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      Metabolic Syndrome Over 10 Years and Cognitive Functioning in Late Midlife : The Whitehall II study

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          Abstract

          OBJECTIVE

          Evidence that the metabolic syndrome is a risk factor for poor cognition is mixed and is focused mainly on the elderly population; rarely is an adjustment made for socioeconomic factors. We examined this association in late midlife, with particular focus on cumulative effects and the role of socioeconomic circumstances.

          RESEARCH DESIGN AND METHODS

          Analyses were performed for 4,150 white participants from the Whitehall II study. Metabolic syndrome, using the National Cholesterol Education Program Adult Treatment Panel III criteria, was assessed three times over the 10-year follow-up (1991–2001). Cognitive function was assessed using a battery of six tests at the end of the follow-up.

          RESULTS

          After adjustment for demographic variables, health behaviors, and health status, participants with persistent metabolic syndrome (at least two of the three screenings) over the 10-year follow-up had lower cognitive performance than participants who never had metabolic syndrome. No significant differences in cognitive function were observed between participants with nonpersistent metabolic syndrome (one of the three screenings) and those who never had metabolic syndrome during the follow-up. Adjustment for adult occupational position attenuated this association by between 41 and 86%, depending on the measure of cognitive function. Adjustment for education had little effect.

          CONCLUSIONS

          Only persistent metabolic syndrome was associated with lower cognitive performance in late midlife. Adult occupational position but not education had a substantial impact on this association; these results highlight the importance of adult socioeconomic circumstances in identifying and targeting risk factors for cognitive aging.

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          Most cited references15

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          The metabolic syndrome, inflammation, and risk of cognitive decline.

          Several studies have reported an association between the metabolic syndrome and cardiovascular disease. Despite an increasing awareness that cardiovascular risk factors increase risk of cognitive decline and dementia, there are few data on the metabolic syndrome and cognition. To determine if the metabolic syndrome is a risk factor for cognitive decline and if this association is modified by inflammation. A 5-year prospective observational study conducted from 1997 to 2002 at community clinics at 2 sites. A total of 2632 black and white elders (mean age, 74 years). Association of the metabolic syndrome (measured using National Cholesterol Education Program guidelines) and high inflammation (defined as above median serum level of interleukin 6 and C-reactive protein) with change in cognition (Modified Mini-Mental State Examination [3MS]) at 3 and 5 years. Cognitive impairment was defined as at least a 5-point decline. Compared with those without the metabolic syndrome (n = 1616), elders with the metabolic syndrome (n = 1016) were more likely to have cognitive impairment (26% vs 21%, multivariate adjusted relative risk [RR], 1.20; 95% confidence interval [CI], 1.02-1.41). There was a statistically significant interaction with inflammation and the metabolic syndrome (P = .03) on cognitive impairment. After stratifying for inflammation, those with the metabolic syndrome and high inflammation (n = 348) had an increased likelihood of cognitive impairment compared with those without the metabolic syndrome (multivariate adjusted RR, 1.66; 95% CI, 1.19-2.32). Those with the metabolic syndrome and low inflammation (n = 668) did not exhibit an increased likelihood of impairment (multivariate adjusted RR, 1.08; 95% CI, 0.89-1.30). Stratified multivariate random-effects models demonstrated that participants with the metabolic syndrome and high inflammation had greater 4-year decline on 3MS (P = .04) compared with those without the metabolic syndrome, whereas those with the metabolic syndrome and low inflammation did not (P = .44). These findings support the hypothesis that the metabolic syndrome contributes to cognitive impairment in elders, but primarily in those with high level of inflammation.
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            Influence of education and occupation on the incidence of Alzheimer's disease.

            Several cross-sectional studies have found an association between Alzheimer's disease (AD) and limited educational experience. It has been difficult to establish whether educational experience is a risk factor for AD because educational attainment can influence performance on diagnostic tests. This study was designed to determine whether limited educational level and occupational attainment are risk factors for incident dementia. Cohort incidence study. General community. A total of 593 nondemented individuals aged 60 years or older who were listed in a registry of individuals at risk for dementia in North Manhattan, NY, were identified and followed up. We reexamined subjects 1 to 4 years later with the identical standardized neurological and neuropsychological measures. Incident dementia. We used Cox proportional hazards models, adjusting for age and gender, to estimate the relative risk (RR) of incident dementia associated with low educational and occupational attainment. Of the 593 subjects, 106 became demented; all but five of these met research criteria for AD. The risk of dementia was increased in subjects with either low education (RR, 2.02; 95% confidence interval [Cl], 1.33 to 3.06) or low lifetime occupational attainment (RR, 2.25; 95% Cl, 1.32 to 3.84). Risk was greatest for subjects with both low education and low life-time occupational attainment (RR, 2.87; 95% Cl, 1.32 to 3.84). The data suggest that increased educational and occupational attainment may reduce the risk of incident AD, either by decreasing ease of clinical detection of AD or by imparting a reserve that delays the onset of clinical manifestations.
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              Metabolic Syndrome and Risk for Incident Alzheimer's Disease or Vascular Dementia

              OBJECTIVE—Associations between metabolic syndrome and its individual components with risk of incident dementia and its different subtypes are inconsistent. RESEARCH DESIGN AND METHODS—The 7,087 community-dwelling subjects aged ≥65 years were recruited from the French Three-City (3C) cohort. Hazard ratios (over 4 years) of incident dementia and its subtypes (vascular dementia and Alzheimer's disease) and association with metabolic syndrome (defined according to the National Cholesterol Education Program Adult Treatment Panel III criteria) and its individual components (hypertension, large waist circumference, high triglycerides, low HDL cholesterol, and elevated fasting glycemia) were estimated in separate Cox proportional hazard models. RESULTS—Metabolic syndrome was present in 15.8% of the study participants. The presence of metabolic syndrome increased the risk of incident vascular dementia but not Alzheimer's disease over 4 years, independent of sociodemographic characteristics and the apolipoprotein (apo) Eɛ4 allele. High triglyceride level was the only component of metabolic syndrome that was significantly associated with the incidence of all-cause (hazard ratio 1.45 [95% CI 1.05–2.00]; P = 0.02) and vascular (2.27 [1.16–4.42]; P = 0.02) dementia, even after adjustment of the apoE genotype. Diabetes, but not impaired fasting glycemia, was significantly associated with all-cause (1.58 [1.05–2.38]; P = 0.03) and vascular (2.53 [1.15–5.66]; P = 0.03) dementia. CONCLUSIONS—The observed relation between high triglycerides, diabetes, and vascular dementia emphasizes the need for detection and treatment of vascular risk factors in older individuals in order to prevent the likelihood of clinical dementia.
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                Author and article information

                Journal
                Diabetes Care
                diacare
                dcare
                Diabetes Care
                Diabetes Care
                American Diabetes Association
                0149-5992
                1935-5548
                January 2010
                16 October 2009
                : 33
                : 1
                : 84-89
                Affiliations
                [1] 1Department of Epidemiology and Public Health, University College London, London, U.K.;
                [2] 2INSERM U 888 and University Montpellier 1, Montpellier, France;
                [3] 3Department of Medicine, Semmelweis University Faculty of Medicine, Budapest, Hungary;
                [4] 4Department of Psychology, University of Helsinki, Helsinki, Finland;
                [5] 5Finnish Institute of Occupational Health, Helsinki, Finland;
                [6] 6INSERM U687 and Centre de Gérontologie, Hôpital Ste Périne, Assistance Publique-Hôpitaux de Paris, Paris, France.
                Author notes
                Corresponding author: Tasnime N. Akbaraly, tasnime.akbaraly@ 123456inserm.fr .
                Article
                1218
                10.2337/dc09-1218
                2797991
                19837794
                2e54f5c5-7345-423a-9479-d33214318fa5
                © 2010 by the American Diabetes Association.

                Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

                History
                : 3 July 2009
                : 7 October 2009
                Categories
                Original Research
                Epidemiology/Health Services Research

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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