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Stress management fails to lower heart disease risk in new study

A year-long cognitive behavioral therapy program helped cardiac patients manage stress better—but didn't reduce the biological markers linked to heart attack risk. The finding suggests that willpower and coping skills alone may be insufficient, forcing health systems and insurers to rethink how they design and measure cardiac prevention programs.

Originaltitel: Stress, Diet and Lifestyle: Cortisol, Carotenoids, and Lifestyle Factors in a Cardiovascular Perspective

Abstrakt

<p>Healthy lifestyle changes that may reduce the risk of cardiovascular disease are often difficult to implement in the general population. This is also true for cardiovascular patients, who usually get well-grounded advice from health professionals as well as opportunities to participate in programs to quit smoking, consume a healthier diet, reduce psychosocial stress, or increase physical activity. The reasons for this resistance and how better intervention compliance could be achieved are unclear.</p><p>Here, the variables psychosocial stress, intake of statins, dietary habits, and sleep quality have been studied in cardiovascular patients and in a group of middle-aged individuals with respect to their role in cardiovascular disease and myocardial infarction.</p><p>In Paper I, the aim was to investigate whether improved stress behavior in coronary artery patients with type A personality traits resulted in altered cortisol secretion after a 1-year cognitive stress management program. The stress management program, based on cognitive behavioral methods, showed a significant improvement in the patients’ ability to cope with perceived stress. However, this was not associated with any changes in diurnal cortisol secretion or levels of cholesterol or C-reactive protein. The pilot study raises questions as to the value of salivary cortisol as a stress marker in cardiac rehabilitation.</p><p>Paper II investigated the association between diet, inflammatory markers, and carotenoid concentrations in a middle-aged population. Carotenoid levels were not solely explained by dietary intake of fruit and vegetables. Instead, significant associations were found to male sex, obesity, low levels of “protective” high-density lipoprotein cholesterol and high levels of the inflammatory marker matrix metalloproteinase-9. It can be speculated that provitamin A carotenoids have athero-protective effects.</p><p>Paper III studied how lipid-lowering statins affect the levels of carotenoids and the inflammatory marker C-reactive protein, which could possibly participate in a cardio-protective mechanism. The study patients, with mild to moderate hypercholesterolemia, received either placebo or simvastatin and were followed up after 6 weeks. After adjustment for lipids, the levels of the carotenoids lutein, lycopene, α-carotene, and β-carotene were found to be significantly increased in the simvastatin group, suggesting an increased ratio of carotenoids per particle. Importantly, there is a risk of misinterpreting the carotenoid status in individuals on statin medication if relying on crude serum or plasma levels.</p><p>Paper IV studied middle-aged individuals (a subgroup in the Swedish CArdioPulmonary bioImage study) with regard to adherence to a healthy diet, psychological factors (stress and sleep), and risk factors for cardiovascular disease. Dietary habits were not linked to stress or sleeping patterns. Instead, participants who lived in areas with low socioeconomic status had higher odds ratio for having more unfavorable apolipo-protein B/apolipoprotein A1 ratio. Moreover, among several predictors, depression emerged as a strong predictor of a poor lipid profile in low SES areas but not in high SES areas. This study highlighted that tailored dietary recommendations, promoting physical activity, and addressing mental health may be of particular importance in low socioeconomic status areas for cardiovascular disease risk reduction in this subgroup of patients.</p>

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