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      Longitudinal Examination of Obesity and Cognitive Function: Results from the Baltimore Longitudinal Study of Aging

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          Abstract

          Background: Obesity indices (i.e. BMI, waist-to-hip ratio) show differential relationships to other health outcomes, though their association to neurocognitive outcome is unclear. Methods: We examined whether central obesity would be more closely associated with cognitive function in 1,703 participants from the Baltimore Longitudinal Study of Aging. Results: Longitudinal mixed-effects regression models showed multiple obesity indices were associated with poorer performance in a variety of cognitive domains, including global screening measures, memory, and verbal fluency tasks. Obesity was associated with better performance on tests of attention and visuospatial ability. An obesity index by age interaction emerged in multiple domains, including memory and attention/executive function. Conclusion: Obesity indices showed similar associations to cognitive function, and further work is needed to clarify the physiological mechanisms that link obesity to poor neurocognitive outcome.

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          Most cited references35

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          Excess deaths associated with underweight, overweight, and obesity.

          As the prevalence of obesity increases in the United States, concern over the association of body weight with excess mortality has also increased. To estimate deaths associated with underweight (body mass index [BMI] or =30) in the United States in 2000. We estimated relative risks of mortality associated with different levels of BMI (calculated as weight in kilograms divided by the square of height in meters) from the nationally representative National Health and Nutrition Examination Survey (NHANES) I (1971-1975) and NHANES II (1976-1980), with follow-up through 1992, and from NHANES III (1988-1994), with follow-up through 2000. These relative risks were applied to the distribution of BMI and other covariates from NHANES 1999-2002 to estimate attributable fractions and number of excess deaths, adjusted for confounding factors and for effect modification by age. Number of excess deaths in 2000 associated with given BMI levels. Relative to the normal weight category (BMI 18.5 to or =30) was associated with 111,909 excess deaths (95% confidence interval [CI], 53,754-170,064) and underweight with 33,746 excess deaths (95% CI, 15,726-51,766). Overweight was not associated with excess mortality (-86,094 deaths; 95% CI, -161,223 to -10,966). The relative risks of mortality associated with obesity were lower in NHANES II and NHANES III than in NHANES I. Underweight and obesity, particularly higher levels of obesity, were associated with increased mortality relative to the normal weight category. The impact of obesity on mortality may have decreased over time, perhaps because of improvements in public health and medical care. These findings are consistent with the increases in life expectancy in the United States and the declining mortality rates from ischemic heart disease.
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            An 18-year follow-up of overweight and risk of Alzheimer disease.

            Overweight and obesity are epidemic in Western societies and constitute a major public health problem because of adverse effects on vascular health. Vascular factors may play a role in the development of a rapidly growing disease of late life, Alzheimer disease (AD). Using body mass index (BMI, calculated as weight in kilograms divided by the square of height in meters), we examined whether overweight is a risk factor for dementia and AD. The relationship between BMI and dementia risk was investigated in a representative cohort of 392 nondemented Swedish adults who were followed up from age 70 to 88 years, with the use of neuropsychiatric, anthropometric, and other measurements. Multivariate Cox proportional hazards regression analyses included BMI, blood pressure, cardiovascular disease, cigarette smoking, socioeconomic status, and treatment for hypertension. During the 18-year follow-up (4184.8 risk-years), 93 participants were diagnosed as having dementia. Women who developed dementia between ages 79 and 88 years were overweight, with a higher average BMI at age 70 years (27.7 vs 25.7; P =.007), 75 years (27.9 vs 25.0; P<.001), and 79 years (26.9 vs 25.1; P =.02) compared with nondemented women. A higher degree of overweight was observed in women who developed AD at 70 years (29.3; P =.009), 75 years (29.6; P<.001), and 79 years (28.2; P =.003) compared with nondemented women. For every 1.0 increase in BMI at age 70 years, AD risk increased by 36%. These associations were not found in men. Overweight is epidemic in Western societies. Our data suggest that overweight at high ages is a risk factor for dementia, particularly AD, in women. This may have profound implications for dementia prevention.
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              Elevated body mass index is associated with executive dysfunction in otherwise healthy adults.

              There is growing evidence that obesity is linked to adverse neurocognitive outcome, including reduced cognitive functioning and Alzheimer disease. However, no study to date has determined whether the relationship between body mass index (BMI) and cognitive performance varies as a function of age. We examined attention and executive function in a cross-section of 408 healthy persons across the adult life span (20-82 years). Bivariate correlation showed that BMI was inversely related to performance on all cognitive tests. After controlling for possible confounding factors, overweight and obese adults (BMI > 25) exhibited poorer executive function test performance than normal weight adults (BMI, 18.5-24.9). No differences emerged in attention test performance, and there was no evidence of a BMI x age interaction for either cognitive domain. These results provide further evidence for the relationship between elevated BMI and reduced cognitive performance and suggest that this relationship does not vary with age. Further research is needed to identify the etiology of these deficits and whether they resolve after weight loss.
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                Author and article information

                Journal
                NED
                Neuroepidemiology
                10.1159/issn.0251-5350
                Neuroepidemiology
                S. Karger AG
                0251-5350
                1423-0208
                2010
                May 2010
                18 March 2010
                : 34
                : 4
                : 222-229
                Affiliations
                aDepartment of Psychology, Kent State University, Kent, Ohio, bDepartment of Psychiatry, Summa Health System, Akron, Ohio, cLaboratory of Personality and Cognition and dClinical Research Branch, National Institute on Aging, National Institutes of Health, Bethesda, Md., USA
                Article
                297742 PMC2883839 Neuroepidemiology 2010;34:222–229
                10.1159/000297742
                PMC2883839
                20299802
                ea644fc4-7f00-4a9a-aaf1-e16deebab05f
                © 2010 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 17 May 2009
                : 08 January 2010
                Page count
                Figures: 1, Tables: 5, References: 55, Pages: 8
                Categories
                Original Paper

                Geriatric medicine,Neurology,Cardiovascular Medicine,Neurosciences,Clinical Psychology & Psychiatry,Public health
                Longitudinal,Age-associated cognitive change,Cognition,Aged,Obesity

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