Body-mass index and all-cause mortality: individual-participant-data meta-analysis of 239 prospective studies in four continents

Background Overweight and obesity are increasing worldwide. To help assess their relevance to mortality in different populations we conducted individual-participant data meta-analyses of prospective studies of body-mass index (BMI), limiting confounding and reverse causality by restricting analyses to never-smokers and excluding pre-existing disease and the first 5 years of follow-up. Methods Of 10 625 411 participants in Asia, Australia and New Zealand, Europe, and North America from 239 prospective studies (median follow-up 13·7 years, IQR 11·4–14·7), 3 951 455 people in 189 studies were never-smokers without chronic diseases at recruitment who survived 5 years, of whom 385 879 died. The primary analyses are of these deaths, and study, age, and sex adjusted hazard ratios (HRs), relative to BMI 22·5–<25·0 kg/m2. Findings All-cause mortality was minimal at 20·0–25·0 kg/m2 (HR 1·00, 95% CI 0·98–1·02 for BMI 20·0–<22·5 kg/m2; 1·00, 0·99–1·01 for BMI 22·5–<25·0 kg/m2), and increased significantly both just below this range (1·13, 1·09–1·17 for BMI 18·5–<20·0 kg/m2; 1·51, 1·43–1·59 for BMI 15·0–<18·5) and throughout the overweight range (1·07, 1·07–1·08 for BMI 25·0–<27·5 kg/m2; 1·20, 1·18–1·22 for BMI 27·5–<30·0 kg/m2). The HR for obesity grade 1 (BMI 30·0–<35·0 kg/m2) was 1·45, 95% CI 1·41–1·48; the HR for obesity grade 2 (35·0–<40·0 kg/m2) was 1·94, 1·87–2·01; and the HR for obesity grade 3 (40·0–<60·0 kg/m2) was 2·76, 2·60–2·92. For BMI over 25·0 kg/m2, mortality increased approximately log-linearly with BMI; the HR per 5 kg/m2 units higher BMI was 1·39 (1·34–1·43) in Europe, 1·29 (1·26–1·32) in North America, 1·39 (1·34–1·44) in east Asia, and 1·31 (1·27–1·35) in Australia and New Zealand. This HR per 5 kg/m2 units higher BMI (for BMI over 25 kg/m2) was greater in younger than older people (1·52, 95% CI 1·47–1·56, for BMI measured at 35–49 years vs 1·21, 1·17–1·25, for BMI measured at 70–89 years; pheterogeneity<0·0001), greater in men than women (1·51, 1·46–1·56, vs 1·30, 1·26–1·33; pheterogeneity<0·0001), but similar in studies with self-reported and measured BMI. Interpretation The associations of both overweight and obesity with higher all-cause mortality were broadly consistent in four continents. This finding supports strategies to combat the entire spectrum of excess adiposity in many populations

Intergenerational change and familial aggregation of body mass index

The relationship between parental BMI and that of their adult offspring, when increased adiposity can become a clinical issue, is unknown. We investigated the intergenerational change in body mass index (BMI) distribution, and examined the sex-specific relationship between parental and adult offspring BMI. Intergenerational change in the distribution of adjusted BMI in 1,443 complete families (both parents and at least one offspring) with 2,286 offspring (1,263 daughters and 1,023 sons) from the west of Scotland, UK, was investigated using quantile regression. Familial correlations were estimated from linear mixed effects regression models. The distribution of BMI showed little intergenerational change in the normal range (\25 kg/m2), decreasing overweightness (25– \30 kg/m2) and increasing obesity (C30 kg/m2). Median BMI was static across generations in males and decreased in females by 0.4 (95% CI: 0.0, 0.7) kg/m2; the 95th percentileincreased by 2.2 (1.1, 3.2) kg/m2 in males and 2.7 (1.4, 3.9) kg/m2 in females. Mothers’ BMI was more strongly associated with daughters’ BMI than was fathers’ (correlation coefficient (95% CI): mothers 0.31 (0.27, 0.36), fathers 0.19 (0.14, 0.25); P = 0.001). Mothers’ and fathers’ BMI were equally correlated with sons’ BMI (correlation coefficient: mothers 0.28 (0.22, 0.33), fathers 0.27 (0.22, 0.33). The increase in BMI between generations was concentrated at the upper end of the distribution. This, alongside the strong parent-offspring correlation, suggests that the increase in BMI is disproportionally greater among offspring of heavier parents. Familial influences on BMI among middle-aged women appear significantly stronger from mothers than father

Parity and body mass index in US women: a prospective 25-year study.

ObjectiveTo investigate long-term body mass index (BMI) changes associated with childbearing.Design and methodsAdjusted mean BMI changes were estimated by race-ethnicity, baseline BMI, and parity using longitudinal regression models for 3,943 young females over 10 and 25 year follow-up from the ongoing 1979 National Longitudinal Survey of Youth cohort.ResultsEstimated BMI increases varied by group, ranging from a low of 2.1 BMI units for white, non-overweight nulliparas over the first 10 years to a high of 10.1 BMI units for black, overweight multiparas over the full 25-year follow-up. Impacts of parity were strongest among overweight multiparas and primaparas at 10 years, ranges 1.4-1.7 and 0.8-1.3 BMI units, respectively. Among non-overweight women, parity-related gain at 10 years varied by number of births among black and white but not Hispanic women. After 25 years, childbearing significantly increased BMI only among overweight multiparous black women.ConclusionChildbearing is associated with permanent weight gain in some women, but the relationship differs by maternal BMI in young adulthood, number of births, race-ethnicity, and length of follow-up. Given that overweight black women may be at special risk for accumulation of permanent, long-term weight after childbearing, effective interventions for this group are particularly needed

Rethinking the Body Mass Index Initiative

In February 2005, the Office for Education Policy published a fact sheet detailing Arkansans’ attitudes toward the Body Mass Index initiative (BMI) and found that the state was roughly divided on the issue. Since 2005, the results of BMI screening have been chronicled in a pair of government reports, and the General Assembly has acted to modify how BMI testing is undertaken. In this policy brief we outline what the research indicates after three years of BMI testing, and how the laws surrounding BMI have changed

Breakfast intake, habits and body composition in New Zealand European women : a thesis presented in partial fulfilment of the requirements for the degree of Master of Science in Nutrition and Dietetics, Massey University, Albany, New Zealand

Background: The rise of obesity and related poor health outcomes is rampant in New Zealand. Dietary factors are key in the aetiology of obesity. One dietary factor with wide reaching implications on health and weight maintenance is breakfast consumption. Breakfast consumption has declined in New Zealand in recent years, and adverse health outcomes have risen concurrently. Breakfast consumption has been associated with lower BMI, improved appetite control, better diet quality, and more stable glycaemia. Objective: The aim of this study was to describe and compare reported and observed breakfast consumption between obese and normal weight New Zealand European women aged 18-45 years, living in Auckland, New Zealand. Methods: In a cross-sectional study, healthy women (n=75 normal BMI, n=82 obese BMI) completed a 5-day food record, an observed ad libitum buffet breakfast assessment and body composition measurements. Nutrient intake, food choices and behavioural aspects, including pace of eating and meal skipping data were obtained and analysed. Results: More normal BMI women (n=69; 84.1%) than obese BMI women (n=56; 74.6%) consumed breakfast daily. Obese BMI women consumed significantly more energy at the observed breakfast (1915 ± 868 kJ) than at the recorded breakfast (1431 ± 690kJ, p<0.001); however neither BMI group met one third of estimated energy requirements at either breakfast occasion. Carbohydrate consumption was lower than recommended (AMDR: 45-65%) in both groups in the recorded breakfast (40.7% and 42.6%; normal BMI and obese BMI respectively), whereas total fat consumption was higher than recommended (AMDR: 20-35%) (36.5% and 35.9% respectively). Protein consumption was within AMDR recommendations (15-25%) for both groups in the recorded breakfast (16.3% and 17.5%) but not in the observed breakfast, (13.0% and 14.0%), obese BMI and normal BMI respectively. Foods with the greatest contribution to energy at the observed breakfast for obese BMI women were discretionary items (fats, cake and biscuits), compared with sweetened cereals, nuts and seeds for normal BMI women. Having a faster pace of eating and consuming foods with a higher energy density significantly increased the likelihood of falling into the obese BMI category (b=3.11, p=0.016; b=1.35, p=0.042 respectively). Conclusions: Consuming a breakfast, particularly one that contains whole grains, fruits and low-fat dairy products, and minimising discretionary items could enable women to more closely meet dietary recommendations, and as a result, improve health outcomes. Key words: breakfast, obesity, energy intake, appetite, pace of eatin

Body mass index and incident coronary heart disease in women: a population-based prospective study

BACKGROUND A high body mass index (BMI) is associated with an increased risk of mortality from coronary heart disease (CHD); however, a low BMI may also be associated with an increased mortality risk. There is limited information on the relation of incident CHD risk across a wide range of BMI, particularly in women. We examined the relation between BMI and incident CHD overall and across different risk factors of the disease in the Million Women Study. METHODS 1.2 million women (mean age=56 years) participants without heart disease, stroke, or cancer (except non-melanoma skin cancer) at baseline (1996 to 2001) were followed prospectively for 9 years on average. Adjusted relative risks and 20-year cumulative incidence from age 55 to 74 years were calculated for CHD using Cox regression. RESULTS After excluding the first 4 years of follow-up, we found that 32,465 women had a first coronary event (hospitalization or death) during follow-up. The adjusted relative risk for incident CHD per 5 kg/m2 increase in BMI was 1.23 (95% confidence interval (CI) 1.22 to 1.25). The cumulative incidence of CHD from age 55 to 74 years increased progressively with BMI, from 1 in 11 (95% CI 1 in 10 to 12) for BMI of 20 kg/m2, to 1 in 6(95% CI 1 in 5 to 7) for BMI of 34 kg/m2. A 10 kg/m2 increase in BMI conferred a similar risk to a 5-year increment in chronological age. The 20 year cumulative incidence increased with BMI in smokers and non-smokers, alcohol drinkers and non-drinkers, physically active and inactive, and in the upper and lower socioeconomic classes. In contrast to incident disease, the relation between BMI and CHD mortality (n=2,431) was J-shaped. For the less than 20 kg/m2 and ≥35 kg/m2 BMI categories, the respective relative risks were 1.27 (95% CI 1.06 to 1.53) and 2.84 (95% CI 2.51 to 3.21) for CHD deaths, and 0.89 (95% CI 0.83 to 0.94) and 1.85 (95% CI 1.78 to 1.92) for incident CHD. CONCLUSIONS CHD incidence in women increases progressively with BMI, an association consistently seen in different subgroups. The shape of the relation with BMI differs for incident and fatal disease.The Million Women Study is funded by Cancer Research UK, the Medical Research Council, and the NHS Breast Screening Programme. The funding organizations were not involved in the study design or conduct, data analysis or interpretation, manuscript preparation or review, final version approval, or decision to submit the manuscript

Excess of weight: is it a modifiable predictive and prognostic factor in locally advanced rectal cancer?

To evaluate the relationship between body mass index (BMI) and rates of treatment tolerance and clinical outcomes in patients with locally advanced rectal cancer treated with a multimodality approach. PATIENTS AND METHODS: This study was conducted on 56 patients with histologically proven rectal adenocarcinoma, staged T3-4, and/or node-positive tumor, which underwent intensified radiochemotherapy (RT-CHT) treatment before surgery. We calculated adiposity indices and analyzed their influence on treatment tolerance and clinical outcomes. RESULTS: Distribution of the 56 patients according to BMI was BMI < 25 kg/m2 (n = 19; 33.9%), BMI 25-29 kg/m2 (n = 29; 51.8%) and BMI ≥ 30 kg/m2 (n = 8; 14.3%). BMI had no significant influence on neo-adjuvant treatment-related toxicity. With a median follow-up of 23 months (range 11-47), the 2-year survival was 85.7%. We did not observe any significant difference among the three BMI categories for any of the outcomes. CONCLUSIONS: This study suggested no evident links between overweight and survival in patients with locally advanced rectal carcinoma treated with neo-adjuvant RT-CHT. Overweight patients tolerate treatment as normal-weight patients

Changes in BMI, Duration of Overweight and Obesity, and Glucose Metabolism: 45 Years of Follow-up of a Birth Cohort

OBJECTIVE: Long-term implications of childhood obesity and BMI change over the life course for risk of type 2 diabetes remain uncertain. The objective was to establish whether there are effects on adult glucose metabolism of 1) sensitive periods of BMI gain or 2) long duration of overweight and obesity. RESEARCH DESIGN AND METHODS: Participants in the 1958 British birth cohort with child to adult BMI and glycosylated hemoglobin (HbA(1c)) at 45 years (n = 7,855). RESULTS: Prevalence of type 2 diabetes or HbA(1c) ≥7 was 2%. BMI gains in child- and adulthood were associated with higher HbA(1c): for every SD of 5-year BMI increase from 0 to 7 years, there was a 75% (95% CI 1.42–2.16) increased risk of HbA(1c) ≥7, increasing to a 4.7-fold (3.12–7.00) risk for the interval 23–33 years. Associations for BMI gain in adulthood were related to attained BMI but were independent for the longer period birth (or 7 years) to 45 years. Duration of obesity was also associated with HbA(1c); compared with the never obese, those with childhood onset had a 23.9-fold risk (13.5–42.1) of HbA(1c) ≥7%; odds ratios were 16.0 (10.6–24.2) and 2.99 (1.77–5.03), respectively, for young and midadulthood onset. Similar trends by onset age were found in mean HbA(1c) levels and for onset of overweight. Those with the earliest age of onset had higher BMI and waist circumference at 45 years, which markedly explained the associations for onset age and HbA(1c). CONCLUSIONS: Excessive BMI gain across the life span and earlier onset of overweight/obesity are associated with impaired glucose metabolism, in part through attained adult BMI