Energy labelling of alcoholic drinks as a public health policy to reduce obesity: An integrative review

Objective: Both excessive alcohol consumption and obesity produce a considerable public health burden. Alcohol is calorie dense, but unlike food products, alcoholic drinks tend to be exempt from nutritional labelling laws that require energy content information to be displayed on packaging or at point of purchase. Design: Here we provide an integrative review on the potential of alcoholic drink energy labelling as a public health policy to reduce obesity. Results: We first outline the contribution that alcohol makes to population level daily energy intake and the role that alcohol consumption may have in promoting obesity. We next discuss the extent to which there is a consumer need for alcoholic drink energy labelling and the potential impact that energy labelling of alcoholic drinks would have on both consumer and industry behaviour. The direct and indirect pathways and mechanisms by which energy labelling of alcoholic drinks could theoretically influence public health are discussed, as well as possible unintended consequences of alcoholic drink energy labelling. Conclusion: We conclude by discussing key questions that will need to be answered by future research in order to determine how effective energy labelling of alcoholic drink policies will be in reducing obesity and improving public health

Energy labelling of alcoholic drinks: An important or inconsequential obesity policy?

Alcohol is calorie dense, but unlike food products, alcoholic drinks tend to be exempt from nutritional labelling laws that require energy content information to be displayed on packaging or at point of purchase. This review provides a perspective on the likely efficacy of alcoholic drink energy labelling as a public health policy to reduce obesity and discusses key questions to be addressed by future research. First, the contribution that alcohol makes to population level daily energy intake and obesity is outlined. Next, consumer need for alcohol energy labelling and the potential impacts on both consumer and industry behavior are discussed. Pathways and mechanisms by which energy labelling of alcoholic drinks could reduce obesity are considered, as well as possible unintended consequences of alcoholic drink energy labelling. Would widespread energy labelling of alcoholic drinks reduce obesity? The unclear effect that alcohol has on population level obesity, the modest contribution calories from alcohol make to daily energy intake and limited impact nutritional labelling policies tend to have on behavior, suggest alcohol energy labelling may have limited impact on population obesity prevalence as a standalone policy. However, there are a number of questions that will need to be answered by future research to make definitive conclusions on the potential for alcohol energy labelling policies to reduce obesity

Energy labelling of alcoholic drinks as a public health policy to reduce obesity: An integrative review

Objective: Both excessive alcohol consumption and obesity produce a considerable public health burden. Alcohol is calorie dense, but unlike food products, alcoholic drinks tend to be exempt from nutritional labelling laws that require energy content information to be displayed on packaging or at point of purchase. Design: Here we provide an integrative review on the potential of alcoholic drink energy labelling as a public health policy to reduce obesity. Results: We first outline the contribution that alcohol makes to population level daily energy intake and the role that alcohol consumption may have in promoting obesity. We next discuss the extent to which there is a consumer need for alcoholic drink energy labelling and the potential impact that energy labelling of alcoholic drinks would have on both consumer and industry behaviour. The direct and indirect pathways and mechanisms by which energy labelling of alcoholic drinks could theoretically influence public health are discussed, as well as possible unintended consequences of alcoholic drink energy labelling. Conclusion: We conclude by discussing key questions that will need to be answered by future research in order to determine how effective energy labelling of alcoholic drink policies will be in reducing obesity and improving public health.</p

Energy labelling of alcoholic drinks : An important or inconsequential obesity policy?

Alcohol is calorie dense, but unlike food products, alcoholic drinks tend to be exempt from nutritional labelling laws that require energy content information to be displayed on packaging or at point of purchase. This review provides a perspective on the likely efficacy of alcoholic drink energy labelling as a public health policy to reduce obesity and discusses key questions to be addressed by future research. First, the contribution that alcohol makes to population level daily energy intake and obesity is outlined. Next, consumer need for alcohol energy labelling and the potential impacts on both consumer and industry behavior are discussed. Pathways and mechanisms by which energy labelling of alcoholic drinks could reduce obesity are considered, as well as possible unintended consequences of alcoholic drink energy labelling. Would widespread energy labelling of alcoholic drinks reduce obesity? The unclear effect that alcohol has on population level obesity, the modest contribution calories from alcohol make to daily energy intake and limited impact nutritional labelling policies tend to have on behavior, suggest alcohol energy labelling may have limited impact on population obesity prevalence as a standalone policy. However, there are a number of questions that will need to be answered by future research to make definitive conclusions on the potential for alcohol energy labelling policies to reduce obesity

Using an Open Educational Resources Platform to Support Underserved Groups

The Open University (OU) United Kingdom manages two platforms for hosting Open Educational Resources (OER): OpenLearn, delivering the OU’s OER, reaching over10 million learners a year, attracting a mostly UK audience, and OpenLearn Create, reaching 3 million learners a year, where anyone can create and share OER, attracting a mostly international – non-UK – audience. Both platforms release OER using a Creative Commons license and afford accessibility to learning materials specifically catering to the needs of underserved groups, in other words, individuals or groups who may have limited access to education or continuing professional development (CPD) either as recipient or as educator. Using case studies, research data analytics and survey data, this chapter reveals how the approach to delivering OER on OpenLearn Create fosters community engagement and outreach across a broad spectrum of projects in a range of languages and format often to those with restricted access to professional development within organizations. The chapter discusses weaknesses in the platform’s usability for delivering online courses, but strengths and recommendations for its use as an adaptable project-based tool. Research data also reveal that where an institution is prepared to minimally support the provision of such a platform, the contribution to humanizing education for OER projects globally is great

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

: Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2-4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

AbstractCritical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease.</jats:p

Mapping the human genetic architecture of COVID-19

AbstractThe genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease.</jats:p