Sokratis Charisis1, Eva Ntanasi1, Mary Yannakoulia1, Costas A Anastasiou1, Mary H Kosmidis1, Efthimios Dardiotis1, Antonios N Gargalionis1, Kostas Patas1, Stylianos Chatzipanagiotou1, Ioannis Mourtzinos1, Katerina Tzima1, Georgios Hadjigeorgiou1, Paraskevi Sakka1, Dimitrios Kapogiannis1, Nikolaos Scarmeas2. 1. From the 1st Department of Neurology (S.C., E.N., N.S.) and Department of Medical Biopathology and Clinical Microbiology (A.N.G., K.P., S.C.), Aiginition Hospital, National and Kapodistrian University of Athens Medical School, Greece; Department of Neurology (S.C.), University of Texas Health Science Center at San Antonio; Department of Nutrition and Dietetics (E.N., M.Y., C.A.A.), Harokopio University, Athens; Lab of Cognitive Neuroscience (M.H.K.), School of Psychology, and Department of Food Science and Technology (I.M.), Faculty of Agriculture, Aristotle University of Thessaloniki; School of Medicine (E.D.), University of Thessaly, Larissa, Greece; Department of Food BioSciences (K.T.), Teagasc Food Research Centre Ashtown, Dublin, Ireland; Department of Neurology (G.H.), Medical School, University of Cyprus; Athens Association of Alzheimer's Disease and Related Disorders (P.S.), Greece; National Institute on Aging/NIH (D.K.), Baltimore, MD; and Taub Institute for Research in Alzheimer's Disease and the Aging Brain (N.S.), Gertrude H. Sergievsky Center, Department of Neurology, Columbia University, New York, NY. 2. From the 1st Department of Neurology (S.C., E.N., N.S.) and Department of Medical Biopathology and Clinical Microbiology (A.N.G., K.P., S.C.), Aiginition Hospital, National and Kapodistrian University of Athens Medical School, Greece; Department of Neurology (S.C.), University of Texas Health Science Center at San Antonio; Department of Nutrition and Dietetics (E.N., M.Y., C.A.A.), Harokopio University, Athens; Lab of Cognitive Neuroscience (M.H.K.), School of Psychology, and Department of Food Science and Technology (I.M.), Faculty of Agriculture, Aristotle University of Thessaloniki; School of Medicine (E.D.), University of Thessaly, Larissa, Greece; Department of Food BioSciences (K.T.), Teagasc Food Research Centre Ashtown, Dublin, Ireland; Department of Neurology (G.H.), Medical School, University of Cyprus; Athens Association of Alzheimer's Disease and Related Disorders (P.S.), Greece; National Institute on Aging/NIH (D.K.), Baltimore, MD; and Taub Institute for Research in Alzheimer's Disease and the Aging Brain (N.S.), Gertrude H. Sergievsky Center, Department of Neurology, Columbia University, New York, NY. ns257@columbia.edu.
Abstract
BACKGROUND AND OBJECTIVES: Aging is characterized by a functional shift of the immune system toward a proinflammatory phenotype. This derangement has been associated with cognitive decline and has been implicated in the pathogenesis of dementia. Diet can modulate systemic inflammation; thus, it may be a valuable tool to counteract the associated risk for cognitive impairment and dementia. The present study aimed to explore the associations between the inflammatory potential of diet, assessed with an easily applicable, population-based, biomarker-validated diet inflammatory index (DII), and the risk for dementia in community-dwelling older adults. METHODS: Individuals from the Hellenic Longitudinal Investigation of Aging and Diet (HELIAD) were included in the present cohort study. Participants were recruited through random population sampling and were followed up for a mean of 3.05 (standard deviation 0.85) years. Dementia diagnosis was based on standard clinical criteria. Those with baseline dementia or missing cognitive follow-up data were excluded from the analyses. The inflammatory potential of diet was assessed through a DII score that considers literature-derived associations of 45 food parameters with levels of proinflammatory and anti-inflammatory cytokines in the blood; higher values indicated a more proinflammatory diet. Consumption frequencies were derived from a detailed food frequency questionnaire and were standardized to representative dietary intake normative data from 11 different countries. Analysis of dementia incidence as a function of baseline DII scores was performed by Cox proportional hazards models. RESULTS: Analyses included 1,059 individuals (mean age 73.1 years, 40.3% male, mean education 8.2 years), 62 of whom developed incident dementia. Each additional unit of DII score was associated with a 21% increase in the risk for dementia incidence (hazard ratio 1.21 [95% confidence interval 1.03-1.42]; p = 0.023). Compared to participants in the lowest DII score tertile, participants in the highest one (maximal proinflammatory diet potential) were 3 (95% confidence interval 1.2-7.3; p = 0.014) times more likely to develop incident dementia. The test for trend was also significant, indicating a potential dose-response relationship (p = 0.014). DISCUSSION: In the present study, higher DII scores (indicating greater proinflammatory diet potential) were associated with an increased risk for incident dementia. These findings might avail the development of primary dementia preventive strategies through tailored and precise dietary interventions.
BACKGROUND AND OBJECTIVES: Aging is characterized by a functional shift of the immune system toward a proinflammatory phenotype. This derangement has been associated with cognitive decline and has been implicated in the pathogenesis of dementia. Diet can modulate systemic inflammation; thus, it may be a valuable tool to counteract the associated risk for cognitive impairment and dementia. The present study aimed to explore the associations between the inflammatory potential of diet, assessed with an easily applicable, population-based, biomarker-validated diet inflammatory index (DII), and the risk for dementia in community-dwelling older adults. METHODS: Individuals from the Hellenic Longitudinal Investigation of Aging and Diet (HELIAD) were included in the present cohort study. Participants were recruited through random population sampling and were followed up for a mean of 3.05 (standard deviation 0.85) years. Dementia diagnosis was based on standard clinical criteria. Those with baseline dementia or missing cognitive follow-up data were excluded from the analyses. The inflammatory potential of diet was assessed through a DII score that considers literature-derived associations of 45 food parameters with levels of proinflammatory and anti-inflammatory cytokines in the blood; higher values indicated a more proinflammatory diet. Consumption frequencies were derived from a detailed food frequency questionnaire and were standardized to representative dietary intake normative data from 11 different countries. Analysis of dementia incidence as a function of baseline DII scores was performed by Cox proportional hazards models. RESULTS: Analyses included 1,059 individuals (mean age 73.1 years, 40.3% male, mean education 8.2 years), 62 of whom developed incident dementia. Each additional unit of DII score was associated with a 21% increase in the risk for dementia incidence (hazard ratio 1.21 [95% confidence interval 1.03-1.42]; p = 0.023). Compared to participants in the lowest DII score tertile, participants in the highest one (maximal proinflammatory diet potential) were 3 (95% confidence interval 1.2-7.3; p = 0.014) times more likely to develop incident dementia. The test for trend was also significant, indicating a potential dose-response relationship (p = 0.014). DISCUSSION: In the present study, higher DII scores (indicating greater proinflammatory diet potential) were associated with an increased risk for incident dementia. These findings might avail the development of primary dementia preventive strategies through tailored and precise dietary interventions.
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