological state in which the respondent is answering the questionnaire. Hence, we do not know to what degree actual misbehaviour of persons in the environment or perception and reporting biases led participants to report self-perceived bullying or violence. Unfortunately, current or previous affect and underlying personality traits are not reported.

It also remains unclear by which mechanisms adverse experiences measured at one time point can impact on disease outcomes up to 12 years later, i.e. how the past experience is conserved for the future. These mechanisms may be entirely biological, such as an increase in atherosclerotic plaque burden occurring during or shortly after the adverse events. The natural progress of atherosclerosis might then simply continue at a normal pace but from a higher level and lead to earlier disease manifestations. Stressful events have also been shown to alter epigenetically determined gene expression lasting beyond the immediate period of stress and leading to altered sensitivity to future stressors.[4] It is, however, likely that psychological and interpersonal sequelae of the stressful event are equally important. Bullying and other adverse interpersonal events are associated with increased and sometimes enduring levels of distress, negative emotions, and overt psychopathology.[5]

Xu and colleagues tried to control for psychological mechanisms by adjusting for baseline mental disorders in sensitivity analyses. However, mental disorders are substantially underdiagnosed both in the community and in the medical setting, and feelings of anxiety or anger can also be normal reactions that do not necessarily justify a mental diagnosis and still increase CVD risk. Hence, controlling for known mental disorder at baseline does not rule out psychological mechanisms. Distress and negative emotions (possibly fulfilling diagnostic criteria for a specific disorder) may also occur with some latency after the stressful event and can persist over years. They are accompanied by direct physiological changes such as activation of autonomic and neuroendocrine stress pathways which can lead to haemodynamic changes, and proinflammatory and procoagulant states. Negative emotions also alter the motivational state of the individual, leading to adverse effects on health behaviours such as smoking, diet, physical activity, and treatment adherence. Furthermore, emotional stress leads to impaired sleep with its adverse health consequences. All these chronic stress effects could serve as mechanisms for the observed association.

In addition to considering psychological sequelae of bullying or violence, one must be aware that both are not entirely external events but mostly results of interpersonal dynamics which only partially depend on environmental factors, such as high work pressure and hostile individuals or group dynamics in the environment. They are also affected by the victim's own work performance and communication style. It is therefore conceivable that self-reports of workplace bullying and violence to some degree indicate pre-existing personality problems or mental health conditions which are again known to predict CVD development and can often be found even in persons without diagnosed mental disorders. Pre-existing exhaustion, hostile or obsessive–compulsive traits, and negative emotions may contribute to workplace victimization:[6] persons who feel exhausted or depressed may perform more poorly at work and have increased times of absence from work, which may annoy their clients, co-workers, or superiors and trigger inappropriate behaviours. Similarly, hostile or overly meticulous persons may inadvertently provoke their colleagues or clients. As pre-existing psychological conditions were incompletely controlled for, their possible contribution to adverse workplace experiences and CVD risk cannot be resolved on the current database.

We therefore do not know to what degree the increased CVD incidence was driven by objective events (that could best be prevented by workplace interventions), subjective perceptions of the events, and psychobiological reactions to them (which might require efforts addressing individual stress resilience and coping) or pre-existing psychological conditions (which are per se associated with increased CVD risk and would call for early recognition, treatment, or even prevention of the underling problems).

There is little doubt that prevention of stress-related illness should include the workplace as a potential source of both psychological stress and support. It should address the workplace itself with its economic, physical, and psychological demands, and create a humane environment for individuals and teams. Helping individuals and teams to cope with remaining demands and internal conflicts may reduce bullying and violence and thus increase well-being, health outcomes, and productivity. However, early recognition of untreated, possibly subthreshold, mental disorders that predispose persons to become perpetrators or victims of bullying or violence may additionally be needed in order to facilitate early initiation of appropriate mental health care and interrupt the vicious cycle of workplace bullying or violence, emotional distress, and its behavioural and physiological consequences. Probably this self-reinforcing vicious cycle is more relevant for increased CVD risk than any single psychosocial factor.

Finally, one should not forget that the basis for personality development, mental disorders, and CVD is laid before persons enter the working environment. Adverse life circumstances in childhood and adolescence lay the ground for interpersonal problems, mental disorders, risk behaviours, and cardiovascular disease in later life.[7] Behavioural interventions for young children from disadvantaged families can lead to better metabolic control in later years,[8] and higher stress resilience in young men may be related to reduced cardiac risk until their mid-50s.[9] It might therefore be wise not only to recognize and solve interpersonal problems at the workplace early but also to consider cardiovascular prevention a lifelong endeavour which might best be initiated in much earlier life stages. Of course, such interventions come too late for today's adults, and preventative efforts for these persons will have to deal with their actual social context, psychological condition, and behaviour. This requires awareness of factors that might contribute to elevated risk and an individualized approach to modifying them. Workplace bullying or violence are two factors that might need more attention in future CVD prevention programmes. Future observational studies and intervention trials should elaborate on their relative relevance in the broader context of psychosocial CVD risk factors.