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Editorial

Saved by the bell: does working too much increase the likelihood of depression?

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Pages 497-499 | Published online: 09 Jan 2014

Depression is a serious public health concern that has been predicted to be the leading cause of the burden of disease in high-income countries by 2030 Citation[1]. In addition to human suffering, depression affects families and communities and is associated with substantial work impairment, lost work days and reduced productivity.

Negative life events have long been a major focus of research on psychosocial risk factors for depression. Life events that possess a high degree of threat, negative emotions and experience of loss have been found to precede the onset of depression (for a review, see Hammen Citation[2]). The hypothesized underlying pathways involve dysregulation of the physiological stress system. The hypothalamic–pituitary–adrenal axis is activated during psychological stress and involves secretion of corticotropin-releasing hormone and cortisol, the hormonal end point of the hypothalamic–pituitary–adrenal activation. Both corticotropin-releasing hormone and cortisol levels have been shown to be elevated in depressed people Citation[3].

Given the link between the stress systems and depression, it is plausible to assume that not only acute stress related to negative life events, but also more chronic psychological stress may be of etiological importance in the development of depression Citation[4]. Recently, an increasing research interest has been focused on possible work-related stress exposures, such as long working hours and mental health. Several issues support the idea that extensive working might be depressogenic. First, employees working long hours are likely to have reduced time available for sleep and recovery from work, potentially leading to chronic fatigue, poor health-related behaviours and, eventually, deterioration in health Citation[5,6]. Second, they may also be exposed for longer periods of time to psychosocial and physical workplace hazards, such as high demands (which can also be an underlying cause of extended working hours) and other poor working conditions, as compared with those working shorter days Citation[6]. Third, prospective cohort studies and case–control studies have linked long working hours to an increased risk of stress-related chronic diseases, such as coronary heart disease Citation[5].

Evidence regarding the association between long working hours and mental health is accumulating, but is not without limitations. To date, more than 20 cross-sectional studies using individual-level data have been published on the effects of long working hours on mental health, for example, looking at symptoms or depression. Of them, slightly more than half failed to find any association, while the rest of them reported a positive association. None of the studies found a negative association (i.e., long working hours being a protective factor for mental health). The problem in cross-sectional studies is their inability to prove the direction of the association. Employees with mental health symptoms may either shorten or lengthen their working hours depending on the circumstances, and the association found can therefore be inflated or attenuated by selection bias and reverse causation, rather than be a result of a true effect Citation[7].

Of the longitudinal studies published, a small field study with a follow-up of 6 months found no association between overtime work and psychological distress symptoms Citation[8], while a Canadian study with a follow-up of 1–2 years found long (>40) weekly working hours to be associated with the onset of a major depressive episode among women but not among men Citation[9]. Null findings have also been reported in two Swedish studies from the same cohort Citation[10,11], in one Japanese study Citation[12] and in one study from the USA Citation[13]. In another Japanese study, working >12 h a day was associated with increased psychological distress symptoms in men Citation[14]. In a small-scale experimental field study, an overtime work week (12 h a day) was associated with increased exhaustion and irritation compared with an 8 h a day work week Citation[15], whereas in a 3-year follow-up of the Maastricht cohort study Citation[16], no association was found between prolonged overtime and psychological distress among women. Surprisingly, in men, working overtime was related to lower chances of distress. However, measurements of working hours and change in psychological distress were overlapping. A study of senior medical consultants did not reveal any association between overtime work and antidepressant use during a 1-year follow-up Citation[17].

Possible explanations for these inconsistencies may relate to nonstandard exposure assessments (e.g., part-time workers in the reference group), small sample sizes or few cases, the cutoff point for overtime being relatively low (e.g., >40 h vs less; for a review, see Citation[5]) and a failure to control for important confounding factors, such as socioeconomic status.

Three prospective analyses on overtime and mental health have recently been published from the Whitehall II cohort of British civil servants Citation[18–20]. A major advantage of this study is the comprehensive data on potential confounding factors and the possibility of examining exposure to working hours in a more stratified manner. Working overtime (>55 h per week) compared with 35–40 h was associated with a doubling of the risk of new-onset depressive and anxiety symptoms in women, while this association was not evident in men Citation[18]. In a cohort combining women and men, a similar association was found for clinical depression, but these data related to a subcohort who had performed a clinical psychiatric interview (sex-specific analysis was not possible to carry out in this subcohort owing to insufficient statistical power) Citation[19].

The participants of the Whitehall II study were screened for cognitive functioning using five cognitive tests in 5-year intervals. Compared with employees working normal 35–40 h per week, those working >55 h per week and those working 41–55 h already performed worse in a vocabulary test at baseline Citation[20]. At follow-up, both these overtime groups again performed worse in a vocabulary test but also had shared a greater decline in test score in a cognitive reasoning test. The latter finding is particularly important, as depression might have contributed to the process of cognitive decline. However, it is also possible that accelerated decline in reasoning resulted from increased sleeping problems, some aspects of unhealthy lifestyle or effects of cardiovascular disease that were all more common among those working long hours Citation[5].

Can we say, based on this evidence, that working too much increases the likelihood of depression? The longitudinal study findings are quite mixed, with many of the individual studies suggesting no association. Positive association was found in a small-scale field study as well as in larger studies including Canadian women, Japanese men and female British civil servants. However, there has been considerable heterogeneity in the study samples, assessment of exposure, outcome and potential confounding factors. In most of the studies, outcomes were mainly based on psychological distress symptoms instead of a clinically verified diagnosis of depression.

A further uncertainty relates to the definition of ‘too much work.’ There was substantial heterogeneity in the operationalization of long working hours, that is, in some studies the cutoff point was 40 h, in some studies 50 h or even more, while some studies used ‘overtime work’, defined as any amount of hours exceeding the normal hours. In addition, it is not clear whether the number of working hours reported by participants at baseline was stable over the follow-up period. This could be a potential source of misclassification of the exposure measurement or represent an actual change in hours worked.

Study design may also have a critical effect on results. For example, many studies included part-time employees in the reference group. This is problematic because of the elevated mental health problems among part-time employees Citation[7,14]. Thus, poor health is a possible reason for working reduced hours and a source of reverse causation bias. In future studies, a reference group with a standard work day of approximately 8 h would therefore be preferable. In addition, as depressive disorders usually initiate at a young age, childhood and pre-employment mental health should be taken into account to remove bias due to reverse causality.

It is known that some employees work long hours because they enjoy their work whereas others are required to work long hours, they are forced to do so or they need the money. It is not known whether this makes a difference in terms of depression risk. It may be necessary to distinguish different types of ‘overtime’ workers based on their underlying motivation: one type is a constructive, highly committed, achievement-oriented employee; another type includes individuals who work long hours in order to get an advantage over the competition in working life or in the hope for rewards; and a third type could be comprised of those working long hours as a result of external factors, such as employer demands or work overload. Caruso and others suggest that there might be factors modifying the effect of long working hours on health outcomes, such as voluntary versus involuntary nature of long hours or the number of hours worked owing to domestic responsibilities Citation[6].

One of the primary motivations for working longer hours is to increase productivity; however, paradoxically, the effect of extended work days on health may result in increased mistakes and accidents and the negative effects of long working hours may also spread to family members Citation[6]. Working long hours is an important exposure for future studies. Valuable information for causality could be obtained from trials where interventions designed to reduce working hours are examined for depression risk.

Financial & competing interests disclosure

This work was supported by grants from the Medical Research Council (G0902037), British Heart Foundation (RG/07/008/23674), Stroke Association, National Heart Lung and Blood Institute (5RO1 HL036310), National Institute on Aging (R01AG034454, 5RO1AG13196) and Agency for Health Care Policy Research (5RO1AG034454), the Academy of Finland (projects 124271, 124322, 126602, 129262 and 132944), and the European Union New OSH ERA Research. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

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