Association of Optimism With Cardiovascular Events and All-Cause Mortality: A Systematic Review and Meta-analysis
[COMPLETE ARTICLE READ IN FULL AT SOURCE, open access at jamanetwork.com, including the mechanisms, clinical-significance and limitations sections] Rozanski, A., Bavishi, C., Kubzansky, L. D., & Cohen, R. (2019). 'Association of Optimism With Cardiovascular Events and All-Cause Mortality: A Systematic Review and Meta-analysis.' JAMA Network Open 2(9), e1912200. doi:10.1001/jamanetworkopen.2019.12200. PubMed, Scopus and PsycINFO from inception to 2 July 2019; MOOSE reporting guideline; Hartung-Knapp-Sidik-Jonkman random-effects model; screening and extraction by two investigators independently. 15 studies, 229,391 participants, 10 reporting cardiovascular events and 9 all-cause mortality; mean follow-up 13.8 years, range 2 to 40. Cardiovascular events: relative risk 0.65 (0.51 to 0.78), p < .001, I-squared 87.4 per cent. All-cause mortality: 0.86 (0.80 to 0.92), p < .001, I-squared 73.2 per cent. Restricted to the revised Life Orientation Test: 0.71 (0.57 to 0.86) and 0.87 (0.78 to 0.96). THE HETEROGENEITY IS THE STORY AND THE AUTHORS SAY SO: 'Although each study adjusted for important covariates, these covariates varied widely from study to study. Thus, we could not systematically assess the independent effects of various individual clinical covariates, including smoking, diabetes, and hypertension. This variability in covariate adjustment may help to account for the considerable heterogeneity found among studies.' STUDIES OF PATIENTS WITH CANCER WERE EXCLUDED BY DESIGN, 'to avoid confounding secondary to terminal sickness', so the pooled estimate everyone quotes contains no cancer patients. Mechanisms are listed as associations with inflammation, impairments in haemostasis and endothelial function, metabolic function, telomerase activity and telomere length, ambulatory blood pressure and hypothalamic-pituitary-adrenocortical function, with their own calibration that 'study of individual mediators remains sparse compared with the study of more established psychosocial mediators, such as depression'. They also raise the asymmetry directly, asking whether 'pessimism is a stronger contributor to pathophysiologic dysfunction' than optimism is for positive physiologic buffering, and they state the field's open question, whether optimism enhanced or induced by intervention carries similar benefits to naturally occurring optimism. They flag the construct problem themselves and record that there was insufficient information in the included studies to address it.
[COMPLETE ARTICLE READ IN FULL AT SOURCE, open access at jamanetwork.com, including the mechanisms, clinical-significance and limitations sections] Rozanski, A., Bavishi, C., Kubzansky, L. D., & Cohen, R. (2019). 'Association of Optimism With Cardiovascular Events and All-Cause Mortality: A Systematic Review and Meta-analysis.' JAMA Network Open 2(9), e1912200. doi:10.1001/jamanetworkopen.2019.12200. PubMed, Scopus and PsycINFO from inception to 2 July 2019; MOOSE reporting guideline; Hartung-Knapp-Sidik-Jonkman random-effects model; screening and extraction by two investigators independently. 15 studies, 229,391 participants, 10 reporting cardiovascular events and 9 all-cause mortality; mean follow-up 13.8 years, range 2 to 40. Cardiovascular events: relative risk 0.65 (0.51 to 0.78), p < .001, I-squared 87.4 per cent. All-cause mortality: 0.86 (0.80 to 0.92), p < .001, I-squared 73.2 per cent. Restricted to the revised Life Orientation Test: 0.71 (0.57 to 0.86) and 0.87 (0.78 to 0.96). THE HETEROGENEITY IS THE STORY AND THE AUTHORS SAY SO: 'Although each study adjusted for important covariates, these covariates varied widely from study to study. Thus, we could not systematically assess the independent effects of various individual clinical covariates, including smoking, diabetes, and hypertension. This variability in covariate adjustment may help to account for the considerable heterogeneity found among studies.' STUDIES OF PATIENTS WITH CANCER WERE EXCLUDED BY DESIGN, 'to avoid confounding secondary to terminal sickness', so the pooled estimate everyone quotes contains no cancer patients. Mechanisms are listed as associations with inflammation, impairments in haemostasis and endothelial function, metabolic function, telomerase activity and telomere length, ambulatory blood pressure and hypothalamic-pituitary-adrenocortical function, with their own calibration that 'study of individual mediators remains sparse compared with the study of more established psychosocial mediators, such as depression'. They also raise the asymmetry directly, asking whether 'pessimism is a stronger contributor to pathophysiologic dysfunction' than optimism is for positive physiologic buffering, and they state the field's open question, whether optimism enhanced or induced by intervention carries similar benefits to naturally occurring optimism. They flag the construct problem themselves and record that there was insufficient information in the included studies to address it.
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Rozanski, A., Bavishi, C., Kubzansky, L. D., & Cohen, R. (2019). Association of Optimism With Cardiovascular Events and All-Cause Mortality: A Systematic Review and Meta-analysis. JAMA Network Open, 2(9), e1912200. doi:10.1001/jamanetworkopen.2019.12200