Body mass index and risk of dementia: Analysis of individual-level data from 1.3 million individuals
Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects. We examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was asce...
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Published in | Alzheimer's & dementia Vol. 14; no. 5; pp. 601 - 609 |
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Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.05.2018
Elsevier, Inc |
Subjects | |
Online Access | Get full text |
ISSN | 1552-5260 1552-5279 1552-5279 |
DOI | 10.1016/j.jalz.2017.09.016 |
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Abstract | Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects.
We examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow-up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis.
Hazard ratios per 5-kg/m2 increase in BMI for dementia were 0.71 (95% confidence interval = 0.66–0.77), 0.94 (0.89–0.99), and 1.16 (1.05–1.27) when BMI was assessed 10 years, 10-20 years, and >20 years before dementia diagnosis.
The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short.
•Data from 1.3 million adults from 39 prospective cohort studies were pooled for the analyses.•Higher BMI was associated with increased risk of dementia when the follow-up was long.•When follow-up was short, lower BMI was linked to increased dementia risk probably due to reverse causation. |
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AbstractList | Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects.INTRODUCTIONHigher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects.We examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow-up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis.METHODSWe examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow-up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis.Hazard ratios per 5-kg/m2 increase in BMI for dementia were 0.71 (95% confidence interval = 0.66-0.77), 0.94 (0.89-0.99), and 1.16 (1.05-1.27) when BMI was assessed 10 years, 10-20 years, and >20 years before dementia diagnosis.RESULTSHazard ratios per 5-kg/m2 increase in BMI for dementia were 0.71 (95% confidence interval = 0.66-0.77), 0.94 (0.89-0.99), and 1.16 (1.05-1.27) when BMI was assessed 10 years, 10-20 years, and >20 years before dementia diagnosis.The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short.CONCLUSIONSThe association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short. Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects. We examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow-up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis. Hazard ratios per 5-kg/m increase in BMI for dementia were 0.71 (95% confidence interval = 0.66-0.77), 0.94 (0.89-0.99), and 1.16 (1.05-1.27) when BMI was assessed 10 years, 10-20 years, and >20 years before dementia diagnosis. The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short. INTRODUCTION: Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects. METHODS: We examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow-up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis. RESULTS: Hazard ratios per 5-kg/m(2) increase in BMI for dementia were 0.71 (95% confidence interval = 0.66-0.77), 0.94 (0.89-0.99), and 1.16 (1.05-1.27) when BMI was assessed 10 years, 10-20 years, and >20 years before dementia diagnosis. CONCLUSIONS: The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short. Introduction: Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects. Methods: We examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow-up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis. Results: Hazard ratios per 5-kg/m2 increase in BMI for dementia were 0.71 (95% confidence interval = 0.66-0.77), 0.94 (0.89-0.99), and 1.16 (1.05-1.27) when BMI was assessed 10 years, 10-20 years, and >20 years before dementia diagnosis. Conclusions: The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short. Introduction: Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects. Methods: We examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow-up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis. Results: Hazard ratios per 5-kg/m(2) increase in BMI for dementia were 0.71 (95% confidence interval = 0.66-0.77), 0.94 (0.89-0.99), and 1.16 (1.05-1.27) when BMI was assessed 10 years, 10-20 years, and >20 years before dementia diagnosis. Conclusions: The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short. • Data from 1.3 million adults from 39 prospective cohort studies were pooled for the analyses. • Higher BMI was associated with increased risk of dementia when the follow-up was long. • When follow-up was short, lower BMI was linked to increased dementia risk probably due to reverse causation. Introduction: Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects. Methods: We examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow-up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis. Results: Hazard ratios per 5-kg/m2 increase in BMI for dementia were 0.71 (95% confidence interval = 0.66-0.77), 0.94 (0.89-0.99), and 1.16 (1.05-1.27) when BMI was assessed 10 years, 10-20 years, and >20 years before dementia diagnosis. Conclusions: The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short. Introduction Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects. Methods We examined this hypothesis in 1,349,857 dementia‐free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow‐up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis. Results Hazard ratios per 5‐kg/m2 increase in BMI for dementia were 0.71 (95% confidence interval = 0.66–0.77), 0.94 (0.89–0.99), and 1.16 (1.05–1.27) when BMI was assessed 10 years, 10‐20 years, and >20 years before dementia diagnosis. Conclusions The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow‐up, and a reverse‐causation effect that makes a higher BMI to appear protective when the follow‐up is short. Highlights Data from 1.3 million adults from 39 prospective cohort studies were pooled for the analyses. Higher BMI was associated with increased risk of dementia when the follow‐up was long. When follow‐up was short, lower BMI was linked to increased dementia risk probably due to reverse causation. Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects. We examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow-up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis. Hazard ratios per 5-kg/m2 increase in BMI for dementia were 0.71 (95% confidence interval = 0.66–0.77), 0.94 (0.89–0.99), and 1.16 (1.05–1.27) when BMI was assessed 10 years, 10-20 years, and >20 years before dementia diagnosis. The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short. •Data from 1.3 million adults from 39 prospective cohort studies were pooled for the analyses.•Higher BMI was associated with increased risk of dementia when the follow-up was long.•When follow-up was short, lower BMI was linked to increased dementia risk probably due to reverse causation. Introduction: Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects. Methods: We examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow-up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis. Results: Hazard ratios per 5-kg/m(2) increase in BMI for dementia were 0.71 (95% confidence interval = 0.66-0.77), 0.94 (0.89-0.99), and 1.16 (1.05-1.27) when BMI was assessed 10 years, 10-20 years, and >20 years before dementia diagnosis. Conclusions: The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short. (C) 2017 The Authors. Published by Elsevier Inc. on behalf of the Alzheimer's Association. |
Author | Singh-Manoux, Archana Kivimäki, Mika Goldberg, Marcel Pentti, Jaana Theorell, Töres Knutsson, Anders Kivipelto, Miia Jokela, Markus Nordin, Maria Koskenvuo, Markku Fransson, Eleonor I. Westerholm, Peter Kuosma, Eeva Shipley, Martin J. Vahtera, Jussi Vuoksimaa, Eero Nyberg, Solja T. Luukkonen, Ritva Kaprio, Jaakko Alfredsson, Lars Suominen, Sakari B. Westerlund, Hugo Batty, G. David Ferrie, Jane E. Zins, Marie |
AuthorAffiliation | k Department of Health Sciences, Mid Sweden University, Sundsvall, Sweden m Folkhälsan Research Center, Folkhälsan, Helsinki, Finland j Population-based Epidemiologic Cohort Unit, UMS 011, Inserm, Villejuif, France d Centre for Cognitive Ageing and Cognitive Epidemiology, Alzheimer Scotland Dementia Research Centre, University of Edinburgh, Edinburgh, UK i Division of Epidemiology, Stress Research Institute, Stockholm University, Stockholm, Sweden n School of Health and Education, University of Skövde, Skövde, Sweden f Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden h School of Health Sciences and Welfare, Jönköping University, Jönköping, Sweden r Department of Neurobiology, Karolinska Institute, Stockholm, Sweden u Institute of Behavioral Sciences, University of Helsinki, Helsinki, Finland p Institute for Molecular Medicine (FIMM), University of Helsinki, Helsinki, Finland t University of Turku, Turku, Finland g Centre for Occupational and Environmental Medicine, Sto |
AuthorAffiliation_xml | – name: e School of Social and Community Medicine, University of Bristol, Bristol, UK – name: t University of Turku, Turku, Finland – name: n School of Health and Education, University of Skövde, Skövde, Sweden – name: u Institute of Behavioral Sciences, University of Helsinki, Helsinki, Finland – name: k Department of Health Sciences, Mid Sweden University, Sundsvall, Sweden – name: i Division of Epidemiology, Stress Research Institute, Stockholm University, Stockholm, Sweden – name: o Turku University Hospital, Turku, Finland – name: g Centre for Occupational and Environmental Medicine, Stockholm County Council, Stockholm, Sweden – name: r Department of Neurobiology, Karolinska Institute, Stockholm, Sweden – name: l Department of Psychology, Umeå University, Umeå, Sweden – name: m Folkhälsan Research Center, Folkhälsan, Helsinki, Finland – name: f Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden – name: b Clinicum, Department of Public Health, Faculty of Medicine, University of Helsinki, Helsinki, Finland – name: d Centre for Cognitive Ageing and Cognitive Epidemiology, Alzheimer Scotland Dementia Research Centre, University of Edinburgh, Edinburgh, UK – name: q Occupational and Environmental Medicine, Uppsala University, Uppsala, Sweden – name: j Population-based Epidemiologic Cohort Unit, UMS 011, Inserm, Villejuif, France – name: s National Institute for Health and Welfare, Helsinki, Finland – name: c Finnish Institute of Occupational Health, Helsinki and Turku, Finland – name: a Department of Epidemiology and Public Health, University College London, London, UK – name: p Institute for Molecular Medicine (FIMM), University of Helsinki, Helsinki, Finland – name: h School of Health Sciences and Welfare, Jönköping University, Jönköping, Sweden |
Author_xml | – sequence: 1 givenname: Mika surname: Kivimäki fullname: Kivimäki, Mika email: m.kivimaki@ucl.ac.uk organization: Department of Epidemiology and Public Health, University College London, London, UK – sequence: 2 givenname: Ritva surname: Luukkonen fullname: Luukkonen, Ritva organization: Clinicum, Department of Public Health, Faculty of Medicine, University of Helsinki, Helsinki, Finland – sequence: 3 givenname: G. David surname: Batty fullname: Batty, G. David organization: Department of Epidemiology and Public Health, University College London, London, UK – sequence: 4 givenname: Jane E. surname: Ferrie fullname: Ferrie, Jane E. organization: School of Social and Community Medicine, University of Bristol, Bristol, UK – sequence: 5 givenname: Jaana surname: Pentti fullname: Pentti, Jaana organization: Clinicum, Department of Public Health, Faculty of Medicine, University of Helsinki, Helsinki, Finland – sequence: 6 givenname: Solja T. surname: Nyberg fullname: Nyberg, Solja T. organization: Clinicum, Department of Public Health, Faculty of Medicine, University of Helsinki, Helsinki, Finland – sequence: 7 givenname: Martin J. surname: Shipley fullname: Shipley, Martin J. organization: Department of Epidemiology and Public Health, University College London, London, UK – sequence: 8 givenname: Lars surname: Alfredsson fullname: Alfredsson, Lars organization: Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden – sequence: 9 givenname: Eleonor I. surname: Fransson fullname: Fransson, Eleonor I. organization: Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden – sequence: 10 givenname: Marcel surname: Goldberg fullname: Goldberg, Marcel organization: Population-based Epidemiologic Cohort Unit, UMS 011, Inserm, Villejuif, France – sequence: 11 givenname: Anders surname: Knutsson fullname: Knutsson, Anders organization: Department of Health Sciences, Mid Sweden University, Sundsvall, Sweden – sequence: 12 givenname: Markku surname: Koskenvuo fullname: Koskenvuo, Markku organization: Clinicum, Department of Public Health, Faculty of Medicine, University of Helsinki, Helsinki, Finland – sequence: 13 givenname: Eeva surname: Kuosma fullname: Kuosma, Eeva organization: Clinicum, Department of Public Health, Faculty of Medicine, University of Helsinki, Helsinki, Finland – sequence: 14 givenname: Maria surname: Nordin fullname: Nordin, Maria organization: Division of Epidemiology, Stress Research Institute, Stockholm University, Stockholm, Sweden – sequence: 15 givenname: Sakari B. surname: Suominen fullname: Suominen, Sakari B. organization: Folkhälsan Research Center, Folkhälsan, Helsinki, Finland – sequence: 16 givenname: Töres surname: Theorell fullname: Theorell, Töres organization: Division of Epidemiology, Stress Research Institute, Stockholm University, Stockholm, Sweden – sequence: 17 givenname: Eero surname: Vuoksimaa fullname: Vuoksimaa, Eero organization: Clinicum, Department of Public Health, Faculty of Medicine, University of Helsinki, Helsinki, Finland – sequence: 18 givenname: Peter surname: Westerholm fullname: Westerholm, Peter organization: Occupational and Environmental Medicine, Uppsala University, Uppsala, Sweden – sequence: 19 givenname: Hugo surname: Westerlund fullname: Westerlund, Hugo organization: Division of Epidemiology, Stress Research Institute, Stockholm University, Stockholm, Sweden – sequence: 20 givenname: Marie surname: Zins fullname: Zins, Marie organization: Population-based Epidemiologic Cohort Unit, UMS 011, Inserm, Villejuif, France – sequence: 21 givenname: Miia surname: Kivipelto fullname: Kivipelto, Miia organization: Department of Neurobiology, Karolinska Institute, Stockholm, Sweden – sequence: 22 givenname: Jussi surname: Vahtera fullname: Vahtera, Jussi organization: Turku University Hospital, Turku, Finland – sequence: 23 givenname: Jaakko surname: Kaprio fullname: Kaprio, Jaakko organization: Clinicum, Department of Public Health, Faculty of Medicine, University of Helsinki, Helsinki, Finland – sequence: 24 givenname: Archana surname: Singh-Manoux fullname: Singh-Manoux, Archana organization: Department of Epidemiology and Public Health, University College London, London, UK – sequence: 25 givenname: Markus surname: Jokela fullname: Jokela, Markus organization: Institute of Behavioral Sciences, University of Helsinki, Helsinki, Finland |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29169013$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-15589$$DView record from Swedish Publication Index https://urn.kb.se/resolve?urn=urn:nbn:se:hj:diva-37998$$DView record from Swedish Publication Index https://urn.kb.se/resolve?urn=urn:nbn:se:miun:diva-32715$$DView record from Swedish Publication Index https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-151281$$DView record from Swedish Publication Index https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-148752$$DView record from Swedish Publication Index https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-336135$$DView record from Swedish Publication Index http://kipublications.ki.se/Default.aspx?queryparsed=id:138275548$$DView record from Swedish Publication Index |
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Snippet | Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such... Introduction Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask... • Data from 1.3 million adults from 39 prospective cohort studies were pooled for the analyses. • Higher BMI was associated with increased risk of dementia... Introduction: Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may... INTRODUCTION: Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may... |
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Title | Body mass index and risk of dementia: Analysis of individual-level data from 1.3 million individuals |
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