Leisure time physical activity, risk of depressive symptoms, and inflammatory mediators: The English Longitudinal Study of Ageing
Introduction
Evidence from prospective cohort studies have generally confirmed inverse associations between physical activity and incident depression (Farmer et al., 1988, Camacho et al., 1991, Paffenbarger et al., 1994, Strawbridge et al., 2002, Brown et al., 2005) and an association between reduced activity and elevated depressive symptomatology (van Gool et al., 2003). Recent clinical trials that have employed credible control groups and considered the confounding effects of psychotherapy have also shown robust effects of exercise on remission of depression (Blumenthal et al., 2007, Mutrie et al., 2007). The mechanisms, however, remain unclear. Exercise is thought to improve a number of biological risk factors such as dyslipidemia, glucose intolerance, inflammation, and vascular dysfunction, which have been highlighted as possible mechanisms in depression (Joynt et al., 2003). The role of inflammation in depression has gained particular attention. For example, recent evidence suggests that inflammatory processes may play a causal role in depression (Gimeno et al., 2008), often referred to as sickness behaviour (Dantzer, 2001). Other data has also shown an elevation in inflammatory markers following the onset of depressive symptoms (Matthews et al., 2007), which might be partly mediated through health behaviour change, including physical activity, smoking and alcohol (Hamer et al., 2009). Thus, the association between inflammation and depression might be bi-directional. Inflammatory cytokines have profound stimulatory effects on various systems in the brain such as dopaminergic, noradrenergic, and serotonergic pathways, and are also thought to play a role in growth factor signaling (Cotman et al., 2007). We are, however, unaware of any epidemiological studies that have directly examined the role of inflammatory mechanisms in relation to physical activity and depression. The aim of the present study was therefore to examine if inflammatory markers (CRP, fibrinogen) might partly explain the association between physical activity and depression in a sample of community dwelling older adults from the English Longitudinal Study of Ageing (ELSA).
Section snippets
Design/setting and participants
ELSA is an ongoing cohort study that contains a nationally representative sample of the English population living in households. The original ELSA cohort consists of men and women born on or before 29 February 1952. The sample was drawn from households that have participated in Health Survey for England (HSE) in 1998, 1999, and 2001. HSE recruits participants using multistage stratified probability sampling with postcode sectors selected at the first stage and household addresses selected at
Results
Approximately 16% of the sample was relatively sedentary, reporting none or only some light activity. In a sub-sample of participants (n = 1685) with detailed information on physical activity from the 1998 HSE, approximately 25% of participants met the current guidelines for physical activity (Haskell et al., 2007), thus suggesting that the sample as a whole was fairly sedentary. In comparison with physically active participants, the sedentary were older, more likely to be female, lower
Discussion
The findings from the present study demonstrate that moderate or vigorous physical activity is associated with lower risk of depressive symptomatology over 4 yrs follow up, which largely confirm the results of others (Farmer et al., 1988, Camacho et al., 1991, Paffenbarger et al., 1994, Strawbridge et al., 2002, Brown et al., 2005). We also demonstrated an association between physical activity and remission of depressive symptoms in participants that were initially depressed at baseline.
Role of funding sources
Drs Hamer and Molloy are supported by the British Heart Foundation, UK. The data were made available through the UK Data Archive. The English Longitudinal Study of Ageing (ELSA) was developed by a team of researchers based at University College London, the Institute of Fiscal Studies and the National Centre for Social Research. The funding is provided by the National Institute on Ageing in the United States (grants 2RO1AG7644-01A1 and 2RO1AG017644) and a consortium of UK government departments
Conflict of interest
None of the authors have any competing interests to declare.
Acknowledgement
None.
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