Laura F. DeFina, MD; Benjamin L. Willis, MD, MPH; Nina B. Radford, MD; Ang Gao, MS; David Leonard, PhD; William L. Haskell, PhD; Myron F. Weiner, MD; Jarett D. Berry, MD, MS
Acknowledgment: The authors thank Kenneth H. Cooper, MD, MPH, for establishing the CCLS; the late Fred R. Meyer, former Chief Executive Officer of The Cooper Institute; the Cooper Clinic for collecting the data; and The Cooper Institute for data management.
Grant Support: By The Cooper Institute. Dr. Berry receives funding from the Dedman Family Scholar in Clinical Care endowment at the University of Texas Southwestern Medical Center; the National Heart, Lung, and Blood Institute; and the American Heart Association.
Potential Conflicts of Interest: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M12-1302.
Reproducible Research Statement: Study protocol: Available from Dr. DeFina (e-mail, firstname.lastname@example.org). Statistical code and data set: Available from Dr. Willis (e-mail, email@example.com).
Corresponding Author: Laura F. DeFina, MD, The Cooper Institute, 12330 Preston Road, Dallas, TX 75230; e-mail, firstname.lastname@example.org.
Current Author Addresses: Drs. DeFina and Willis: The Cooper Institute, 12330 Preston Road, Dallas, TX 75230.
Dr. Radford: The Cooper Clinic, 12200 Preston Road, Dallas, TX 75230.
Ms. Gao and Dr. Berry: Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390.
Dr. Leonard: Department of Clinical Science, Division of Biostatistics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390.
Dr. Haskell: Stanford Prevention Research Center, Stanford University School of Medicine, 1070 Arastradero Road, Suite 100, Palo Alto, CA 94304-1334.
Dr. Weiner: Department of Psychiatry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390.
Author Contributions: Conception and design: L.F. DeFina, B.L. Willis, W.L. Haskell, J.D. Berry.
Analysis and interpretation of the data: L.F. DeFina, B.L. Willis, A. Gao, D. Leonard, M.F. Weiner, J.D. Berry.
Drafting of the article: L.F. DeFina, B.L. Willis, N.B. Radford, M.F. Weiner, J.D. Berry.
Critical revision of the article for important intellectual content: L.F. DeFina, B.L. Willis, N.B. Radford, D. Leonard, W.L. Haskell, M.F. Weiner, J.D. Berry.
Final approval of the article: L.F. DeFina, B.L. Willis, N.B. Radford, A. Gao, D. Leonard, W.L. Haskell, J.D. Berry.
Statistical expertise: B.L. Willis, A. Gao, D. Leonard.
Obtaining of funding: J.D. Berry.
Administrative, technical, or logistic support: L.F. DeFina, B.L. Willis, J.D. Berry.
Collection and assembly of data: L.F. DeFina, B.L. Willis.
DeFina LF, Willis BL, Radford NB, Gao A, Leonard D, Haskell WL, et al. The Association Between Midlife Cardiorespiratory Fitness Levels and Later-Life Dementia: A Cohort Study. Ann Intern Med. 2013;158:162-168. doi: 10.7326/0003-4819-158-3-201302050-00005
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Published: Ann Intern Med. 2013;158(3):162-168.
Primary prevention of Alzheimer disease and other types of dementia (all-cause dementia) is an important public health goal. Evidence to date is insufficient to recommend any lifestyle change to prevent or delay the onset of dementia.
To assess the association between objectively measured midlife cardiorespiratory fitness (“fitness”) levels and development of all-cause dementia in advanced age.
Prospective, observational cohort study.
Preventive medicine clinic.
19 458 community-dwelling, nonelderly adults who had a baseline fitness examination.
Fitness levels, assessed using the modified Balke treadmill protocol between 1971 and 2009, and incident all-cause dementia using Medicare Parts A and B claims data from 1999 to 2009.
1659 cases of incident all-cause dementia occurred during 125 700 person-years of Medicare follow-up (median follow-up, 25 years [interquartile range, 19 to 30 years]). After multivariable adjustment, participants in the highest quintile of fitness level had lower hazard of all-cause dementia than those in the lowest quintile (hazard ratio, 0.64 [95% CI, 0.54 to 0.77]). Higher fitness levels were associated with lower hazard of all-cause dementia with previous stroke (hazard ratio, 0.74 [CI, 0.53 to 1.04]) or without previous stroke (hazard ratio, 0.74 [CI, 0.61 to 0.90]).
Dementia diagnoses were based on Medicare claims, and participants generally were non-Hispanic white, healthy, and well-educated and had access to preventive health care. This study evaluated fitness levels, so a specific exercise prescription cannot be generated from results and the findings may not be causal.
Higher midlife fitness levels seem to be associated with lower hazards of developing all-cause dementia later in life. The magnitude and direction of the association were similar with or without previous stroke, suggesting that higher fitness levels earlier in life may lower risk for dementia later in life, independent of cerebrovascular disease.
The Cooper Institute; University of Texas Southwestern Medical Center; National Heart, Lung, and Blood Institute; and American Heart Association.
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Dementia, Geriatric Medicine, Neurology, Prevention/Screening.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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