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Smoking and reverse causation create an obesity paradox in cardiovascular disease
OBJECTIVE: Many studies find that excess weight is associated with better survival among individuals with cardiovascular disease (CVD). Investigations were carried out to see whether this “obesity paradox” can be explained by biases. METHODS: The association between weight status and mortality in th...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4701612/ https://www.ncbi.nlm.nih.gov/pubmed/26421898 http://dx.doi.org/10.1002/oby.21239 |
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author | Stokes, Andrew Preston, Samuel H. |
author_facet | Stokes, Andrew Preston, Samuel H. |
author_sort | Stokes, Andrew |
collection | PubMed |
description | OBJECTIVE: Many studies find that excess weight is associated with better survival among individuals with cardiovascular disease (CVD). Investigations were carried out to see whether this “obesity paradox” can be explained by biases. METHODS: The association between weight status and mortality in the US population ages 35 and above with CVD was investigated. Data were obtained from the National Health and Nutrition Examination Survey, 1988‐2010, linked to mortality records through 2011. To minimize biases resulting from illness‐induced weight loss, a reference category consisting of individuals who have always maintained normal weight was used. Age‐standardized mortality rates and Cox models were estimated, comparing overweight/obesity (body mass index (BMI) ≥25.0 kg m(−2)) to normal weight (BMI 18.5‐24.9 kg m(−2)). RESULTS: The paradox was present among those with overweight/obesity at the time of survey (hazard ratio (HR) = 0.89; 95% confidence interval (CI) 0.78‐1.01). However, when the reference category was limited to the always‐normal‐weight, the paradox disappeared (HR = 1.16; 95% CI 0.95‐1.41). When analysis was additionally confined to never‐smokers, mortality risks were significantly higher in the overweight/obesity group (HR = 1.51; 95% CI 1.07‐2.15; P = 0.021). CONCLUSIONS: The findings provide support for the hypothesis that lower mortality among individuals with CVD and overweight/obesity is a product of biases involving reverse causation and confounding by smoking. |
format | Online Article Text |
id | pubmed-4701612 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-47016122016-05-18 Smoking and reverse causation create an obesity paradox in cardiovascular disease Stokes, Andrew Preston, Samuel H. Obesity (Silver Spring) Original Articles OBJECTIVE: Many studies find that excess weight is associated with better survival among individuals with cardiovascular disease (CVD). Investigations were carried out to see whether this “obesity paradox” can be explained by biases. METHODS: The association between weight status and mortality in the US population ages 35 and above with CVD was investigated. Data were obtained from the National Health and Nutrition Examination Survey, 1988‐2010, linked to mortality records through 2011. To minimize biases resulting from illness‐induced weight loss, a reference category consisting of individuals who have always maintained normal weight was used. Age‐standardized mortality rates and Cox models were estimated, comparing overweight/obesity (body mass index (BMI) ≥25.0 kg m(−2)) to normal weight (BMI 18.5‐24.9 kg m(−2)). RESULTS: The paradox was present among those with overweight/obesity at the time of survey (hazard ratio (HR) = 0.89; 95% confidence interval (CI) 0.78‐1.01). However, when the reference category was limited to the always‐normal‐weight, the paradox disappeared (HR = 1.16; 95% CI 0.95‐1.41). When analysis was additionally confined to never‐smokers, mortality risks were significantly higher in the overweight/obesity group (HR = 1.51; 95% CI 1.07‐2.15; P = 0.021). CONCLUSIONS: The findings provide support for the hypothesis that lower mortality among individuals with CVD and overweight/obesity is a product of biases involving reverse causation and confounding by smoking. John Wiley and Sons Inc. 2015-09-30 2015-12 /pmc/articles/PMC4701612/ /pubmed/26421898 http://dx.doi.org/10.1002/oby.21239 Text en © 2015 The Authors Obesity published by Wiley Periodicals, Inc. on behalf of The Obesity Society (TOS) This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs (http://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Original Articles Stokes, Andrew Preston, Samuel H. Smoking and reverse causation create an obesity paradox in cardiovascular disease |
title | Smoking and reverse causation create an obesity paradox in cardiovascular disease |
title_full | Smoking and reverse causation create an obesity paradox in cardiovascular disease |
title_fullStr | Smoking and reverse causation create an obesity paradox in cardiovascular disease |
title_full_unstemmed | Smoking and reverse causation create an obesity paradox in cardiovascular disease |
title_short | Smoking and reverse causation create an obesity paradox in cardiovascular disease |
title_sort | smoking and reverse causation create an obesity paradox in cardiovascular disease |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4701612/ https://www.ncbi.nlm.nih.gov/pubmed/26421898 http://dx.doi.org/10.1002/oby.21239 |
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