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Try out PMC Labs and tell us what you think. Learn More. We examined whether obesity at ages 50, 60, and 70 years is associated with subsequent dementia. Changes in body mass index BMI for more than 28 years before dementia diagnosis were compared with Free sex texting in Whitehall in BMI in those free of dementia.

BMI was assessed six times and cases of dementia were recorded. Obesity in midlife and weight loss in the preclinical phase characterizes dementia; the current obesity epidemic may affect future dementia rates. Prospective studies, particularly those with extended follow-up [1]suggest midlife obesity is a risk factor for dementia [2][3][4][5].

Meta-analyses and systematic reviews show the excess risk to be similar for Alzheimer's disease and all-cause dementia [6][7][8]with effects being stronger in studies with a follow-up longer than 10 years, and when body mass index BMI is assessed before age 60 years [6].

The hypothesis that midlife obesity increases risk for dementia has been challenged by two sets of recent findings. The first using electronic patient records from 2 million adults showed lower rates of dementia in the obese and progressively decreasing risk with increasing obesity [9]. As meta-analyses suggesting midlife obesity to be a risk factor for dementia are based on less than 50, persons overall [2][6][7]inclusion of this new study in future meta-analyses would undoubtedly change conclusions. The second set of studies was based on a Mendelian randomization MR approach, which uses genetic variants as proxies for exposures, to show no association between obesity and dementia [10][11].

These findings taken together raise questions about the inclusion of midlife obesity in guidelines for dementia prevention, such as the one published last year [12]. BMI in older adults with dementia is typically lower than age peers, with weight loss starting 10 years or more before clinical onset [13]. Pathophysiological processes underlying dementia are known to span several years, perhaps decades [14][15]and may lead to weight loss before disease onset [16].

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However, the BMI trajectory in those with dementia remains poorly characterized. The few studies with repeat BMI data over the adult life course show those with dementia to gain less weight [17]or experience accelerated weight loss in old age [13][18]but no differences in BMI in midlife. The inconsistencies are likely to be because of the analysis of change in BMI being anchored by wave of BMI assessment rather than the etiologic stage of dementia. We use an innovative analytic approach with two objectives. First, to understand when in midlife obesity carries risk for dementia, we model the risk associated with obesity at ages 50, 60, and 70 years.

Our method allows better insight into the manner in which age modifies the association between obesity and dementia. Second, to study changes in BMI, we use repeat data and model trajectories of BMI for more than 28 years, using a backward timescale anchored to the year of dementia diagnosis. This method allows BMI differences between dementia cases and those free of dementia to be estimated for each of the 28 years preceding dementia diagnosis. Analyses were repeated with waist circumference and waist-to-hip ratio to determine whether their associations with dementia are similar to that obtained for BMI.

The Whitehall II study is an ongoing cohort study of men and women originally employed by the British civil service in London-based offices [19].

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Since the baseline medical examination, follow-up examinations have taken place approximately every 5 years. Weight was measured in underwear to the nearest 0. Height was measured in bare feet to the nearest 1 mm using a stadiometer with the participant standing erect with head in the Frankfurt plane. Waist and hip circumferences, starting at the to assessment, were measured with subjects in the standing position in light clothing, using a fiberglass tape measure at g tension. Waist circumference was taken as the smallest circumference at or below the costal margin and hip circumference at the level of the greater trochanter.

We used comprehensive tracing of electronic health records for dementia ascertainment using three databases: the national hospital episode statistics database, the Mental Health Services Data Set, and the national mortality register. The National Health Service provides most of the health care; hospital episode statistics and Mental Health Services Data Set are national databases with information on both inpatient and outpatient care, with the latter also including data on care in the community.

Record linkage until March 31, identified cases of dementia, cases were first recorded in the hospitalization register, in the mental health register, and eight in the mortality register. The validity of dementia cases in our study is supported by modeling changes in the global cognitive score, composed of tests of memory, reasoning, and phonemic and semantic fluency administered to the participants in,and [23]. These show accelerated decline in global cognitive score in the 8 to 10 years before dementia diagnosis Supplementary Fig.

Free sex texting in Whitehall was reported by the participant as the highest level of education achieved and regrouped into five standard hierarchic levels: no formal education, lower secondary education, higher secondary education, university degree, and higher university degree. Cardiovascular disease CVDdiabetes, and medication : ascertainment of these conditions was based on two methods: study specific assessments,, and and linkage to electronic health records for nonresponders and chronic conditions occurring between study waves.

A lead resting electrocardiogram recording, coded using the Minnesota system, was used for coronary heart disease. Medication for CVD was reported by the participants at each wave. We undertook two sets of analyses; first, Cox regression to examine associations of adiposity measures at ages 50, 60, and 70 years three separate models with subsequent dementia. Analyses were based on all participants with data on obesity, follow-up for dementia commencing on the date of the obesity measure.

Second, we compared changes in BMI trajectories in those with dementia with other participants using a backward timescale. Age ranges of the participants at the six clinical evaluations between to and to were 35 to 55, 40 to 64, 45 to 69, 50 to 74, 55 to 79, and 60 to 84 years. We extracted data on adiposity measures at ages 50, 60, and 70 years for each participant across the data waves. The analyses were first run with dementia as an outcome and repeated with mortality; both using Cox regression with date of entry being the date of clinical assessment from which the obesity measure separate models for age 50, 60, and 70 years was drawn.

In the analysis for dementia, those who died free of dementia were censored at death so that participants were followed until the record of dementia, death, or March 31,whichever came first. For analysis of mortality, they were followed until the record of death or March 31,whichever came first. All analyses were adjusted for age, sex, and education. In Supplementary Tables, we show analyses with further adjustment for diabetes, CVD, and medication for these conditions.

Trajectories of BMI for more than 28 years were modeled using a backward timescale such that year 0 was year of dementia for dementia cases, year of death for those who died during the follow-up, and March 31, end of follow-up for all others. Dementia coded as 1 for cases and 0 for others and its interaction with time and time squared to allow for nonlinear change were Free sex texting in Whitehall to the model to test for differences in BMI trajectories between cases and others.

The slope terms time and time squared allow the assessment of changes in BMI for more than the 28 years. Analyses were adjusted for age, sex, education, their interactions with time and time squared, and for 5-year birth cohort to take cohort effects into.

These analyses on BMI trajectories anchored to the year of dementia diagnosis were repeated using a case-control approach to for period effects in measures of BMI and dementia. Year 0 for both cases and control subjects was the year of dementia diagnosis. Each case was individually matched to six control subjects drawn randomly from the study population using the following criteria: age 5-year age group at the index yearsex, education university degree or notbeing alive at year 0, and without a diagnosis of dementia at the end of follow-up.

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The case-control analyses were also undertaken for waist circumference and waist-to-hip ratio on the same cases and control subjects, albeit with a shorter follow-up of 22 years. The software SAS 9. Increasing age hazard ratio [HR] for 1 year greater age at study baseline associated with a 1.

Table 1 presents study characteristics as a function of dementia status in the total population and in cases and control subjects. A total of Analyses of waist circumference and waist-to-hip ratio are shown in Supplementary Tables 2 and 3 in the minimally and fully adjusted models. Theseusing a backward timescale, showed that those with dementia had higher BMI in midlife and accelerated decline in the decade before dementia diagnosis. Analyses with the backward timescale were repeated using a case-control de Fig.

Trajectories of BMI in the 28 years before dementia. Mean of observations per participant is 3. Trajectories of waist circumference A and waist-to-hip ratio B in the 22 years before dementia.

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Note: 1 The figure represents marginal effects of dementia on trajectories of waist circumference and waist-to-hip ratio, adjusted for age, sex, and education. Mean of observations per participant is 2. This association was greatly attenuated when BMI was assessed at ages 60 and 70 years. These findings were corroborated in analysis of trajectories where BMI differences between those with dementia and those free of dementia were examined for each of the 28 years preceding dementia diagnosis.

Taken together, the present data demonstrate that the association between obesity and dementia is modified by age at obesity measurement, such that midlife obesity is a risk factor for dementia but BMI begins to decline in those with dementia in the years before diagnosis. Data from several studies show increased dementia risk with midlife obesity [1][3][4][25][26][27][28][29]these are reflected in conclusions of meta-analyses [2][6][7]. As the reported analyses were based on only a third of the eligible sample because of missing data on BMI, selection bias is likely to affect.

Furthermore, a follow-up of less than 10 years is perhaps too short a period to remove effects of preclinical dementia, given that changes underlying dementia are known to unfold over many years [15]. In our data, use of a backward timescale on all participants shows the BMI trajectories to intersect 12 years before the diagnosis of dementia, this was reduced to 8 years in analysis using a case-control de, which adjusted for covariates better and took period effects into.

The risk of dementia associated with obesity at older ages is either attenuated or reversed [30]. A combination of predementia apathy, loss of initiative, and reduced olfactory function could explain this association [13]. As evidence of the risk associated with high BMI in midlife and low BMI at older ages comes from separate data sets, the findings on BMI have been interpreted as being conflicting or inconsistent.

At least two studies used two BMI assessments, one in midlife and the second at older ages [28][29]and both show higher BMI in midlife and lower BMI in late life to carry risk for dementia. Our study is the first to model BMI trajectories for more than nearly three decades before dementia using an analytic strategy anchored to the etiology of disease. The advantage of this method is that the timescale used in the analysis is years before dementia diagnosis rather than age which can vary between individuals for dementia onset or data collection cycle which conflates the effects of age and stage of Free sex texting in Whitehall.

Two recent MR studies, using overlapping data on older adults [11][33]showed no association between obesity and dementia.

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These studies might be affected by selective BMI-related survival [33]. The AD Genetics Consortium, which contributed the bulk of cases and control subjects to both articles, is based on cases where the mean age of dementia onset was The exact mechanisms explaining the increased risk of dementia associated with obesity are poorly understood. Obesity in midlife [35] and at older ages [36] is associated with brain atrophy. There is also evidence suggesting a variant of the fat mass and obesity-associated FTO gene affects brain structure, causing deficits in the frontal and occipital lobes [37][38].

Obesity is also likely to influence cognition through its impact on vascular risk factors and pathology, and some authors have highlighted the role of adipocyte hormones and cytokines [16].

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Genome-wide association studies, in turn, show genetic risk variants that influence vascular and inflammatory pathways to be associated with dementia [39][40]. Potential avenues of further research include brain atrophy, disruption in cerebrovascular function, development of amyloid pathology, breakdown in the blood-brain barrier, and systemic and neuroinflammation. The major strength of our study is the use of BMI data covering a period of 28 years, which allowed us to assess both the risk associated with obesity at specific ages and model trajectories of BMI for more than 28 years before dementia onset.

Our use of both BMI and other indices of adiposity at specific ages and their trajectories over the adult life course allow the natural history of this relationship to be established. The case-control de analysis strategy ensured a better control for period effects the effects of calendar time on dementia diagnosis or adiposity and confounders age, sex, and education. The use of three markers of obesity also allows us to conclude that BMI, the most widely used measure because of ease of data collection, is suitable for the assessment of risk of dementia and death.

A key limitation of our study is underascertainment of dementia because of use of linkage to electronic health records. A similar pattern is likely in our study because of universal health coverage in the UK, where electronic health records have been shown to be reliable for dementia [42]. There was no evidence in our Free sex texting in Whitehall that BMI affected age of dementia diagnosis.

In analyses on BMI at 50 years the age of dementia diagnosis was Thus, any misclassification of dementia status is likely to be random, that is, the probability of dementia status being misclassified is independent of BMI. This means that under conditions of high specificity, Free sex texting in Whitehall association between risk factor and outcome is unlikely to be biased by underascertainment of the outcome [43].

Furthermore, consistency in between the survival analysis and that using trajectories of adiposity markers suggests that these are also robust to nonrandom misclassification. The advantage of our passive case finding approach is that dementia status was available on all participants and not only on those who continued to participate in the study over the follow-up, thus increasing the generalizability of findings. We were unable to examine the sub of dementia because of small s but reports show similar findings for the association of obesity with dementia subtypes [4][18][27][28][31].

Finally, the prevalence of obesity was relatively low in this cohort and it was not possible to undertake detailed analyses stratified by degrees of obesity; for example, only 2. Our findings have important implications. Considerable improvements in cardiovascular health and education over the second half of the last century are suggested to be responsible for the leveling of the incidence rates of dementia [44]. In the past 40 years, however, there has been a startling increase in the of obese persons, rising from million in to million in Our suggest midlife obesity is a risk factor for dementia, and the extent to which the continuing obesity epidemic will create a surge in future dementia rates is an important public health issue.

Systematic review. We searched PubMed, to identify the scientific literature on the association between obesity and dementia. However, a publication on 2 million adults showed lower dementia risk in the obese, with the risk decreasing with increasing obesity. Obesity at age 50 years but not at ages 60 and 70 years was associated with increased risk of dementia. Natural history of body mass index BMIanchored to dementia diagnosis such that changes in BMI were modeled over 28 years preceding dementia diagnosis, shows obesity in midlife and weight loss in the preclinical phase to characterize BMI changes in those with dementia.

Future directions. Obesity in midlife carries risk for dementia; not ing for the preclinical phase explains inconsistency in from studies. Our highlight the importance of the analytic framework used to identify putative risk factors for dementia. The ongoing obesity epidemic may well impact dementia incidence in the future. The authors thank all the participating civil service departments and their welfare, personnel, and establishment officers; the British Occupational Health and Safety Agency; the British Council of Civil Service Unions; all participating civil servants in the Whitehall II Study; and all members of the Whitehall II Study team.

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The Whitehall II Study team comprised research scientists, statisticians, study coordinators, nurses, data managers, administrative assistants, and data entry staff, who made the study possible. Conflicts of interest: The authors have no conflicts of interest to declare.

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email: [email protected] - phone:(247) 725-4970 x 2690

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