SummaryBackgroundHealthy life expectancy (HALE) and disability-adjusted life-years (DALYs) provide summary measures of health across geographies and time that can inform assessments of epidemiological patterns and health system performance, help to prioritise investments in research and development, and monitor progress toward the Sustainable Development Goals (SDGs). We aimed to provide updated HALE and DALYs for geographies worldwide and evaluate how disease burden changes with development.MethodsWe used results from the Global Burden of Diseases, Injuries, and Risk Factors Study 2015 (GBD 2015) for all-cause mortality, cause-specific mortality, and non-fatal disease burden to derive HALE and DALYs by sex for 195 countries and territories from 1990 to 2015. We calculated DALYs by summing years of life lost (YLLs) and years of life lived with disability (YLDs) for each geography, age group, sex, and year. We estimated HALE using the Sullivan method, which draws from age-specific death rates and YLDs per capita. We then assessed how observed levels of DALYs and HALE differed from expected trends calculated with the Socio-demographic Index (SDI), a composite indicator constructed from measures of income per capita, average years of schooling, and total fertility rate.FindingsTotal global DALYs remained largely unchanged from 1990 to 2015, with decreases in communicable, neonatal, maternal, and nutritional (Group 1) disease DALYs offset by increased DALYs due to non-communicable diseases (NCDs). Much of this epidemiological transition was caused by changes in population growth and ageing, but it was accelerated by widespread improvements in SDI that also correlated strongly with the increasing importance of NCDs. Both total DALYs and age-standardised DALY rates due to most Group 1 causes significantly decreased by 2015, and although total burden climbed for the majority of NCDs, age-standardised DALY rates due to NCDs declined. Nonetheless, age-standardised DALY rates due to several high-burden NCDs (including osteoarthritis, drug use disorders, depression, diabetes, congenital birth defects, and skin, oral, and sense organ diseases) either increased or remained unchanged, leading to increases in their relative ranking in many geographies. From 2005 to 2015, HALE at birth increased by an average of 2·9 years (95% uncertainty interval 2·9–3·0) for men and 3·5 years (3·4–3·7) for women, while HALE at age 65 years improved by 0·85 years (0·78–0·92) and 1·2 years (1·1–1·3), respectively. Rising SDI was associated with consistently higher HALE and a somewhat smaller proportion of life spent with functional health loss; however, rising SDI was related to increases in total disability. Many countries and territories in central America and eastern sub-Saharan Africa had increasingly lower rates of disease burden than expected given their SDI. At the same time, a subset of geographies recorded a growing gap between observed and expected levels of DALYs, a trend driven mainly by rising burden due to war, interpersonal violen...

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Background: Previous research suggested that nutritionally stunted children may have increased risk of obesity, but little is known about potential underlying mechanisms. Objective: We sought to test the hypothesis that stunted children have a low metabolic rate and impaired fat oxidation relative to nonstunted children. Design: The subjects were 58 prepubertal boys and girls aged 8-11 y from the shantytowns of São Paulo, Brazil. Twenty-eight were stunted (height-for-age z score < Ϫ1.5) and 30 had similar weight-for-height but normal height (height-for-age z score > Ϫ1.5). Parents of children in the 2 groups had equivalent height and body mass index values. Fasting and postprandial energy expenditure, respiratory quotient (RQ), and substrate oxidation were measured with indirect calorimetry in a 3-d resident study in which all food was provided and body composition was measured with dual-energy X-ray absorptiometry. Results: Stunted children had normal resting energy expenditure relative to body composition compared with control children (4559 ± 90 and 4755 ± 86 kJ/d, respectively; P = 0.14) and had normal postprandial thermogenesis (2.4 ± 0.3% and 2.0 ± 0.3% of meal load, respectively; P = 0.42). However, fasting RQ was significantly higher in the stunted group (0.92 ± 0.009 compared with 0.89 ± 0.007; P = 0.04) and consequently, fasting fat oxidation was significantly lower (25 ± 2% compared with 34 ± 2% of energy expenditure; P < 0.01). Conclusions: Childhood nutritional stunting is associated with impaired fat oxidation, a factor that predicted obesity in other atrisk populations. This finding may help explain recent increases in body fatness and the prevalence of obesity among stunted adults and adolescents in developing countries.Am J Clin Nutr 2000;72:702-7.

SummaryBackgroundEfforts to establish the 2015 baseline and monitor early implementation of the UN Sustainable Development Goals (SDGs) highlight both great potential for and threats to improving health by 2030. To fully deliver on the SDG aim of “leaving no one behind”, it is increasingly important to examine the health-related SDGs beyond national-level estimates. As part of the Global Burden of Diseases, Injuries, and Risk Factors Study 2017 (GBD 2017), we measured progress on 41 of 52 health-related SDG indicators and estimated the health-related SDG index for 195 countries and territories for the period 1990–2017, projected indicators to 2030, and analysed global attainment.MethodsWe measured progress on 41 health-related SDG indicators from 1990 to 2017, an increase of four indicators since GBD 2016 (new indicators were health worker density, sexual violence by non-intimate partners, population census status, and prevalence of physical and sexual violence [reported separately]). We also improved the measurement of several previously reported indicators. We constructed national-level estimates and, for a subset of health-related SDGs, examined indicator-level differences by sex and Socio-demographic Index (SDI) quintile. We also did subnational assessments of performance for selected countries. To construct the health-related SDG index, we transformed the value for each indicator on a scale of 0–100, with 0 as the 2·5th percentile and 100 as the 97·5th percentile of 1000 draws calculated from 1990 to 2030, and took the geometric mean of the scaled indicators by target. To generate projections through 2030, we used a forecasting framework that drew estimates from the broader GBD study and used weighted averages of indicator-specific and country-specific annualised rates of change from 1990 to 2017 to inform future estimates. We assessed attainment of indicators with defined targets in two ways: first, using mean values projected for 2030, and then using the probability of attainment in 2030 calculated from 1000 draws. We also did a global attainment analysis of the feasibility of attaining SDG targets on the basis of past trends. Using 2015 global averages of indicators with defined SDG targets, we calculated the global annualised rates of change required from 2015 to 2030 to meet these targets, and then identified in what percentiles the required global annualised rates of change fell in the distribution of country-level rates of change from 1990 to 2015. We took the mean of these global percentile values across indicators and applied the past rate of change at this mean global percentile to all health-related SDG indicators, irrespective of target definition, to estimate the equivalent 2030 global average value and percentage change from 2015 to 2030 for each indicator.FindingsThe global median health-related SDG index in 2017 was 59·4 (IQR 35·4–67·3), ranging from a low of 11·6 (95% uncertainty interval 9·6–14·0) to a high of 84·9 (83·1–86·7). SDG index values in countries assessed at the subnational level...

Epidemiologic and clinical research has provided a large body of evidence supporting the developmental origins of health and disease (DOHaD), but there has been a relative dearth of mechanistic studies in humans due to the complexity of working with large, longitudinal cohorts. Nonetheless, animal models of undernutrition have provided substantial evidence for the potential epigenetic, metabolic, and endocrine mechanisms behind DOHaD. Furthermore, recent research has explored the interaction between the environment and the gastrointestinal system by investigating how the gut microbial ecology may impact the capacity for nutrient processing and absorption in a manner that may limit growth. This review presents a summary of current research that supports the concept of DOHaD, as well as potential mechanisms and interactions that explain how nutrition in utero and during early childhood influences lifelong health.

Students entering their first year of college are faced with many stresses and changes, including changes in eating and exercise behavior. A common but often undocumented myth among college students is that there is a high risk of gaining 15 pounds of weight during freshman year. The objective of this study was to measure changes in body weight and percentage of body fat among first-year college students. Using a digital scale with bio-electrical impedance, the authors measured height, weight, and percentage of body fat for a sample of students who volunteered to be weighed during a health assessment in the university dining halls. The authors sent e-mails inviting those same students to complete a second measurement in February of the academic year. Sixty-seven of the 217 students who volunteered for the health assessment agreed to undergo a second set of measurements in the spring. The mean change in body weight was 2.86 pounds (1.3 kg, SD = 4.0 kg), and the mean change in percentage of body fat was 0.7% (SD = 4.0%). For those students who gained weight only, the mean increase in body weight (as measured by body mass index, weight divided by height in kg/m2) was 6.82 pounds (3.1 +/- 2.4 kg) and percentage of body fat was 0.9 +/- 3.8%. The authors found that the first year of college is a period in which weight and fat gain may occur. The exact causes behind these changes are unclear and warrant further research to plan or improve intervention and prevention.

The aim of the present study was to analyse the changes in body composition of stunted children during a follow-up period and to test the hypothesis of a tendency to accumulate body fat as a consequence of undernutrition early in life. We selected fifty boys and girls aged 11 to 15, who were residents of slums in Sao Paulo, Brazil. Twenty were stunted (S) and thirty had normal stature (NS). The children's nutritional status and body composition were assessed through anthropometry and dual-energy X-ray absorptiometry, at the beginning of the present study and after 3 years, and changes in lean mass (LM and LM%) and fat mass (FM and FM%) were calculated. Stunted boys accumulated more body fat (FM%: S=1.62%, NS=-3.40%; P=0.003) and gained less lean mass (LM%: S=-1.46, NS=3.21%; P=0.004). Stunted girls gained less lean mass (S=7.87 kg, NS=11.96 kg; P=0.032) and had significantly higher values of FM% at follow-up when compared with their baseline values (P=0.008), whereas non-stunted girls had a non-significant difference in FM% over time (P=0.386). These findings are important to understand the factors involved in the increased prevalence of overweight and obesity among poor populations, which appear to be associated with hunger during infancy and/or childhood.

Background Emerging evidence implicates circadian abnormalities as a component of the pathophysiology of major depressive disorder (MDD). The suprachiasmatic nucleus (SCN) of the hypothalamus coordinates rhythms throughout the brain and body. On a cellular level, rhythms are generated by transcriptional, translational, and post-translational feedback loops of core circadian genes and proteins. In patients with MDD, recent evidence suggests reduced amplitude of molecular rhythms in extra-SCN brain regions. We investigated whether unpredictable chronic mild stress (UCMS), an animal model that induces a depression-like physiological and behavioral phenotype, induces circadian disruptions similar to those seen with MDD. Methods Activity and temperature rhythms were recorded in C57BL/6J mice before, during, and after exposure to UCMS, and brain tissue explants were collected from Period2 luciferase (Per2::luc) mice following UCMS to assess cellular rhythmicity. Results UCMS significantly decreased circadian amplitude of activity and body temperature in mice, similar to findings in MDD patients and these changes directly correlate with depression-related behavior. While amplitude of molecular rhythms in the SCN was decreased following UCMS, surprisingly, rhythms in the nucleus accumbens were amplified with no changes seen in the prefrontal cortex or amygdala. These molecular rhythm changes in the SCN and the nucleus accumbens (NAc) also directly correlated with mood-related behavior. Conclusions These studies find that circadian rhythm abnormalities directly correlate with depression-related behavior following UCMS and suggest a desynchronization of rhythms in the brain with an independent enhancement of rhythms in the NAc.