Mikko Myrskylä1, Neil K Mehta, Virginia W Chang. 1. Research Group Lifecourse Dynamics and Demographic Change, Max Planck Institute for Demographic Research, Rostock, Germany. myrskyla@demogr.mpg.de
Abstract
OBJECTIVES: We sought to analyze how early exposure to the 1918 influenza pandemic is associated with old-age mortality by cause of death. METHODS: We analyzed the National Health Interview Survey (n = 81,571; follow-up 1989-2006; 43,808 deaths) and used year and quarter of birth to assess timing of pandemic exposure. We used Cox proportional and Fine-Gray competing hazard models for all-cause and cause-specific mortality, respectively. RESULTS: Cohorts born during pandemic peaks had excess all-cause mortality attributed to increased noncancer mortality. We found evidence for a trade-off between noncancer and cancer causes: cohorts with high noncancer mortality had low cancer mortality, and vice versa. CONCLUSIONS: Early disease exposure increases old-age mortality through noncancer causes, which include respiratory and cardiovascular diseases, and may trigger a trade-off in the risk of cancer and noncancer causes. Potential mechanisms include inflammation or apoptosis. The findings contribute to our understanding of the causes of death behind the early disease exposure-later mortality association. The cancer-noncancer trade-off is potentially important for understanding the mechanisms behind these associations.
OBJECTIVES: We sought to analyze how early exposure to the 1918 influenza pandemic is associated with old-age mortality by cause of death. METHODS: We analyzed the National Health Interview Survey (n = 81,571; follow-up 1989-2006; 43,808 deaths) and used year and quarter of birth to assess timing of pandemic exposure. We used Cox proportional and Fine-Gray competing hazard models for all-cause and cause-specific mortality, respectively. RESULTS: Cohorts born during pandemic peaks had excess all-cause mortality attributed to increased noncancer mortality. We found evidence for a trade-off between noncancer and cancer causes: cohorts with high noncancer mortality had low cancer mortality, and vice versa. CONCLUSIONS: Early disease exposure increases old-age mortality through noncancer causes, which include respiratory and cardiovascular diseases, and may trigger a trade-off in the risk of cancer and noncancer causes. Potential mechanisms include inflammation or apoptosis. The findings contribute to our understanding of the causes of death behind the early disease exposure-later mortality association. The cancer-noncancer trade-off is potentially important for understanding the mechanisms behind these associations.
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