ECE2018 Poster Presentations: Diabetes, Obesity and Metabolism Obesity (78 abstracts)
Obesity and dementia: the misleading “obesity paradox”
Adriana Pané 1 , Jordi Pegueroles 2, , Sabina Ruiz 1 , Laura Videla 2, , Maria Carmona-Iragui 2, , Eduard Vilaplana 2, , Victor Montal 2, , Anna Casajoana 5 , Josep Vidal 1, , Juan Fortea 2, & Amanda Jiménez 1,
1Endocrinology Department, Obesity Unit of Hospital Clínic, Barcelona, Spain; 2Department of Neurology, Memory Unit. Hospital de la Santa Creu i Sant Pau, Barcelona, Spain; 3Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastián, Spain; 4Barcelona Down Medical Center, Barcelona, Spain; 5General Surgery Service, Hospital de Barcelona-SCIAS, Barcelona, Spain; 6Institut d’Investigacions Biomèdiques August Pi Sunyer, Barcelona, Spain; 7Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain.
Background: Mid-life obesity is a risk factor for Alzheimer’s disease (AD). On the contrary, late-life obesity has been identified as a protective factor for dementia. Recent published studies have shown that weight loss predicts and precedes dementia diagnosis by decades. Thus, paradoxical effect of body weight across lifespan, the so called “obesity paradox”, might be explained by reverse causality. Structural magnetic resonance imaging (MRI) has been extensively used to characterize healthy and pathological aging. Establishing the relationship between BMI and brain structural changes would help to better understand the effects of adiposity on the brain.
Objectives: We aimed to assess the association between late-life obesity and brain structure considering the potential confounding effect of weight loss.
Methods: We included 131 cognitively normal elderly subjects (mean age: 73.4±6.2 years) with available 3T MRI scan from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohort. Significant weight loss was defined as relative weight loss ≥5% of baseline weight. We compared the cross-sectional cortical thickness (CTh) related to the BMI in (1) all the cohort and (2) after the exclusion of individuals with significant weight loss. CTh was extracted using Free Surfer Software. All analysis were adjusted by potential confounders (age, sex and APOE genotype).
Results: After a mean follow-up of 50.5±30.5 months, 31 (23.6%) subjects experienced significant weight loss (FWE<0.05). At baseline, these individuals presented decreased CTh in temporal regions of the right hemisphere (FWE<0.05). When the whole cohort was included in the analysis, there was a weak, although significant, lineal correlation between BMI and cortical thinning. This association was restricted to the occipital region (FWE<0.05). Results significantly changed after having excluded the subjects with weight loss. In this context, several clusters of linear association emerged in widespread areas of both hemispheres including occipital, temporal and frontal regions (FWE<0.05).
Conclusions: Late-life unintentional weight loss is related to cortical thinning. Similarly, late-life obesity is associated with cortical thinning. However, weight loss negatively confounds this association.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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