Rising rural body-mass index is the main driver of the global obesity epidemic in adults

Body-mass index (BMI) has increased steadily in most countries in parallel with a rise in the proportion of the population who live in cities(.)(1,2) This has led to a widely reported view that urbanization is one of the most important drivers of the global rise in obesity(3-6). Here we use 2,009 population-based studies, with measurements of height and weight in more than 112 million adults, to report national, regional and global trends in mean BMI segregated by place of residence (a rural or urban area) from 1985 to 2017. We show that, contrary to the dominant paradigm, more than 55% of the global rise in mean BMI from 1985 to 2017-and more than 80% in some low- and middle-income regions-was due to increases in BMI in rural areas. This large contribution stems from the fact that, with the exception of women in sub-Saharan Africa, BMI is increasing at the same rate or faster in rural areas than in cities in low- and middle-income regions. These trends have in turn resulted in a closing-and in some countries reversal-of the gap in BMI between urban and rural areas in low- and middle-income countries, especially for women. In high-income and industrialized countries, we noted a persistently higher rural BMI, especially for women. There is an urgent need for an integrated approach to rural nutrition that enhances financial and physical access to healthy foods, to avoid replacing the rural undernutrition disadvantage in poor countries with a more general malnutrition disadvantage that entails excessive consumption of low-quality calories.Peer reviewe

Height and body-mass index trajectories of school-aged children and adolescents from 1985 to 2019 in 200 countries and territories: a pooled analysis of 2181 population-based studies with 65 million participants

Summary Background Comparable global data on health and nutrition of school-aged children and adolescents are scarce. We aimed to estimate age trajectories and time trends in mean height and mean body-mass index (BMI), which measures weight gain beyond what is expected from height gain, for school-aged children and adolescents. Methods For this pooled analysis, we used a database of cardiometabolic risk factors collated by the Non-Communicable Disease Risk Factor Collaboration. We applied a Bayesian hierarchical model to estimate trends from 1985 to 2019 in mean height and mean BMI in 1-year age groups for ages 5–19 years. The model allowed for non-linear changes over time in mean height and mean BMI and for non-linear changes with age of children and adolescents, including periods of rapid growth during adolescence. Findings We pooled data from 2181 population-based studies, with measurements of height and weight in 65 million participants in 200 countries and territories. In 2019, we estimated a difference of 20 cm or higher in mean height of 19-year-old adolescents between countries with the tallest populations (the Netherlands, Montenegro, Estonia, and Bosnia and Herzegovina for boys; and the Netherlands, Montenegro, Denmark, and Iceland for girls) and those with the shortest populations (Timor-Leste, Laos, Solomon Islands, and Papua New Guinea for boys; and Guatemala, Bangladesh, Nepal, and Timor-Leste for girls). In the same year, the difference between the highest mean BMI (in Pacific island countries, Kuwait, Bahrain, The Bahamas, Chile, the USA, and New Zealand for both boys and girls and in South Africa for girls) and lowest mean BMI (in India, Bangladesh, Timor-Leste, Ethiopia, and Chad for boys and girls; and in Japan and Romania for girls) was approximately 9–10 kg/m2. In some countries, children aged 5 years started with healthier height or BMI than the global median and, in some cases, as healthy as the best performing countries, but they became progressively less healthy compared with their comparators as they grew older by not growing as tall (eg, boys in Austria and Barbados, and girls in Belgium and Puerto Rico) or gaining too much weight for their height (eg, girls and boys in Kuwait, Bahrain, Fiji, Jamaica, and Mexico; and girls in South Africa and New Zealand). In other countries, growing children overtook the height of their comparators (eg, Latvia, Czech Republic, Morocco, and Iran) or curbed their weight gain (eg, Italy, France, and Croatia) in late childhood and adolescence. When changes in both height and BMI were considered, girls in South Korea, Vietnam, Saudi Arabia, Turkey, and some central Asian countries (eg, Armenia and Azerbaijan), and boys in central and western Europe (eg, Portugal, Denmark, Poland, and Montenegro) had the healthiest changes in anthropometric status over the past 3·5 decades because, compared with children and adolescents in other countries, they had a much larger gain in height than they did in BMI. The unhealthiest changes—gaining too little height, too much weight for their height compared with children in other countries, or both—occurred in many countries in sub-Saharan Africa, New Zealand, and the USA for boys and girls; in Malaysia and some Pacific island nations for boys; and in Mexico for girls. Interpretation The height and BMI trajectories over age and time of school-aged children and adolescents are highly variable across countries, which indicates heterogeneous nutritional quality and lifelong health advantages and risks

Heterogeneous contributions of change in population distribution of body mass index to change in obesity and underweight NCD Risk Factor Collaboration (NCD-RisC)

From 1985 to 2016, the prevalence of underweight decreased, and that of obesity and severe obesity increased, in most regions, with significant variation in the magnitude of these changes across regions. We investigated how much change in mean body mass index (BMI) explains changes in the prevalence of underweight, obesity, and severe obesity in different regions using data from 2896 population-based studies with 187 million participants. Changes in the prevalence of underweight and total obesity, and to a lesser extent severe obesity, are largely driven by shifts in the distribution of BMI, with smaller contributions from changes in the shape of the distribution. In East and Southeast Asia and sub-Saharan Africa, the underweight tail of the BMI distribution was left behind as the distribution shifted. There is a need for policies that address all forms of malnutrition by making healthy foods accessible and affordable, while restricting unhealthy foods through fiscal and regulatory restrictions

Genetic variants in the Desmoglein-2 Gene in patients with familial dilated cardiomyopathy

Die dilatative Kardiomyopathie (DCM) ist eine primäre Erkrankung des Herzmuskels und stellt mit einer Prävalenz von 36/100.000 die häufigste Ursache für eine Herztransplantation dar. In etwa 20-30% tritt die DCM familiär gehäuft auf. Die genetische Ätiologie der familiären DCM (fDCM) ist allerdings sehr heterogen und in der Mehrzahl der Patienten mit fDCM bleibt die zu Grunde liegende genetische Variante unklar. Von den bislang bekannten Krankheitsgenen für die fDCM kodieren die meisten für Proteine der kardialen Kraftproduktion und Impulsübertragung. Interessanterweise können Varianten in den gleichen Genen unterschiedliche Formen von Kardiomyopathien verursachen. Desmoglein-2 (DSG2) ist ein Kalzium-bindendes transmembranäres Glykoprotein, welches in den kardialen Glanzstreifen lokalisiert ist und die zelluläre Kraftübertragung vermittelt. DSG2 wurde bereits als wichtiges Krankheitsgen für die arrhythmogene rechtsventrikuläre Kardiomyopathie (ARVC/D) identifiziert. Um zu untersuchen, ob Sequenzvarianten im DSG2 Gen auch bei der fDCM eine Rolle spielen, wurden die 15 kodierenden Exons bei 73 Patienten mit fDCM sequenziert und kodierende Varianten zusätzlich in 180 Kontrollprobanden untersucht. Es konnten insgesamt 15 Varianten im DSG2-Gen identifiziert werden, darunter waren sechs Kodierende. Zwei dieser kodierenden Varianten (V56M und V920G) waren in dem Kontrollkollektiv nicht nachweisbar. Interessanterweise wurden beide dieser Varianten kurz zuvor als ursächlich für die familiäre ARVC/D beschrieben. Die genetischen Analysen bei den betroffenen Angehörigen der beiden Variantenträger zeigten allerdings, dass nur die Variante V56M mit einem autosomal-dominanten Erbgang der fDCM innerhalb des Stammbaums vereinbar ist. Zudem konnte in einer Fall-Kontrollstudie mit 538 Patienten mit idiopathischer DCM und 432 Kontrollindividuen gezeigt werden, dass die V56M Variante signifikant mit dem Auftreten einer DCM assoziiert ist (p>0.007). Die Variante V56M im DSG2-Gen könnte folglich eine neue Risikovariante für die DCM darstellen.Dilated cardiomyopathy (DCM) is with a prevalence of 36/100.000 a frequent heart disease and the most frequent cause for heart transplantation. Familial DCM (fDCM) may be present in about 20-30% of the cases. Numerous single gene mutations have been described in fDCM subjects indicating a highly heterogenous backround. In many cases of fDCM the genetic cause of the disease is still unknown. Recent investigations suggest that diminished cellular anchorage and lateral myocyte integration via the intercalated disc (ID) are involved in the DCM pathogenesis. Mutations in such genes can cause different phenotypes of cardiomyopathy suggesting a shared molecular etiology of the different cardiomyopathy phenotypes. Desmoglein- 2 (DSG2) is a desmosomal cadherin highly expressed in the ID mediating cardiomyocyte adhesion by calcium dependent dimerization. Mutations in DSG2 were identified in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). However, mutations in other ID genes have also been shown to cause DCM in humans. To investigate the pathogenetic impact of genetic variants in DSG2 on pathogenesis of DCM all 15 exons of DSG2 were sequenced and 180 control probands were screened for the detected coding variants. 15 genetic variants, six of them coding, were identified in DSG2. Two of the coding variants (V56M and V920G) were absent in 180 control probands. Suprisingly, both variants were recently reported in patients with ARVC. Yet, In this study only the V56M variant showed segregation with DCM in a family pedigree. Subsequent, analysis of 538 patients with idiopathic DCM and 617 consecutive contol individuals resulted in identification of thirteen V56M carriers with DCM, whereas only three control subjects harbored the variant. Thus, the variant shows a high association to the disease in this case-control study. Wether or not the V56M variant is a new risk variant for DCM remains to be investigated

“Do no further harm” – Why shall we sedate unresponsive patients?

Ziel: Adipositas ist hochprävalent und mit einer Reihe von Folgeerkrankungen und einem erhöhten Mortalitätsrisiko assoziiert. Die Entstehung und Aufrechterhaltung der Adipositas wurde dabei mit einer veränderten Reaktion auf Nahrungsmittelreize, der sogenannten Reizreaktivität, in Verbindung gebracht. Die funktionelle Kernspintomographie stellt ein innovatives Verfahren zur Untersuchung der neurobiologischen Grundlage der Reizreaktivität auf Nahrungsmittelreize dar und ermöglicht zudem eine Prüfung der Zusammenhänge der neuralen Reizreaktivtät mit der klinisch beobachteten Symptomatik und erlaubt es zudem Parallelen zu Abhängigkeitserkrankungen zu untersuchen. Methode, Ergebnisse und Schlussfolgerungen: In diesem narrativen Review werden die Befunde zur neuralen Reizreaktivität auf Nahrungsmittelreize sowie deren Zusammenhang mit Essverhalten und dem Erfolg gewichtsreduzierender Maßnahmen zusammenfassend dargestellt und ebenso Befunde zu Determinanten der neuralen Reizreaktivität erörtert. Darüber hinaus werden die Limitationen der bisherigen Studien und der genutzten Bildgebungs-Methodik diskutiert

Diminishing benefits of urban living for children and adolescents’ growth and development

Optimal growth and development in childhood and adolescence is crucial for lifelong health and well-being1–6. Here we used data from 2,325 population-based studies, with measurements of height and weight from 71 million participants, to report the height and body-mass index (BMI) of children and adolescents aged 5–19 years on the basis of rural and urban place of residence in 200 countries and territories from 1990 to 2020. In 1990, children and adolescents residing in cities were taller than their rural counterparts in all but a few high-income countries. By 2020, the urban height advantage became smaller in most countries, and in many high-income western countries it reversed into a small urban-based disadvantage. The exception was for boys in most countries in sub-Saharan Africa and in some countries in Oceania, south Asia and the region of central Asia, Middle East and north Africa. In these countries, successive cohorts of boys from rural places either did not gain height or possibly became shorter, and hence fell further behind their urban peers. The difference between the age-standardized mean BMI of children in urban and rural areas was <1.1 kg m–2 in the vast majority of countries. Within this small range, BMI increased slightly more in cities than in rural areas, except in south Asia, sub-Saharan Africa and some countries in central and eastern Europe. Our results show that in much of the world, the growth and developmental advantages of living in cities have diminished in the twenty-first century, whereas in much of sub-Saharan Africa they have amplified

Heterogeneous contributions of change in population distribution of body mass index to change in obesity and underweight

From 1985 to 2016, the prevalence of underweight decreased, and that of obesity and severe obesity increased, in most regions, with significant variation in the magnitude of these changes across regions. We investigated how much change in mean body mass index (BMI) explains changes in the prevalence of underweight, obesity, and severe obesity in different regions using data from 2896 population-based studies with 187 million participants. Changes in the prevalence of underweight and total obesity, and to a lesser extent severe obesity, are largely driven by shifts in the distribution of BMI, with smaller contributions from changes in the shape of the distribution. In East and Southeast Asia and sub-Saharan Africa, the underweight tail of the BMI distribution was left behind as the distribution shifted. There is a need for policies that address all forms of malnutrition by making healthy foods accessible and affordable, while restricting unhealthy foods through fiscal and regulatory restrictions