SummaryBackgroundOverweight 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.MethodsOf 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.FindingsAll-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.InterpretationThe 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.FundingUK Medical Research Council, British Heart Foundation, National Institute for Health Research, US National Institutes of Health.
Prolonged sitting is a risk factor for all-cause mortality, independent of physical activity. Public health programs should focus on reducing sitting time in addition to increasing physical activity levels.
Many children live in families where one or both parents work evenings, nights, or weekends. Do these work schedules affect family relationships or well‐being? Using cross‐sectional survey data from dual‐earner Canadian families (N= 4,306) with children aged 2 – 11 years (N= 6,156), we compared families where parents worked standard weekday times with those where parents worked nonstandard schedules. Parents working nonstandard schedules reported worse family functioning, more depressive symptoms, and less effective parenting. Their children were also more likely to have social and emotional difficulties, and these associations were partially mediated through family relationships and parent well‐being. For some families, work in the 24‐hour economy may strain the well‐being of parents and children.
Background Tobacco smoking is a leading cause of cardiovascular disease (CVD) morbidity and mortality. Evidence on the relation of smoking to different subtypes of CVD, across fatal and non-fatal outcomes, is limited. Methods A prospective study of 188,167 CVD- and cancer-free individuals aged ≥ 45 years from the Australian general population joining the 45 and Up Study from 2006 to 2009, with linked questionnaire, hospitalisation and death data up to the end of 2015. Hazard ratios (HRs) for hospitalisation with or mortality from CVD among current and past versus never smokers were estimated, including according to intensity and recency of smoking, using Cox regression, adjusting for age, sex, urban/rural residence, alcohol consumption, income and education. Population-attributable fractions were estimated. Results During a mean 7.2 years follow-up (1.35 million person-years), 27,511 (crude rate 20.4/1000 person-years) incident fatal and non-fatal major CVD events occurred, including 4548 (3.2) acute myocardial infarction (AMI), 3991 (2.8) cerebrovascular disease, 3874 (2.7) heart failure and 2311 (1.6) peripheral arterial disease (PAD) events. At baseline, 8% of participants were current and 34% were past smokers. Of the 36 most common specific CVD subtypes, event rates for 29 were increased significantly in current smokers. Adjusted HRs in current versus never smokers were as follows: 1.63 (95%CI 1.56–1.71) for any major CVD, 2.45 (2.22–2.70) for AMI, 2.16 (1.93–2.42) for cerebrovascular disease, 2.23 (1.96–2.53) for heart failure, 5.06 (4.47–5.74) for PAD, 1.50 (1.24–1.80) for paroxysmal tachycardia, 1.31 (1.20–1.44) for atrial fibrillation/flutter, 1.41 (1.17–1.70) for pulmonary embolism, 2.79 (2.04–3.80) for AMI mortality, 2.26 (1.65–3.10) for cerebrovascular disease mortality and 2.75 (2.37–3.19) for total CVD mortality. CVD risks were elevated at almost all levels of current smoking intensity examined and increased with smoking intensity, with HRs for total CVD mortality in current versus never smokers of 1.92 (1.11–3.32) and 4.90 (3.79–6.34) for 4–6 and ≥ 25 cigarettes/day, respectively. Risks diminished with quitting, with excess risks largely avoided by quitting before age 45. Over one third of CVD deaths and one quarter of acute coronary syndrome hospitalisations in Australia aged < 65 can be attributed to smoking. Conclusions Current smoking increases the risk of virtually all CVD subtypes, at least doubling the risk of many, including AMI, cerebrovascular disease and heart failure. Paroxysmal tachycardia is a newly identified smoking-related risk. Where comparisons are possible, smoking-associated relative risks for fatal and non-fatal outcomes are similar. Quitting reduces the risk substantially. In an established smoking epidemic, with declining and low current smoking prevalence, smoking accounts for a substantial proportion of premature CVD events. Electronic supplementary mater...
Background : Body mass index (BMI) is an important measure of adiposity. While BMI derived from self‐reported data generally agrees well with that derived from measured values, evidence from Australia is limited, particularly for the elderly. Methods : We compared self‐reported with measured height and weight in a random sample of 608 individuals aged ≥45 from the 45 and Up Study, an Australian population‐based cohort study. We assessed degree of agreement and correlation between measures, and calculated sensitivity and specificity to quantify BMI category misclassification. Results : On average, in males and females respectively, height was overestimated by 1.24cm (95% CI: 0.75–1.72) and 0.59cm (0.26–0.92); weight was underestimated by 1.68kg (–1.99– ‐1.36) and 1.02kg (–1.24– ‐0.80); and BMI based on self‐reported measures was underestimated by 0.90kg/m2 (–1.09– ‐0.70) and 0.60 kg/m2 (–0.75– ‐0.45). Underestimation increased with increasing measured BMI. There were strong correlations between self‐reported and measured height, weight and BMI (r=0.95, 0.99 and 0.95, respectively, p<0.001). While there was excellent agreement between BMI categories from self‐reported and measured data (kappa=0.80), obesity prevalence was underestimated. Findings did not differ substantially between middle‐aged and elderly participants. Conclusions : Self‐reported data on height and weight quantify body size appropriately in middle‐aged and elderly individuals for relative measures, such as quantiles of BMI. However, caution is necessary when reporting on absolute BMI and standard BMI categories, based on self‐reported data, particularly since use of such data is likely to result in underestimation of the prevalence of obesity.
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