Depression and cardiovascular disease: The role of diet, lifestyle and health

Engelstalig abstract Cardiovascular diseases (CVD) were the main causes of mortality world wide in 2002 and are also projected to stay the main causes of mortality till 2030. In addition, depression and CVD are both predicted to become main contributors of disability in 2030. Not only are depression and CVD highly prevalent and main contributors of disability, many studies have also shown that they are more closely related and indicate that depression may be causally related to CVD. However, underlying mechanisms to explain this relation are not well understood. The aim of this thesis was to investigate whether depression was associated with CVD in elderly men, and in addition, to investigate the role of diet, lifestyle and health in this relationship. Data were used from the FINE (acronym for Finland, Italy and the Netherlands Elderly) Study and the Zutphen elderly Study, prospective population-based cohort studies on risk factors of CVD in elderly men. To determine depressive symptoms before the onset of CVD we excluded men with prevalent CVD and diabetes at baseline. Depressive symptoms increased the risk of cardiovascular mortality, a 5-point increase in depressive symptoms at baseline was associated with a 15% increased risk of cardiovascular mortality (hazard ratio (HR) 1.15 ; 95% CI 1.08-1.23), after adjusting for classical cardiovascular risk factors. This risk was stronger for mortality from stroke and heart failure in comparison with mortality from coronary heart disease and other degenerative heart diseases. There were no significant differences in hazard ratios between Finland, Italy and the Netherlands. To investigate whether a poor diet and unhealthy lifestly may explain the relation between depression and CVD, we assesed whether dietary intake of folate, vitamin B6, vitamin B12 and levels of serum homocysteine were associated with depressive symptoms. However intake of B-vitamin and homocysteine levels were not associated with depression and are therefore not likely to explain the relation between depression and CVD. In addition, a high intake of n-3 fatty acids was associated with a lower risk of depressive symptoms, but could not explain the increased risk of depressive symptoms on CVD mortality. The results indicated that depressed persons were less physically active, but physical inactivity also could not explain the relationship between depressive symptoms and CVD mortality. However, the combination of more depressive symptoms and low physical activity may lead to an extra increased risk of cardiovascular mortality. To investigate the role of health we assessed that high resting heart rate and a worse subjective health status, measured by self-rated health and self-reported disability in activities of daily living, were both also associated with more depressive symptoms at baseline as well as with a lower risk of CVD mortality. While indicators of autonomic dysfunction could not explain the relation between depression and CVD mortality, subjective health status did explain part of the relationship between depressive symptoms and cardiovascular mortality. However, a significant risk of depressive symptoms on cardiovascular mortality remained (HR 1.25; 95% CI 1.09-1.43). Finally, we discussed whether depression is a cause, consequence, or innocent bystander of CVD