Association of anthropometry and weight change with risk of dementia and its major subtypes : A meta-analysis consisting 2.8 million adults with 57 294 cases of dementia

Uncertainty exists regarding the relation of body size and weight change with dementia risk. As populations continue to age and the global obesity epidemic shows no sign of waning, reliable quantification of such associations is important. We examined the relationship of body mass index, waist circumference, and annual percent weight change with risk of dementia and its subtypes by pooling data from 19 prospective cohort studies and four clinical trials using meta-analysis. Compared with body mass index-defined lower-normal weight (18.5-22.4 kg/m(2)), the risk of all-cause dementia was higher among underweight individuals but lower among those with upper-normal (22.5-24.9 kg/m(2)) levels. Obesity was associated with higher risk in vascular dementia. Similarly, relative to the lowest fifth of waist circumference, those in the highest fifth had nonsignificant higher vascular dementia risk. Weight loss was associated with higher all-cause dementia risk relative to weight maintenance. Weight gain was weakly associated with higher vascular dementia risk. The relationship between body size, weight change, and dementia is complex and exhibits non-linear associations depending on dementia subtype under scrutiny. Weight loss was associated with an elevated risk most likely due to reverse causality and/or pathophysiological changes in the brain, although the latter remains speculative.Peer reviewe

Height, wealth, and health: an overview with new data from three longitudinal studies

This overview, based on a literature review and new data from the three cohorts (Whitehall Studies I and II, and the Vietnam Experience Study), has four objectives: (a) to outline the major determinants of height, so providing an indication as to what exposures this characteristic may capture; (b) to summarise, by reviewing reports from large scale studies, the relation between adult height and a range of disease outcomes - both somatic and psychiatric - with particular emphasis on coronary heart disease (CHD) and stroke; (c) to discuss why these relationships may exist, in particular, the role, if any, of socioeconomic position in explaining the apparent associations; and, finally (d) to outline future research directions in this field. The large majority of evidence for predictors of height, and its health consequences, comes from observational studies. While genetic predisposition is a major determinant of height, secular rises in childhood and adult stature across successive birth cohorts suggest that early life environment also has an important impact. Plausible non-genetic determinants of height include nutrition, illness, socioeconomic status, and psychosocial stress. Evidence for an association between height and a series of health endpoints is accumulating. Thus, shorter people appear to experience increased risk of CHD, and these associations appear to be independent of socioeconomic position and other potentially confounding variables. For stroke, and its sub-types, findings are less clear. In contrast to CHD, some cancers, such as carcinoma of the colorectum, prostate, breast (in women), central nervous system, skin, endometrium, thyroid and blood (haematopoietic) are more common in taller people. While height may be negatively related to the risk of completed suicide, conclusions about the links between stature and other health endpoints is problematic given the paucity of evidence, which should be addressed. Ultimately, for want of better data, investigators in this area have used height as a proxy for a range of pre-adult exposures. In future, research should aim to explore the predictive capacity of direct measures of diet, psychosocial stress, childhood chronic illness and so on, rather than focus on height or its components. The problem is that extended follow-up of child cohorts with such data are required, and studies which hold these data are not currently available, although several are either maturing to the point where they offer sufficient clinical outcomes to facilitate analyses or are in the advanced planning stage

Height, wealth, and health: An overview with new data from three longitudinal studies

This overview, based on a literature review and new data from the three cohorts (Whitehall Studies I and II, and the Vietnam Experience Study), has four objectives: (a) to outline the major determinants of height, so providing an indication as to what exposures this characteristic may capture; (b) to summarise, by reviewing reports from large scale studies, the relation between adult height and a range of disease outcomes - both somatic and psychiatric - with particular emphasis on coronary heart disease (CHD) and stroke; (c) to discuss why these relationships may exist, in particular, the role, if any, of socioeconomic position in explaining the apparent associations; and, finally (d) to outline future research directions in this field. The large majority of evidence for predictors of height, and its health consequences, comes from observational studies. While genetic predisposition is a major determinant of height, secular rises in childhood and adult stature across successive birth cohorts suggest that early life environment also has an important impact. Plausible non-genetic determinants of height include nutrition, illness, socioeconomic status, and psychosocial stress. Evidence for an association between height and a series of health endpoints is accumulating. Thus, shorter people appear to experience increased risk of CHD, and these associations appear to be independent of socioeconomic position and other potentially confounding variables. For stroke, and its sub-types, findings are less clear. In contrast to CHD, some cancers, such as carcinoma of the colorectum, prostate, breast (in women), central nervous system, skin, endometrium, thyroid and blood (haematopoietic) are more common in taller people. While height may be negatively related to the risk of completed suicide, conclusions about the links between stature and other health endpoints is problematic given the paucity of evidence, which should be addressed. Ultimately, for want of better data, investigators in this area have used height as a proxy for a range of pre-adult exposures. In future, research should aim to explore the predictive capacity of direct measures of diet, psychosocial stress, childhood chronic illness and so on, rather than focus on height or its components. The problem is that extended follow-up of child cohorts with such data are required, and studies which hold these data are not currently available, although several are either maturing to the point where they offer sufficient clinical outcomes to facilitate analyses or are in the advanced planning stage.Height Cardiovascular disease Cancer Suicide Coronary heart disease Stroke

Association of anthropometry and weight change with risk of dementia and its major subtypes: A meta-analysis consisting 2.8 million adults with 57 294 cases of dementia.

Uncertainty exists regarding the relation of body size and weight change with dementia risk. As populations continue to age and the global obesity epidemic shows no sign of waning, reliable quantification of such associations is important. We examined the relationship of body mass index, waist circumference, and annual percent weight change with risk of dementia and its subtypes by pooling data from 19 prospective cohort studies and four clinical trials using meta-analysis. Compared with body mass index-defined lower-normal weight (18.5-22.4 kg/m2 ), the risk of all-cause dementia was higher among underweight individuals but lower among those with upper-normal (22.5-24.9 kg/m2 ) levels. Obesity was associated with higher risk in vascular dementia. Similarly, relative to the lowest fifth of waist circumference, those in the highest fifth had nonsignificant higher vascular dementia risk. Weight loss was associated with higher all-cause dementia risk relative to weight maintenance. Weight gain was weakly associated with higher vascular dementia risk. The relationship between body size, weight change, and dementia is complex and exhibits non-linear associations depending on dementia subtype under scrutiny. Weight loss was associated with an elevated risk most likely due to reverse causality and/or pathophysiological changes in the brain, although the latter remains speculative

Association of anthropometry and weight change with risk of dementia and its major subtypes: A meta-analysis consisting 2.8 million adults with 57 294 cases of dementia.

Uncertainty exists regarding the relation of body size and weight change with dementia risk. As populations continue to age and the global obesity epidemic shows no sign of waning, reliable quantification of such associations is important. We examined the relationship of body mass index, waist circumference, and annual percent weight change with risk of dementia and its subtypes by pooling data from 19 prospective cohort studies and four clinical trials using meta-analysis. Compared with body mass index-defined lower-normal weight (18.5-22.4 kg/m2 ), the risk of all-cause dementia was higher among underweight individuals but lower among those with upper-normal (22.5-24.9 kg/m2 ) levels. Obesity was associated with higher risk in vascular dementia. Similarly, relative to the lowest fifth of waist circumference, those in the highest fifth had nonsignificant higher vascular dementia risk. Weight loss was associated with higher all-cause dementia risk relative to weight maintenance. Weight gain was weakly associated with higher vascular dementia risk. The relationship between body size, weight change, and dementia is complex and exhibits non-linear associations depending on dementia subtype under scrutiny. Weight loss was associated with an elevated risk most likely due to reverse causality and/or pathophysiological changes in the brain, although the latter remains speculative.Adult Changes in Thought Study was funded by a National Institutes of Health Grant U01 AG0006781. The Cache County Memory Study was funded by NIA grants R01 AG011380 and R01 AG018712; Dr Hayden’s effort on this project was supported by NIA R01 AG042633. JKaprio acknowledges support for the Finnish Twin Cohort by the Academy of Finland (grants 265240, 263278, 308248, 312073). This work was supported by the dedication of the Framingham Heart Study participants. This work and the investigators received grant support from the National Heart, Lung, and Blood Institute’s Framingham Heart Study (contracts no. N01-HC-25195 and HHSN268201500001I) and grants from the National Institute of Neurological Disorders and Stroke (NS17950 and UH2 NS100605), the National Institute on Aging (R01 AG054076, R01 AG049607, R01 AG033193, U01 AG049505 and U01 AG052409). The Study of Osteoporotic Fractures (SOF) is supported by National Institutes of Health funding. The National Institute on Aging (NIA) provides support under the following grant numbers: R01 AG005407, R01 AR35582, R01 AR35583, R01 AR35584, R01 AG005394, R01 AG027574, and R01 AG027576. The Three-City Study is conducted under a partnership agreement between the INSERM, the ISPED of the University of Bordeaux, and Sanofi-Aventis. The Foundation pour la Recherche Médicale funded the preparation and initiation of the study. TheThree-City Study is also supported by the Caisse Nationale Maladie des Travailleurs Salariés, Direction Générale de la Santé, Mutuelle Générale de l’Education Nationale, Institut de la Longévité, Conseils Régionaux of Aquitaine and Bourgogne, Fondation de France, and Ministry of Research-INSERM Programme « Cohortes et collections de données biologiques », French National Research Agency COGINUT ANR-06-PNRA-005, COGICARE ANR Longvie (LVIE-003-01), the Fondation Plan Alzheimer (FCS 2009–2012), and the Caisse Nationale pour la Solidarité et l’Autonomie. This research has been conducted using the UK Biobank Resource under Application number 7439. SBell and EDA are supported by core funding from: NIHR Blood and Transplant Research Unit in Donor Health and Genomics (NIHR BTRU-2014-10024), UK Medical Research Council (MR/L003120/1), British Heart Foundation (RG/13/13/30194), and the NIHR Cambridge BRC. GDB is supported by the UK Medical Research Council (MR/P023444/1) and the US National Institute on Aging (1R56AG052519-01; 1R01AG052519-01A1). Whitehall II was supported by the Medical Research Council (MR/R024227/1), the NIH National Institute on Aging (R01AG056477) and British Heart Foundation (32334). EVuoksimaa was supported by the Academy of Finland (grants 314639 & 320109)