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Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci ( P  < 5 × 10 −8 ), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for ∼2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis. A genome-wide association study and Metabochip meta-analysis of body mass index (BMI) detects 97 BMI-associated loci, of which 56 were novel, and many loci have effects on other metabolic phenotypes; pathway analyses implicate the central nervous system in obesity susceptibility and new pathways such as those related to synaptic function, energy metabolism, lipid biology and adipogenesis. Genetic correlates of obesity In the second of two Articles in this issue from the GIANT Consortium, Elizabeth Speliotes and collegues conducted a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), commonly used to define obesity and assess adiposity, to find 97 BMI-associated loci, of which 56 were novel. Many of these loci have significant effects on other metabolic phenotypes. The 97 loci account for about 2.7% of BMI variation, and genome-wide estimates suggest common variation accounts for more than 20% of BMI variation. Pathway analyses implicate the central nervous system in obesity susceptibility including synaptic function, glutamate signaling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.

For most Americans, staying \"mentally sharp\" as they age is a very high priority. Declines in memory and decision-making abilities may trigger fears of Alzheimer's disease or other neurodegenerative diseases. However, cognitive aging is a natural process that can have both positive and negative effects on cognitive function in older adults - effects that vary widely among individuals. At this point in time, when the older population is rapidly growing in the United States and across the globe, it is important to examine what is known about cognitive aging and to identify and promote actions that individuals, organizations, communities, and society can take to help older adults maintain and improve their cognitive health. Cognitive Aging assesses the public health dimensions of cognitive aging with an emphasis on definitions and terminology, epidemiology and surveillance, prevention and intervention, education of health professionals, and public awareness and education. This report makes specific recommendations for individuals to reduce the risks of cognitive decline with aging. Aging is inevitable, but there are actions that can be taken by individuals, families, communities, and society that may help to prevent or ameliorate the impact of aging on the brain, understand more about its impact, and help older adults live more fully and independent lives. Cognitive aging is not just an individual or a family or a health care system challenge. It is an issue that affects the fabric of society and requires actions by many and varied stakeholders. Cognitive Aging offers clear steps that individuals, families, communities, health care providers and systems, financial organizations, community groups, public health agencies, and others can take to promote cognitive health and to help older adults live fuller and more independent lives. Ultimately, this report calls for a societal commitment to cognitive aging as a public health issue that requires prompt action across many sectors.

This book lays out the reasons why we should study cognitive development in adulthood, and presents the history, latest data, and results from the Seattle Longitudinal Study (SLS), which now extends to over forty-five years. The SLS is organized around five questions: does intelligence change uniformly throughout adulthood, or are there different life-course-ability patterns? At what age and at what magnitude can decrement in ability be reliably detected? What are the patterns and magnitude of generational differences? What accounts for individual differences in age-related change in adulthood? Can the intellectual decline that increases with age be reversed by educational intervention? Based on work on the SLS, this book presents a conceptual model. The model represents this book's author's view on the factors that influence cognitive development throughout the human lifespan, and provides a rationale for the various influences that have been investigated — genetic factors, early and current family environment, life styles, the experience of chronic disease, and various personality attributes. The data in this volume include the 1998 longitudinal cycle of the SLS. In light of both new data and revised analyses, psychometric and neuropsychological assessments have been linked in long-term data to aid in the early identification of risk for dementia in later life. The book also presents new data and concludes on the impact of personality on cognition. It includes correlation matrices and web-access information for select data sets.

AbstractObjectivesTo use the estimates from the Global Burden of Disease Study 2016 to describe patterns of suicide mortality globally, regionally, and for 195 countries and territories by age, sex, and Socio-demographic index, and to describe temporal trends between 1990 and 2016.DesignSystematic analysis.Main outcome measuresCrude and age standardised rates from suicide mortality and years of life lost were compared across regions and countries, and by age, sex, and Socio-demographic index (a composite measure of fertility, income, and education).ResultsThe total number of deaths from suicide increased by 6.7% (95% uncertainty interval 0.4% to 15.6%) globally over the 27 year study period to 817 000 (762 000 to 884 000) deaths in 2016. However, the age standardised mortality rate for suicide decreased by 32.7% (27.2% to 36.6%) worldwide between 1990 and 2016, similar to the decline in the global age standardised mortality rate of 30.6%. Suicide was the leading cause of age standardised years of life lost in the Global Burden of Disease region of high income Asia Pacific and was among the top 10 leading causes in eastern Europe, central Europe, western Europe, central Asia, Australasia, southern Latin America, and high income North America. Rates for men were higher than for women across regions, countries, and age groups, except for the 15 to 19 age group. There was variation in the female to male ratio, with higher ratios at lower levels of Socio-demographic index. Women experienced greater decreases in mortality rates (49.0%, 95% uncertainty interval 42.6% to 54.6%) than men (23.8%, 15.6% to 32.7%).ConclusionsAge standardised mortality rates for suicide have greatly reduced since 1990, but suicide remains an important contributor to mortality worldwide. Suicide mortality was variable across locations, between sexes, and between age groups. Suicide prevention strategies can be targeted towards vulnerable populations if they are informed by variations in mortality rates.

This book examines the various ways in which age affects the process and the product of foreign language learning in a school setting. It presents studies that cover a wide range of topics, from phonetics to learning strategies. It will be of interest to students and researchers working in SLA research, language planning and language teaching.

Examination of approximately 10,000 specimens obtained during surgery for intractable seizures in children and adults resulted in 36 distinct diagnoses in seven categories; the most common diagnoses were hippocampal sclerosis, ganglioglioma, and focal cortical dysplasia.

The future of disability in America will depend on how well the U.S. prepares for and manages the demographic, fiscal, and technological developments that will unfold during the next two to three decades. Building upon two prior studies from the Institute of Medicine (the 1991 Institute of Medicine's report Disability in America and the 1997 report Enabling America ), The Future of Disability in America examines both progress and concerns about continuing barriers that limit the independence, productivity, and participation in community life of people with disabilities. This book offers a comprehensive look at a wide range of issues, including the prevalence of disability across the lifespan; disability trends the role of assistive technology; barriers posed by health care and other facilities with inaccessible buildings, equipment, and information formats; the needs of young people moving from pediatric to adult health care and of adults experiencing premature aging and secondary health problems; selected issues in health care financing (e.g., risk adjusting payments to health plans, coverage of assistive technology); and the organizing and financing of disability-related research. The Future of Disability in America is an assessment of both principles and scientific evidence for disability policies and services. This book's recommendations propose steps to eliminate barriers and strengthen the evidence base for future public and private actions to reduce the impact of disability on individuals, families, and society.

The COVID-19 pandemic has shown a markedly low proportion of cases among children 1 – 4 . Age disparities in observed cases could be explained by children having lower susceptibility to infection, lower propensity to show clinical symptoms or both. We evaluate these possibilities by fitting an age-structured mathematical model to epidemic data from China, Italy, Japan, Singapore, Canada and South Korea. We estimate that susceptibility to infection in individuals under 20 years of age is approximately half that of adults aged over 20 years, and that clinical symptoms manifest in 21% (95% credible interval: 12–31%) of infections in 10- to 19-year-olds, rising to 69% (57–82%) of infections in people aged over 70 years. Accordingly, we find that interventions aimed at children might have a relatively small impact on reducing SARS-CoV-2 transmission, particularly if the transmissibility of subclinical infections is low. Our age-specific clinical fraction and susceptibility estimates have implications for the expected global burden of COVID-19, as a result of demographic differences across settings. In countries with younger population structures—such as many low-income countries—the expected per capita incidence of clinical cases would be lower than in countries with older population structures, although it is likely that comorbidities in low-income countries will also influence disease severity. Without effective control measures, regions with relatively older populations could see disproportionally more cases of COVID-19, particularly in the later stages of an unmitigated epidemic. A new epidemiological study shows reduced susceptibility to SARS-CoV-2 and decreased risk of developing severe symptoms in people aged younger than 20 years, suggesting that children have limited contribution to spread of COVID-19.

Ageing and age-related diseases share some basic mechanistic pillars that largely converge on inflammation. During ageing, chronic, sterile, low-grade inflammation — called inflammaging — develops, which contributes to the pathogenesis of age-related diseases. From an evolutionary perspective, a variety of stimuli sustain inflammaging, including pathogens (non-self), endogenous cell debris and misplaced molecules (self) and nutrients and gut microbiota (quasi-self). A limited number of receptors, whose degeneracy allows them to recognize many signals and to activate the innate immune responses, sense these stimuli. In this situation, metaflammation (the metabolic inflammation accompanying metabolic diseases) is thought to be the form of chronic inflammation that is driven by nutrient excess or overnutrition; metaflammation is characterized by the same mechanisms underpinning inflammaging. The gut microbiota has a central role in both metaflammation and inflammaging owing to its ability to release inflammatory products, contribute to circadian rhythms and crosstalk with other organs and systems. We argue that chronic diseases are not only the result of ageing and inflammaging; these diseases also accelerate the ageing process and can be considered a manifestation of accelerated ageing. Finally, we propose the use of new biomarkers (DNA methylation, glycomics, metabolomics and lipidomics) that are capable of assessing biological versus chronological age in metabolic diseases.

Older people have been reported to be at higher risk of COVID-19 mortality. This study explored the factors mediating this association and whether older age was associated with increased mortality risk in the absence of other risk factors. In UK Biobank, a population cohort study, baseline data were linked to COVID-19 deaths. Poisson regression was used to study the association between current age and COVID-19 mortality. Among eligible participants, 438 (0.09%) died of COVID-19. Current age was associated exponentially with COVID-19 mortality. Overall, participants aged ≥75 years were at 13-fold (95% CI 9.13-17.85) mortality risk compared with those <65 years. Low forced expiratory volume in 1 second, high systolic blood pressure, low handgrip strength, and multiple long-term conditions were significant mediators, and collectively explained 39.3% of their excess risk. The associations between these risk factors and COVID-19 mortality were stronger among older participants. Participants aged ≥75 without additional risk factors were at 4-fold risk (95% CI 1.57-9.96, P = 0.004) compared with all participants aged <65 years. Higher COVID-19 mortality among older adults was partially explained by other risk factors. 'Healthy' older adults were at much lower risk. Nonetheless, older age was an independent risk factor for COVID-19 mortality.