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Objectives: To extend existing research on the US health disadvantage relative to Europe by studying the relationships of disability with age from midlife to old age in the US and four European regions (England/Northern and Western Europe/Southern Europe/Eastern Europe) including their wealth-related differences, using a flexible statistical approach to model the age-functions. Methods: We used data from three studies on aging, with nationally representative samples of adults aged 50 to 85 from 15 countries (N = 48225): the US-American Health and Retirement Study (HRS), the English Longitudinal Study of Ageing (ELSA) and the Survey of Health, Ageing and Retirement in Europe (SHARE). Outcomes were mobility limitations and limitations in instrumental activities of daily living. We applied fractional polynomials of age to determine best fitting functional forms for age on disability in each region, while controlling for socio-demographic characteristics and important risk factors (hypertension, diabetes, obesity, smoking, physical inactivity). Results: Findings showed high levels of disability in the US with small age-related changes between 50 and 85. Levels of disability were generally lower in Eastern Europe, followed by England and Southern Europe and lowest in Northern and Western Europe. In these latter countries age-related increases of disability, though, were steeper than in the US, especially in Eastern and Southern Europe. For all countries and at all ages, disability levels were higher among adults with low wealth compared to those with high wealth, with largest wealth-related differences among those in early old age in the USA. Conclusions: This paper illustrates considerable variations of disability and its relationship with age. It supports the hypothesis that less developed social policies and more pronounced socioeconomic inequalities are related to higher levels of disability and an earlier onset of disability. [ABSTRACT FROM AUTHOR]

Background: Observational studies implicate higher dietary energy density (DED) as a potential risk factor for weight gain and obesity. It has been hypothesized that DED may also be associated with risk of type 2 diabetes (T2D), but limited evidence exists. Therefore, we investigated the association between DED and risk of T2D in a large prospective study with heterogeneity of dietary intake. Methodology/Principal Findings: A case-cohort study was nested within the European Prospective Investigation into Cancer (EPIC) study of 340,234 participants contributing 3.99 million person years of follow-up, identifying 12,403 incident diabetes cases and a random subcohort of 16,835 individuals from 8 European countries. DED was calculated as energy (kcal) from foods (except beverages) divided by the weight (gram) of foods estimated from dietary questionnaires. Prentice-weighted Cox proportional hazard regression models were fitted by country. Risk estimates were pooled by random effects meta-analysis and heterogeneity was evaluated. Estimated mean (sd) DED was 1.5 (0.3) kcal/g among cases and subcohort members, varying across countries (range 1.4–1.7 kcal/g). After adjustment for age, sex, smoking, physical activity, alcohol intake, energy intake from beverages and misreporting of dietary intake, no association was observed between DED and T2D (HR 1.02 (95% CI: 0.93–1.13), which was consistent across countries (I2 = 2.9%). Conclusions/Significance: In this large European case-cohort study no association between DED of solid and semi-solid foods and risk of T2D was observed. However, despite the fact that there currently is no conclusive evidence for an association between DED and T2DM risk, choosing low energy dense foods should be promoted as they support current WHO recommendations to prevent chronic diseases. [ABSTRACT FROM AUTHOR]

Background: Prevalence of type 2 diabetes (T2D) is increasing worldwide. T2D prevention by lifestyle intervention is effective. Pragmatic scalable interventions are needed, with evidence to efficiently target and monitor such interventions. We report pooled analyses of data from three European trial cohorts: to analyse T2D incidence, sustained weight loss and utility of risk predictors. Methods: We analysed data on 749 adults with impaired glucose tolerance (278 men and 471 women, mean age 56 years, mean BMI 31 kgm−2) recruited between 1993 and 2003, and randomised to intensive lifestyle intervention (I) or lifestyle advice control (C). The intervention aimed to increase physical activity, modify diet, and promote weight loss≥5%. Using Cox-regression survival analysis, we assessed T2D incidence and the impact on T2D incidence of sustained weight loss, and of baseline cut-point values of FINDRISC score, fasting plasma glucose (FPG), and HbA1c. Results: Mean follow-up duration was 3.1 years. T2D was diagnosed in 139 participants (I = 45/379, C = 94/370). Cumulative T2D incidence was 57% lower in the intervention compared with the control group (HR 0.42 (95% CI 0.29 to 0.60) P<0.001). Participants with ≥5% weight loss at one year had 65% lower T2D incidence (HR 0.35 (95% CI 0.22 to 0.56) P<0.001); maintaining ≥5% weight loss for two and three years further reduced T2D incidence. Recommended cut-points to identify those at high risk for T2D would have identified different proportions of European Diabetes Prevention Study (EDIPS) participants with similar hazard-ratios for intervention effect. Conclusions: Pooled analysis of EDIPS trial data reinforces evidence for T2D prevention by lifestyle intervention. Analysis showed the preventive effect of ≥5% weight loss, especially if maintained long term, which has utility for intervention monitoring. Analysis of proposed cut-points demonstrates difficulties in balancing risk and benefit, to efficiently target interventions and suggests evidence is needed to define clinical policy. Trial registrations: The Finnish Diabetes Prevention study, Helsinki, Finland: ClinicalTrials.gov; NCT00518167 The SLIM diabetes prevention study, Maastricht, The Netherlands: Clinical Trials.gov; NCT00381186 The EDIPS-Newcastle diabetes prevention study, Newcastle upon Tyne, UK: International Standard Randomised Controlled Trial Number; ISRCTN15670600. [ABSTRACT FROM AUTHOR]