Association of change in cardiovascular risk factors with incident dementia
Sedaghat, Sanaz; Lutsey, Pamela L; Ji, Yuekai; Empana, Jean-Philippe; Sorond, Farzaneh; Hughes, Timothy M; Mosley, Thomas H; Gottesman, Rebecca F; Knopman, David S; Walker, Keenan A; Gudnason, Vilmundur; Launer, Lenore J; van Sloten, Thomas T
(2023) Alzheimer's & Dementia, volume 19, issue 5, pp. 1821 - 1831
(Article)
Abstract
INTRODUCTION: We evaluated whether better cardiovascular health at midlife and improvement of cardiovascular health within midlife were associated with dementia risk. METHODS: Two longitudinal population-based studies were used: Atherosclerosis Risk in Communities (ARIC) (n = 11,460/visits at ages 54 and 60), and Age, Gene/Environment Susceptibility (AGES)-Reykjavik (n = 3907/visit at
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age 51). A cardiovascular health score (range 0-12/0-14, depending on diet availability) including six/seven items was calculated at each visit, with weight assigned to each item as poor (0), intermediate (1), or ideal (2). Cardiovascular health was defined as low (score 0-4/0-5), intermediate (5-7/6-9), or high (8-12/10-14). Incident dementia was ascertained through linkage to health records and with neuropsychological examinations. RESULTS: Midlife high compared to low cardiovascular health (hazard ratios [HRs]: for ARIC: 0.60 [95% confidence interval: 0.52, 0.69]); for AGES-Reykjavik: 0.83 [0.66, 0.99] and improvement of cardiovascular health score within midlife (HR per one-point increase: ARIC: 0.94 [0.92, 0.96]) were associated with lower dementia risk. DISCUSSION: Better cardiovascular health at midlife and improvement of cardiovascular health within midlife are associated with lower dementia risk. HIGHLIGHTS: Cardiovascular health and dementia were studied in two large cohort studies. Better cardiovascular health at midlife relates to lower dementia risk. Improvement of cardiovascular health within midlife relates to lower dementia risk. Promotion of cardiovascular health at midlife can help to reduce dementia risk.
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Keywords: cardiovascular health, dementia, life course, longitudinal, primordial prevention, Clinical Neurology, Geriatrics and Gerontology, Psychiatry and Mental health, Cellular and Molecular Neuroscience, Health Policy, Developmental Neuroscience, Epidemiology, Journal Article
ISSN: 1552-5260
Publisher: John Wiley & Sons, Ltd.
Note: Funding Information: The authors thank the staff and participants of the ARIC and AGES-Reykjavik studies for their important contributions. The Atherosclerosis Risk in Communities study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts (HHSN268201700001I, HHSN268201700002I, HHSN268201700003I, HHSN268201700004I, HHSN268201700005I). Neurocognitive data are collected by U01 2U01HL096812, 2U01HL096814, 2U01HL096899, 2U01HL096902, 2U01HL096917 from the NIH (NHLBI, NINDS, NIA, and NIDCD), and with previous brain magnetic resonance imaging examinations funded by R01-HL70825 from the NHLBI. The AGES-Reykjavik was funded by contracts N01-AG-12100 and HHSN27120120022C from the National Institutes of Health; the Intramural Research Program of the National Institute on Aging; and by the Icelandic Heart Association and the Icelandic Parliament. Sanaz Sedaghat is supported by a McKnight Clinical Translational Research Scholarship in Cognitive Aging and Age-Related Memory Loss. Thomas van Sloten is supported by a VENI research grant (916.19.074) from the Netherlands Organization for Scientific Research and a Dutch Heart Foundation research grant (2018T025). Pamela Lutsey is supported by K24 HL159246. Rebecca Gottesman is supported by the Intramural Research Program of the National Institute of Neurological Disorders and Stroke. Keenan Walker is supported by the Intramural Research Program of the National Institute on Aging. Funding Information: The authors thank the staff and participants of the ARIC and AGES‐Reykjavik studies for their important contributions. The Atherosclerosis Risk in Communities study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts (HHSN268201700001I, HHSN268201700002I, HHSN268201700003I, HHSN268201700004I, HHSN268201700005I). Neurocognitive data are collected by U01 2U01HL096812, 2U01HL096814, 2U01HL096899, 2U01HL096902, 2U01HL096917 from the NIH (NHLBI, NINDS, NIA, and NIDCD), and with previous brain magnetic resonance imaging examinations funded by R01‐HL70825 from the NHLBI. The AGES‐Reykjavik was funded by contracts N01‐AG‐12100 and HHSN27120120022C from the National Institutes of Health; the Intramural Research Program of the National Institute on Aging; and by the Icelandic Heart Association and the Icelandic Parliament. Sanaz Sedaghat is supported by a McKnight Clinical Translational Research Scholarship in Cognitive Aging and Age‐Related Memory Loss. Thomas van Sloten is supported by a VENI research grant (916.19.074) from the Netherlands Organization for Scientific Research and a Dutch Heart Foundation research grant (2018T025). Pamela Lutsey is supported by K24 HL159246. Rebecca Gottesman is supported by the Intramural Research Program of the National Institute of Neurological Disorders and Stroke. Keenan Walker is supported by the Intramural Research Program of the National Institute on Aging. Publisher Copyright: © 2022 The Authors. Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.
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