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      Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies

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          Summary

          Background

          The main associations of body-mass index (BMI) with overall and cause-specific mortality can best be assessed by long-term prospective follow-up of large numbers of people. The Prospective Studies Collaboration aimed to investigate these associations by sharing data from many studies.

          Methods

          Collaborative analyses were undertaken of baseline BMI versus mortality in 57 prospective studies with 894 576 participants, mostly in western Europe and North America (61% [n=541 452] male, mean recruitment age 46 [SD 11] years, median recruitment year 1979 [IQR 1975–85], mean BMI 25 [SD 4] kg/m 2). The analyses were adjusted for age, sex, smoking status, and study. To limit reverse causality, the first 5 years of follow-up were excluded, leaving 66 552 deaths of known cause during a mean of 8 (SD 6) further years of follow-up (mean age at death 67 [SD 10] years): 30 416 vascular; 2070 diabetic, renal or hepatic; 22 592 neoplastic; 3770 respiratory; 7704 other.

          Findings

          In both sexes, mortality was lowest at about 22·5–25 kg/m 2. Above this range, positive associations were recorded for several specific causes and inverse associations for none, the absolute excess risks for higher BMI and smoking were roughly additive, and each 5 kg/m 2 higher BMI was on average associated with about 30% higher overall mortality (hazard ratio per 5 kg/m 2 [HR] 1·29 [95% CI 1·27–1·32]): 40% for vascular mortality (HR 1·41 [1·37–1·45]); 60–120% for diabetic, renal, and hepatic mortality (HRs 2·16 [1·89–2·46], 1·59 [1·27–1·99], and 1·82 [1·59–2·09], respectively); 10% for neoplastic mortality (HR 1·10 [1·06–1·15]); and 20% for respiratory and for all other mortality (HRs 1·20 [1·07–1·34] and 1·20 [1·16–1·25], respectively). Below the range 22·5–25 kg/m 2, BMI was associated inversely with overall mortality, mainly because of strong inverse associations with respiratory disease and lung cancer. These inverse associations were much stronger for smokers than for non-smokers, despite cigarette consumption per smoker varying little with BMI.

          Interpretation

          Although other anthropometric measures (eg, waist circumference, waist-to-hip ratio) could well add extra information to BMI, and BMI to them, BMI is in itself a strong predictor of overall mortality both above and below the apparent optimum of about 22·5–25 kg/m 2. The progressive excess mortality above this range is due mainly to vascular disease and is probably largely causal. At 30–35 kg/m 2, median survival is reduced by 2–4 years; at 40–45 kg/m 2, it is reduced by 8–10 years (which is comparable with the effects of smoking). The definite excess mortality below 22·5 kg/m 2 is due mainly to smoking-related diseases, and is not fully explained.

          Funding

          UK Medical Research Council, British Heart Foundation, Cancer Research UK, EU BIOMED programme, US National Institute on Aging, and Clinical Trial Service Unit (Oxford, UK).

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          Most cited references18

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          Body-mass index and mortality in Korean men and women.

          Obesity is associated with diverse health risks, but the role of body weight as a risk factor for death remains controversial. We examined the association between body weight and the risk of death in a 12-year prospective cohort study of 1,213,829 Koreans between the ages of 30 and 95 years. We examined 82,372 deaths from any cause and 48,731 deaths from specific diseases (including 29,123 from cancer, 16,426 from atherosclerotic cardiovascular disease, and 3362 from respiratory disease) in relation to the body-mass index (BMI) (the weight in kilograms divided by the square of the height in meters). In both sexes, the average baseline BMI was 23.2, and the rate of death from any cause had a J-shaped association with the BMI, regardless of cigarette-smoking history. The risk of death from any cause was lowest among patients with a BMI of 23.0 to 24.9. In all groups, the risk of death from respiratory causes was higher among subjects with a lower BMI, and the risk of death from atherosclerotic cardiovascular disease or cancer was higher among subjects with a higher BMI. The relative risk of death associated with BMI declined with increasing age. Underweight, overweight, and obese men and women had higher rates of death than men and women of normal weight. The association of BMI with death varied according to the cause of death and was modified by age, sex, and smoking history. Copyright 2006 Massachusetts Medical Society.
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            How useful is body mass index for comparison of body fatness across age, sex, and ethnic groups?

            This study tested the hypothesis that body mass index (BMI) is representative of body fatness independent of age, sex, and ethnicity. Between 1986 and 1992, the authors studied a total of 202 black and 504 white men and women who resided in or near New York City, were ages 20-94 years, and had BMIs of 18-35 kg/m2. Total body fat, expressed as a percentage of body weight (BF%), was assessed using a four-compartment body composition model that does not rely on assumptions known to be age, sex, or ethnicity dependent. Statistically significant age dependencies were observed in the BF%-BMI relations in all four sex and ethnic groups (p values < 0.05-0.001) with older persons showing a higher BF% compared with younger persons with comparable BMIs. Statistically significant sex effects were also observed in BF%-BMI relations within each ethnic group (p values < 0.001) after controlling first for age. For an equivalent BMI, women have significantly greater amounts of total body fat than do men throughout the entire adult life span. Ethnicity did not significantly influence the BF%-BMI relation after controlling first for age and sex even though both black women and men had longer appendicular bone lengths relative to stature (p values < 0.001 and 0.02, respectively) compared with white women and men. Body mass index alone accounted for 25% of between-individual differences in body fat percentage for the 706 total subjects; adding age and sex as independent variables to the regression model increased the variance (r2) to 67%. These results suggest that BMI is age and sex dependent when used as an indicator of body fatness, but that it is ethnicity independent in black and white adults.
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              Changing patterns in the incidence of esophageal and gastric carcinoma in the United States.

              Incidence rates for esophageal adenocarcinoma previously were reported to be increasing rapidly, especially among white males. Rates for gastric cardia adenocarcinoma also were observed to be rising, although less rapidly. In this article, the authors update the incidence trends through 1994 and further consider the trends by age group. Surveillance, Epidemiology, and End Results (SEER) program data were used to calculate age-adjusted incidence rates for esophageal carcinoma by histologic type and gastric adenocarcinoma by anatomic subsite. Among white males, the incidence of adenocarcinoma of the esophagus rose > 350% since the mid-1970s, surpassing squamous cell carcinoma around 1990. Rates also rose among black males, but remained at much lower levels. To a lesser extent, there were continuing increases in gastric cardia adenocarcinoma among white and black males, which nearly equaled the rates for noncardia tumors of the stomach in white men. The upward trend for both tumors was much greater among older than younger men. Although the incidence also rose among females, rates remained much lower than among males. Previously reported increases of esophageal adenocarcinoma are continuing, most notably among white males. Cigarette smoking may contribute to the trend through an early stage carcinogenic effect, along with obesity, which may increase intraabdominal pressure and predispose to gastroesophageal reflux disease. Further research into esophageal and gastric cardia adenocarcinoma is needed to clarify the risk factors and mechanisms responsible for the upward trends as well as the racial and gender disparities in incidence.
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                Author and article information

                Journal
                Lancet
                Lancet
                Lancet Publishing Group
                0140-6736
                1474-547X
                28 March 2009
                28 March 2009
                : 373
                : 9669
                : 1083-1096
                Author notes
                [* ]Correspondence to: PSC secretariat, Clinical Trial Service Unit and Epidemiological Studies Unit (CTSU), Richard Doll Building, University of Oxford, Oxford OX3 7LF, UK psc@ 123456ctsu.ox.ac.uk
                [‡]

                PSC collaborators listed at end of paper

                Article
                LANCET60318
                10.1016/S0140-6736(09)60318-4
                2662372
                19299006
                fde7d14d-41db-4698-baa1-e45e79401202
                © 2009 Elsevier Ltd. All rights reserved.

                This document may be redistributed and reused, subject to certain conditions.

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