Association between late-life body mass index and dementia The Kame Project

Department of Psychiatry, University of Pittsburgh, PA 15213, USA.
Neurology (Impact Factor: 8.29). 06/2009; 72(20):1741-6. DOI: 10.1212/WNL.0b013e3181a60a58
Source: PubMed


To examine the association between body mass index (BMI), waist circumference (WC), and waist-to-hip ratio (WHR) and risk of dementia and its subtypes in late life.
Participants were members of the Kame Project, a population-based prospective cohort study of 1,836 Japanese Americans living in King County, WA, who had a mean age of 71.8 years and were dementia-free at baseline (1992-1994), and were followed for incident dementia through 2001. Cox proportional hazards models were used to estimate the risk of dementia, Alzheimer disease (AD), and vascular dementia (VaD) controlling for demographic and lifestyle characteristics and vascular comorbidities as a function of baseline BMI, WC, and WHR and change in BMI over time.
Higher baseline BMI was significantly associated with a reduced risk of AD (hazard ratio [HR] = 0.56, 95% confidence interval [CI] = 0.33-0.97) in the fully adjusted model. Slower rate of decline in BMI was associated with a reduced risk of dementia (HR = 0.37, 95% CI = 0.14-0.98), with the association stronger for those who were overweight or obese (HR = 0.18, 95% CI = 0.05-0.58) compared to normal or underweight (HR = 1.00, 95% CI = 0.18-5.66) at baseline.
Higher baseline body mass index (BMI) and slower declining BMI in late life are associated with a reduced risk of dementia, suggesting that low BMI or a faster decline in BMI in late life may be preclinical indicators of an underlying dementing illness, especially for those who were initially overweight or obese.

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Available from: Amy R. Borenstein (Graves), Oct 07, 2015
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    • "Several epidemiologic studies also suggested that overweight and obesity in late life are associated with reduced risk for dementia [6] [7], whereas others have found that a higher BMI at older ages predicts dementia [8]. Because it is widely accepted that malnutrition and unintended weight loss not only occur MACM was involved in the conception and design of the study; generation, collection, assembly, analysis, and interpretation of data; and drafting of the manuscript. "
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    ABSTRACT: Objective: Although dementia and nutritional status have been shown to be strongly associated, differences in body composition (BC) among older people with dementia have not yet been firmly established. The aim of this study was to assess BC through conventional and vector bioimpedance analysis (BIA and BIVA, respectively) in a sample of institutionalized older men with and without dementia, in order to detect dementia-related BC changes. Methods: Forty-one institutionalized men ages ≥ 65 y (23 without dementia [CG] and 18 with dementia [DG]) were measured with BIA and interpreted with BIVA and predictive equations. Results: Age (74.4 and 75.7 y) and body mass index (22.5 and 23.6 kg/m(2)) were similar for DG and CG, respectively. Resistance and ratio of resistance to height did not differ significantly between the two groups. Reactance and ratio of reactance to height were 21.2% and 20.4% lower in DG than in CG. Phase angle was significantly lower in DG (mean = 4.0; 95% confidence interval [CI], 3.6°-4.3°) than in CG (mean = 4.7; 95% CI, 4.3°-5.1°). Mean fat mass index (6 and 7 kg/m(2)), and mean fat-free mass index (16.4 and 16.6 kg/m(2)) were similar in both groups. BIVA showed a significant downward migration of the ellipse in DG with respect to CG (T(2) = 15.1; P < 0.01). Conclusion: Conventional BIA showed no significant differences in BC between DG and CG, although reactance and ratio of reactance to height were about 21% lower in DG. Nevertheless, a body cell mass depletion and an increase in the ratio of extracellular to intracellular water were identified in DG using BIVA. BIVA reflects dementia-related changes in BC better than BIA.
    Nutrition 07/2014; 31(1). DOI:10.1016/j.nut.2014.06.006 · 2.93 Impact Factor
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    • "The observed risk reduction of late-life obesity on dementia is viewed controversially and should probably be regarded as an absence of weight loss. Weight loss in itself might be viewed as a marker of disease progression [Gustafson et al., 2003; Atti et al., 2008; Dahl et al., 2008; Sturman et al., 2008; Hughes et al., 2009; Coin et al., 2012]. A relationship between underweight in midlife and dementia risk has also been described [Chiang et al., 2007; Whitmer, 2007; Beydoun et al., 2008a,b; Chen et al., 2010], but not in all studies [Loef and Walach, 2013]. "
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    ABSTRACT: Deviations from normal body weight are observed prior to and after the onset of Alzheimer's disease (AD). Midlife obesity confers increased AD risk in later life, whereas late-life obesity is associated with decreased AD risk. The role of underweight and weight loss for AD risk is controversial. Based on the hypothesis of shared genetic variants for both obesity and AD, we analyzed the variants identified for AD or obesity from genome-wide association meta-analyses of the GERAD (AD, cases = 6,688, controls = 13,685) and GIANT (body mass index [BMI] as measure of obesity, n = 123,865) consortia. Our cross-disorder analysis of genome-wide significant 39 obesity SNPs and 23 AD SNPs in these two large data sets revealed that: (1) The AD SNP rs10838725 (pAD = 1.1 × 10−08) at the locus CELF1 is also genome-wide significant for obesity (pBMI = 7.35 × 10−09). (2) Four additional AD risk SNPs were nominally associated with obesity (rs17125944 at FERMT2, pBMI = 4.03 × 10−05, pBMI corr = 2.50 × 10−03; rs3851179 at PICALM; pBMI = 0.002, rs2075650 at TOMM40/APOE, pBMI = 0.024, rs3865444 at CD33, pBMI = 0.024). (3) SNPs at two of the obesity risk loci (rs4836133 downstream of ZNF608; pAD = 0.002 and at rs713586 downstream of RBJ/DNAJC27; pAD = 0.018) were nominally associated with AD risk. Additionally, among the SNPs used for confirmation in both studies the AD risk allele of rs1858973, with an AD association just below genome-wide significance (pAD = 7.20 × 10−07), was also associated with obesity (SNP at IQCK/GPRC5B; pBMI = 5.21 × 10−06; pcorr = 3.24 × 10−04). Our first GWAS based cross-disorder analysis for AD and obesity suggests that rs10838725 at the locus CELF1 might be relevant for both disorders. © 2014 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 06/2014; 165(4). DOI:10.1002/ajmg.b.32234 · 3.42 Impact Factor
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    • "A recent meta-analysis reported that, compared to normal weight, midlife obesity nearly doubles the risk of dementia later in life (Loef and Walach, 2013). Whereas obesity in midlife may confer an increased risk of later dementia, many studies have found an opposite effect in older adults (Atti et al., 2008; Chu et al., 2009; Dahl et al., 2008; Fitzpatrick et al., 2009; Hughes et al., 2009; West and Haan, 2009). Lower BMI has been associated with the development of Alzheimer's disease (Johnson et al., 2006) and a higher degree of AD pathology (Buchman et al., 2006). "
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    ABSTRACT: Cognitive decline in elderly people often derives from the interaction between aging-related changes and age-related diseases and covers a large spectrum of clinical manifestations, from intact cognition through mild cognitive impairment and dementia. Epidemiological evidence supports the hypothesis that modifiable lifestyle-related factors are associated with cognitive decline, opening new avenues for prevention. Diet in particular has become the object of intense research in relation to cognitive aging and neurodegenerative disease. We reviewed the most recent findings in this rapidly expanding field. Some nutrients, such as vitamins and fatty acids, have been studied longer than others, but strong scientific evidence of an association is lacking even for these compounds. Specific dietary patterns, like the Mediterranean diet, may be more beneficial than a high consumption of single nutrients or specific food items. A strong link between vascular risk factors and dementia has been shown, and the association of diet with several vascular and metabolic diseases is well known. Other plausible mechanisms underlying the relationship between diet and cognitive decline, such as inflammation and oxidative stress, have been established. In addition to the traditional etiological pathways, new hypotheses, such as the role of the intestinal microbiome in cognitive function, have been suggested and warrant further investigation.
    Mechanisms of ageing and development 12/2013; 136-137. DOI:10.1016/j.mad.2013.11.011 · 3.40 Impact Factor
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