Excess adiposity is an established risk factor for all-cause mortality, likely mediated mainly through its effects on a wide range of chronic diseases, including several types of cancer, type 2 diabetes, and cardiovascular disease. In their population-based cohort study published in The Lancet Diabetes & Endocrinology, Krishnan Bhaskaran and colleagues1Bhaskaran K dos-Santos-Silva I Leon DA Douglas IJ Smeeth L Association of BMI with overall and cause-specific mortality: a population-based cohort study of 3·6 million adults in the UK.Lancet Diabetes Endocrinol. 2018; (published online Oct 30.)http://dx.doi.org/10.1016/S2213-8587(18)30288-2Summary Full Text Full Text PDF PubMed Scopus (438) Google Scholar found a J-shaped association between BMI and overall mortality among 3·6 million adults in the UK. This study provides further support for the strong association between increasing BMI and excess mortality at BMI of 25 kg/m2 or higher (estimated hazard ratio per 5 kg/m2 increase 1·21 [95% CI 1·20–1·22]). These observations are consistent with several recent studies, collectively representing tens of millions of participants globally.2Global BMI Mortality CollaborationBody-mass index and all-cause mortality: individual-participant-data meta-analysis of 239 prospective studies in four continents.Lancet. 2016; 388: 776-786Summary Full Text Full Text PDF PubMed Scopus (1306) Google Scholar, 3GBD 2015 Obesity CollaboratorsHealth effects of overweight and obesity in 195 countries over 25 years.N Engl J Med. 2017; 377: 13-27Crossref PubMed Scopus (3646) Google Scholar, 4Aune D Sen A Prasad M et al.BMI and all cause mortality: systematic review and non-linear dose-response meta-analysis of 230 cohort studies with 3·74 million deaths among 30·3 million participants.BMJ. 2016; 353: i2156Crossref PubMed Scopus (453) Google Scholar The authors also report the association between BMI and deaths from specific causes, with optimal BMI in the range of 21–25 kg/m2 for cancer, cardiovascular, and respiratory deaths. Causes of death with weak or no biological link to excess bodyweight, such as mental health, behavioural, neurological and accidental causes, and suicide, were not associated with increased BMI, but with underweight (<18·5 kg/m2). With a large sample size, the authors analytically controlled for biases that often underestimate the magnitude of the association of BMI with mortality in their primary analyses, by limiting their analyses to never smokers and excluding deaths occurring less than 5 years from BMI ascertainment. Participants with prevalent chronic diseases that affect bodyweight and subsequent mortality risk (eg, cancer, neurological diseases, and cardiovascular disease) were included in the main analyses, although they were excluded in sensitivity analyses that confirmed the main results. In this study, the J-shaped association between BMI and all-cause mortality was partly driven by the associations between lower BMI or underweight and increased mortality from mental and behavioural, neurological, and external causes. There is a high likelihood that these associations reflect methodological issues such as reverse causation (ie, low BMI is the consequence rather than the cause of these conditions), but further research is needed to disentangle complex associations between these mental health and neurological conditions and bodyweight. This study also quantified the population attributable fraction (PAF), an estimate of the contribution of overweight and obesity to total mortality, or the potential population-level reduction in mortality given the hypothetical scenario in which everyone had been of optimal bodyweight. Because this metric accounts for the prevalence of exposure in the population, it arguably better reflects the disproportionate burden for underweight versus overweight and obese categories than the J-shaped association. As such, the authors estimated that, assuming causality, overweight and obesity (BMI ≥25 kg/m2) contributed to 5·5% of total deaths, whereas underweight contributed to 0·7%, in their UK-based study population. The estimate for excess bodyweight with mortality is similar to that of the 2015 Global Burden of Disease Study,3GBD 2015 Obesity CollaboratorsHealth effects of overweight and obesity in 195 countries over 25 years.N Engl J Med. 2017; 377: 13-27Crossref PubMed Scopus (3646) Google Scholar which estimated that, globally, overweight and obesity contributed to approximately 7·1% (95% uncertainty interval 4·9–9·6) of total deaths. PAF estimates are expected to vary across study populations according to the time period of data collection, socioeconomic development, and the ranking of common causes of mortality. Estimates of PAF for excess bodyweight with mortality will also continue to be a moving target as the population distribution of BMI shifts. Regardless, this metric provides a useful tool for health-care providers and stakeholders to appreciate the importance of overweight and obesity as an important driver of excess mortality. This study adds to the overwhelming evidence about the public health importance of the obesity epidemic to overall and cause-specific mortality. It also has important clinical and public health implications for obesity prevention, especially for the prevention of further increase in bodyweight and waist size among moderately overweight individuals. Although the debate might persist as to the precise point at which the association between continuous BMI with excess mortality becomes statistically significant, it is important to note that most people will gain weight throughout midlife, which is associated with increased subsequent risk of chronic diseases and mortality.5Zheng Y Manson JE Yuan C et al.Associations of weight gain from early to middle adulthood with major health outcomes later in life.JAMA. 2017; 318: 255-269Crossref PubMed Scopus (290) Google Scholar Many individuals with a BMI in the range of overweight (25·0–29·9 kg/m2) are already on a trajectory of gaining more weight that will transition them into the BMI range of obesity (≥30·0 kg/m2). Therefore, although the excess mortality associated with overweight is relatively small, it is important for overweight individuals to prevent further weight gain. Even among older populations, a plateau or decline in bodyweight often masks a trajectory of fat mass gain, offset by losses in lean body mass (ie, decreases in muscle tissue and bone density).6Sheehan TJ DuBrava S DeChello LM Fang Z Rates of weight change for black and white Americans over a twenty year period.Int J Obes Relat Metab Disord. 2003; 27: 498-504Crossref PubMed Scopus (160) Google Scholar Therefore, it is important for older individuals to prevent an increase in waist size, a marker of abdominal obesity, while minimising loss of muscle mass. Additional studies might shed more light on the role of body fat distributions and different fat depots in chronic disease morbidity and mortality. Meanwhile, current efforts need to be intensified to identify more effective and impactful strategies for prevention of weight gain and obesity-related comorbidities. FBH reports grants from the California Walnut Commission and personal fees from Standard Process, Metagenics, and Diet Quality Photo Navigation, outside the submitted work; FBH's research is funded by US National Institutes of Health (NIH) grants HL60712, HL118264, and DK112940. DKT declares no competing interests. Association of BMI with overall and cause-specific mortality: a population-based cohort study of 3·6 million adults in the UKBMI had J-shaped associations with overall mortality and most specific causes of death; for mental and behavioural, neurological, and external causes, lower BMI was associated with increased mortality risk. Full-Text PDF Open Access
A rapid, low‐cost technique of microfabrication for feature sizes of 20 μm or more is described, which is useful for the rapid production of limited numbers of microsensor and optical structures. The pattern can be designed on a PC and printed out on transparent films of polymers using a commercial image‐setting system. The Figure shows an SEM image of a relief pattern generated on photoresistant film using this method. magnified image
The effect of void nucleation and growth on overall stress-strain behavior is investigated for solids undergoing plastic straining under axisymmetric and shearing conditions. Contact between the void surface and the nucleating particle is taken into account and is found to be important under shear and under axisymmetric straining when the stress triaxiality is low. The notion of the macroscopic stress drop due to nucleation of a void is defined and computed, both for isolated voids and for voids in periodic arrays. The stress drop for an isolated void in an infinite matrix can be used to predict softening due to void nucleation when the void concentration is dilute. Interaction between voids in shear during nucleation is analysed numerically and softening effects are calculated along with large strain aspects of void deformation during subsequent growth.
Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
The purpose of this study was to describe gender differences in children's health until the age of 7 y. The study cohort consisted of all children born in Finland in 1987 (n = 60 254), of whom 99.9% were identified in the follow-up. Childhood health data were received from five national registers (1987-94), from regional registers of intellectual disabilities (1987-96) and from education registers in the largest county (1996). Boys had a 20% higher risk for a low 5-min Apgar score and an 11% higher risk for being preterm. After the perinatal period, boys had a 64% higher cumulative incidence of asthma, a 43% higher cumulative incidence of intellectual disability, a 22% higher incidence of mortality and a higher, but not statistically significant, incidence of epilepsy and vision disorders. No male excess was found for diabetes or hearing disorders. The healthcare-related indicators showed poorer health for boys, who had a 37% higher mean of hospital days, a 28% higher risk for receiving social benefits due to health problems and a 13% higher risk for long-term medication. The differences in the socially defined indicators were greatest, and boys had a two- to three-fold risk of having delayed development, postponed school start or attendance in special education programmes. Gender differences in different social classes were similar. Boys' shorter gestational age at birth did not explain the gender differences in childhood health. Some of boys' poorer health seemed to be biologically based, but the social causes of health problems are amenable to change. In particular, the potential of the school system to reduce ill health among boys should be investigated.
ADVERTISEMENT RETURN TO ISSUEPREVCommunicationNEXTShape-Selective Recognition and Self-Assembly of mm-Scale ComponentsInsung S. Choi, Ned Bowden, and George M. WhitesidesView Author Information Department of Chemistry and Chemical Biology Harvard University, 12 Oxford Street Cambridge, Massachusetts 02138 Cite this: J. Am. Chem. Soc. 1999, 121, 8, 1754–1755Publication Date (Web):February 13, 1999Publication History Received8 May 1998Revised10 December 1998Published online13 February 1999Published inissue 1 March 1999https://doi.org/10.1021/ja9816032Copyright © 1999 American Chemical SocietyRIGHTS & PERMISSIONSArticle Views445Altmetric-Citations24LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InReddit Read OnlinePDF (46 KB) Get e-AlertsSupporting Info (1)»Supporting Information Supporting Information SUBJECTS:Hydrophobicity,Interfaces,Ligands,Receptors,Self organization Get e-Alerts
Covers advancements in spacecraft and tactical and strategic missile systems, including subsystem design and application, mission design and analysis, materials and structures, developments in space sciences, space processing and manufacturing, space operations, and applications of space technologies to other fields.
To the Editor: In their meta-analysis of BMI and mortality "to inform decision making in the clinical setting," Dr Flegal and colleagues1 found that mortality was not increased up to a BMI of less than 35.
We present simulations of 3 D dynamic fracture which suggest that a persistent elastic wave is generated in response to a localized perturbation of a propagating crack front, e.g., by a local heterogeneity of critical fracture energy. The wave propagates along the moving crack front and spreads, relative to its origin point on the fractured surface, at a speed slightly below the Rayleigh speed. The simulations were done using the spectral elastodynamic methodology of Geubelle and Rice (1995). They model failure by a displacement-weakening cohesive model, which corresponds in the singular crack limit to crack growth at a critical fracture energy. Confirmation that crack front waves with properties like in our simulation do exist has been provided by Ramanathan and Fisher (1997). Through a derivation based on the linearized perturbation analysis of dynamic singular tensile crack growth by Willis and Movchan (1995), those authors found by numerical evaluation that a transfer function thereby introduced has a simple pole at a certain ω κ ratio, corresponding to a non-dispersive wave. Further, we show that as a consequence of these persistent waves, when a crack grows through a region of small random fluctuations in fracture energy, the variances of both the local propagation velocity and the deformed slope of the crack front increase, according to linearized perturbation theory, in direct proportion to distance of growth into the randomly heterogeneous region. That rate of disordering is more rapid than the growth of the variances with the logarithm of distance established by Perrin and Rice (1994) for a model elastodynamic fracture theory based on a scalar wave equation. That scalar case, which shows slowly decaying (as t− 1 2 ) rather than persistent crack front waves, is analyzed here too.
