![]() The Nord-Trøndelag County of Norway covers a mainly rural area, with a total population of 127,000 at the time of the study commencement. The HUNT study represents one of the largest and most comprehensive population-based health surveys ever undertaken. First, does exercise provide protection against new-onset depression and anxiety? Second, if so, what intensity and total amount of exercise is required to gain protection? Third, what causal mechanisms underlie any association between exercise and later depression and anxiety? The aim of the present study was to utilize a large (N=33,908) prospective cohort to address three questions. While many agencies are keen to promote the potential mental health benefits of exercise, at present the literature is unable to provide the most basic information needed for effective, targeted, evidence-based public health campaigns concerning depression and anxiety. Other explanations for any association between exercise and depression and anxiety focus on the physical health, self-esteem, or social benefits of exercise.Īddressing the uncertainty surrounding the relationship between exercise and depression and anxiety is important. ![]() Alterations in autonomic nervous system activity have been observed in those suffering from depression, and vagal nerve stimulation has been used to treat depression ( 21). Regular exercise increases parasympathetic vagal tone, leading to physiological changes such as resting bradycardia ( 23). One purported biological mechanism is alteration in the activity of the autonomic nervous system ( 21, 22). ![]() Exercise is associated with a number of biological changes that could have an impact on mental health. However, systematic reviews of the evidence for exercise in preventing new-onset depression and/or anxiety have needed to be more tempered in their conclusions, particularly regarding the relative importance of the intensity and amount of exercise required to convey any protective effect ( 20).Ī number of theories have been proposed as to how exercise may prevent mental illness, yet to date none of these have been formally evaluated in prospective epidemiological studies ( 5). Recent analyses of the data used in these reviews have added further evidence for the antidepressant effect of exercise, with findings that both publication bias and enhanced control group responses may have led to an underestimate of the true effect size of exercise as an intervention in depression ( 18, 19). The evidence base for exercise as a treatment for current depression is more established, with numerous reviews concluding that exercise is moderately effective for reducing the symptoms of depression ( 16, 17). The evidence base has been further confused by many, but not all, of the published reports conflating depression and anxiety disorders, despite each having unique risk factors and distinct biological processes ( 15). Some studies have found no prospective association between levels of exercise and depression and anxiety ( 9– 11), while others have suggested that any beneficial effects of exercise may be limited to certain subgroups or age groups, or only associated with intensive exercise ( 12– 14). To date, the results of prospective studies have been more mixed. However, the possibility of reverse causation (low mood or anxiety leading to reduced levels of exercise) has limited the interpretation of such studies. A variety of health surveys have demonstrated a cross-sectional association between exercise and lower rates of both depression and anxiety ( 7, 8). There is, however, some emerging evidence that lifestyle factors, such as physical inactivity, may be potential targets for strategies aimed at preventing depression and anxiety ( 5, 6). However, most of the known risk factors for depression and anxiety, such as familial risk, socioeconomic position, and life events, are difficult or impossible to modify ( 4). ![]() Such strategies are well established for the prevention of other conditions, such as cardiovascular disease. Rose ( 3) argued that the most appropriate method for preventing common, multifactorial diseases is to shift the entire population distribution of known risk factors. As a result, a number of agencies have begun to consider strategies aimed at primary prevention of both depression and anxiety. Although effective treatments are available, cost-effectiveness models suggest that even in the unlikely event of optimal treatment being delivered in all cases, only 35%–50% of the overall burden of depression and anxiety would be alleviated ( 2). While the need to address the growing burden of these common mental disorders is not in doubt, there has been little consensus on how this should be executed. The rising costs associated with depression and anxiety constitute a major public health problem across the developed and developing world ( 1).
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