MRC Epidemiology Unit

Cambridge, United Kingdom

MRC Epidemiology Unit

Cambridge, United Kingdom

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News Article | April 25, 2017
Site: www.biosciencetechnology.com

The largest genomic analysis of puberty timing in men and women conducted to date has identified 389 genetic signals associated with puberty timing, four times the number that were previously known. The study, published in Nature Genetics and led by researchers from the Medical Research Council (MRC) Epidemiology Unit at the University of Cambridge and other scientists in the international ReproGen consortium, also found new genetic evidence linking earlier timing of puberty to higher risk of several cancers known to be sensitive to sex-hormones in later life, including breast, ovary and endometrial cancers in women, and prostate cancer in men. These influences remained after controlling for body weight, which is important as body weight itself influences both the timing of puberty and the risk of some cancers. Dr. John Perry, Senior Investigator Scientist from the MRC Epidemiology Unit and senior author on the paper, says: "Previous studies suggested that the timing of puberty in childhood was associated with risks of disease decades later, but until now it was unclear if those were circumstantial observations, for example secondary to other factors such as body weight. “Our current study identifies direct causal links between earlier puberty timing itself and increased cancer risk. This link could possibly be explained by higher levels of sex hormones throughout life, but we need to do more work to understand the exact mechanisms involved. We aim to understand these disease links and thereby contribute to the prevention of diseases in later life." The timing of puberty varies widely between individuals but tends to run closely within families. Earlier puberty timing may have advantages for some adolescents, for example for boys who engage actively in sports, but it appears to have largely negative effects on later health, such as higher risks of heart disease and some cancers. By performing detailed assessments of genetic variants across the whole genome in 329,345 women, comprising data from 40 studies in the ReproGen consortium, UK Biobank, and consented 23andMe customers, this study identified 389 independent genetic signals for age at puberty in women. This observation was then confirmed in a further 39,543 women from the deCODE study, Iceland. Many of these genetic associations were also found to influence age at voice breaking, a comparable measure of puberty timing in men. These findings shed light on the mechanisms that regulate puberty timing. Perry adds: "These newly identified genetic factors explain one quarter of the estimated heritability of puberty timing. Our findings highlight the remarkable biological complexity of puberty timing, with likely thousands of genetic factors, in combination with numerous environmental triggers, acting together to control the timing of this key transition from childhood to adult life.” Dr. Ken Ong, also from the MRC Epidemiology Unit and joint senior author on the paper, says: "One of the more remarkable findings concerns the role of certain types of genes called imprinted genes, which are only active in your body when inherited specifically from one parent but not the other. We identified rare variants in two genes, which both lower the age of puberty when inherited from your father, but have no effect when inherited from your mother. This is intriguing as it suggests that mothers and fathers might benefit differently from puberty occurring at earlier or later ages in their children."


News Article | April 24, 2017
Site: www.eurekalert.org

The largest genomic analysis of puberty timing in men and women conducted to date has identified 389 genetic signals associated with puberty timing, four times the number that were previously known. The study, published today in Nature Genetics and led by researchers from the Medical Research Council (MRC) Epidemiology Unit at the University of Cambridge and other scientists in the international ReproGen consortium, also found new genetic evidence linking earlier timing of puberty to higher risk of several cancers known to be sensitive to sex-hormones in later life, including breast, ovary and endometrial cancers in women, and prostate cancer in men. These influences remained after controlling for body weight, which is important as body weight itself influences both the timing of puberty and the risk of some cancers. Dr John Perry, Senior Investigator Scientist from the MRC Epidemiology Unit and senior author on the paper, says: "Previous studies suggested that the timing of puberty in childhood was associated with risks of disease decades later, but until now it was unclear if those were circumstantial observations, for example secondary to other factors such as body weight. "Our current study identifies direct causal links between earlier puberty timing itself and increased cancer risk. This link could possibly be explained by higher levels of sex hormones throughout life, but we need to do more work to understand the exact mechanisms involved. We aim to understand these disease links and thereby contribute to the prevention of diseases in later life." The timing of puberty varies widely between individuals but tends to run closely within families. Earlier puberty timing may have advantages for some adolescents, for example for boys who engage actively in sports, but it appears to have largely negative effects on later health, such as higher risks of heart disease and some cancers. By performing detailed assessments of genetic variants across the whole genome in 329,345 women, comprising data from 40 studies in the ReproGen consortium, UK Biobank, and consented 23andMe customers, this study identified 389 independent genetic signals for age at puberty in women. This observation was then confirmed in a further 39,543 women from the deCODE study, Iceland. Many of these genetic associations were also found to influence age at voice breaking, a comparable measure of puberty timing in men. These findings shed light on the mechanisms that regulate puberty timing. Dr Perry adds: "These newly identified genetic factors explain one quarter of the estimated heritability of puberty timing. Our findings highlight the remarkable biological complexity of puberty timing, with likely thousands of genetic factors, in combination with numerous environmental triggers, acting together to control the timing of this key transition from childhood to adult life." Dr Ken Ong, also from the MRC Epidemiology Unit and joint senior author on the paper, says: "One of the more remarkable findings concerns the role of certain types of genes called imprinted genes, which are only active in your body when inherited specifically from one parent but not the other. We identified rare variants in two genes, which both lower the age of puberty when inherited from your father, but have no effect when inherited from your mother. This is intriguing as it suggests that mothers and fathers might benefit differently from puberty occurring at earlier or later ages in their children." Felix R. Day, Deborah J. Thompson, Hannes Helgason et al. Genomic analyses identify hundreds of variants associated with age at menarche and support a role for puberty timing in cancer risk. Nature Genetics; 24 April 2017; DOI: 10.1038/ng.3841


News Article | November 29, 2016
Site: www.eurekalert.org

People who receive personalized genetic and phenotypic information on their risk of developing diabetes don't significantly increase their physical activity compared to those who get broader, generic information on diabetes, according to a randomized controlled trial of more than 500 healthy adults published in PLOS Medicine by Job Godino from the University of Cambridge School of Clinical Medicine, UK, and colleagues. Information about someone's risk of developing type 2 diabetes can now be calculated both from a genetic standpoint--by detecting the presence of certain risk genes in their DNA -- and from a phenotypic standpoint, using formulas that take into consideration age, body mass index, and other data. But whether informing patients of their risk motivates them to change their behavior has never been clear. In the new study, researchers recruited 569 men and women born between 1950 and 1975 who were already enrolled in the ongoing Fenland Study in England and who had no previous diabetes diagnosis or other chronic diseases. They collected blood samples from the participants to screen for genetic variants and then randomly assigned each person to either a control group who received only standard lifestyle advice on preventing diabetes, or groups that also received either their genetic risk estimate or phenotypic risk estimate of developing diabetes. 8 weeks later, participants were fitted with a device to monitor physical activity for six days. Compared to the control group, receipt of a genetic or phenotypic risk estimate was not associated with more physical activity; the difference in adjusted mean change from baseline in the genetic risk group versus control group was 0.85 kJ/kg/d (95% Confidence interval (CI) ?2.07 to 3.77, p = 0.57), and in the phenotypic risk group versus control group was 1.32 kJ/kg/d (95% CI -1.61 to 4.25, p = 0.38). Nor did the researchers find differences in self-reported behavior, diet, or weight changes. However, the patients who were given their personalized risk of developing diabetes did have a better perception of risk at the conclusion of the study. More research is needed to shed light on whether these results hold true for personalized risk information as it relates to other diseases and whether someone's perception of their risk before the study had any impact on the outcome. "The results of the current study provide further evidence for a shift in focus for promoting healthy changes in habitual, environmentally patterned behaviors, such as physical activity and diet, away from interventions solely based on provision of information and advice to individuals towards interventions that target the wider collective determinants of disease," the authors say. This trial was conducted at the MRC Epidemiology Unit in Cambridge, UK. It was funded by the Medical Research Council (MC_U106179474), the Sixth Framework Programme (LSHM-CT-2006-037197), and the National Institute for Health Research (RP-PG-0606-1259). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The authors have declared that no competing interests exist. Godino JG, van Sluijs EMF, Marteau TM, Sutton S, Sharp SJ, Griffin SJ (2016) Lifestyle Advice Combined with Personalized Estimates of Genetic or Phenotypic Risk of Type 2 Diabetes, and Objectively Measured Physical Activity: A Randomized Controlled Trial. PLoS Med 13(11): e1002185. doi:10.1371/journal.pmed.1002185 MRC Epidemiology Unit, University of Cambridge School of Clinical Medicine, Cambridge, United Kingdom Center for Wireless and Population Health Systems, Department of Family Medicine and Public Health and Calit2's Qualcomm Institute, University of California, San Diego, La Jolla, California, United States of America Behaviour and Health Research Unit, University of Cambridge School of Clinical Medicine, Institute of Public Health, Cambridge, United Kingdom Behavioural Science Group, University of Cambridge School of Clinical Medicine, Institute of Public Health, University of Cambridge, Cambridge, United Kingdom Primary Care Unit, University of Cambridge School of Clinical Medicine, Institute of Public Health, University of Cambridge, Cambridge, United Kingdom IN YOUR COVERAGE PLEASE USE THIS URL TO PROVIDE ACCESS TO THE FREELY AVAILABLE PAPER:http://journals.


News Article | November 21, 2016
Site: www.eurekalert.org

A study published today in the journal PLOS Medicine has identified the five genetic variants associated with higher levels of the branched-chain amino acids isoleucine, leucine and valine. The researchers also found that these genetic variants were associated with an increased risk of type 2 diabetes. The researchers, led by the Medical Research Council (MRC) Epidemiology Unit at the University of Cambridge, used large-scale genetic data together with detailed measurements of the branched-chain amino acids and their metabolites in the blood of more than 16,000 volunteers*. Branched-chain amino acids have fundamental roles in human metabolism and are building blocks of proteins. Unlike some of the other 20 amino acids, they cannot be made by the human body. This means that their levels depend entirely on external sources, from food sources or dietary supplements, and the ability of our body to metabolise them. To date, while higher circulating levels of branched-chain amino acids have been found to be associated with type 2 diabetes, no study has been able to establish whether this link is causal. This is important, because if the relationship is found to be causal, reducing dietary intake or altering the metabolism of these amino acids could help to prevent diabetes, an increasingly common and serious disease. The researchers studied over 10 million genetic variants in more than 16,000 men and women and discovered five regions of the human genome with genetic differences that are associated with higher levels of circulating branched-chain amino acids. They then found that in 300,000 individuals**, including 40,000 diabetes patients, those carrying the genetic differences associated with higher levels of branched-chain amino acids were also found to be at increased risk of type 2 diabetes, providing strong evidence of a causal link. PPM1K, the gene found to be most strongly associated with levels of all three amino acids and also with a higher risk of diabetes, encodes a known regulator of the key step in the breakdown of branched-chain amino acids. This suggests that an impaired breakdown of these amino acids may put individuals at higher risk of type 2 diabetes. Intervening on this pathway may reduce diabetes risk. "Our results suggest that treatment strategies which target metabolism of branched-chain amino acids could help to reduce the risk of diabetes, and we already know which molecules target this metabolic pathway", says Dr Claudia Langenberg from the MRC Epidemiology Unit at the University of Cambridge. Clinical trials will now need to be carried out to establish if drugs that target the breakdown of branched-chain amino acids can reduce the risks of type 2 diabetes. *16,000 volunteers were from the Fenland Study & meta-analysis of KORA and TwinsUK studies. ** 300,000 individuals were from the Diabetes Genetics Replication and Meta-analysis, EPIC_InterAct, GoDART and UK Biobank For further information or to request an interview with a researcher involved with the study, please contact the MRC press office on +44(0)207 395 2345 (Out of Hours: +44(0)7818 428 297) or email press.office@headoffice.mrc.ac.uk Paper details: Genetic Predisposition to an Impaired Metabolism of the Branched-Chain Amino Acids and Risk of Type 2 Diabetes: A Mendelian Randomisation Analysis. Luca Lotta et al. PLOS Medicine. After embargo paper will be available here: http://dx. The Medical Research Council is at the forefront of scientific discovery to improve human health. Founded in 1913 to tackle tuberculosis, the MRC now invests taxpayers' money in some of the best medical research in the world across every area of health. Thirty-one MRC-funded researchers have won Nobel prizes in a wide range of disciplines, and MRC scientists have been behind such diverse discoveries as vitamins, the structure of DNA and the link between smoking and cancer, as well as achievements such as pioneering the use of randomised controlled trials, the invention of MRI scanning, and the development of a group of antibodies used in the making of some of the most successful drugs ever developed. Today, MRC-funded scientists tackle some of the greatest health problems facing humanity in the 21st century, from the rising tide of chronic diseases associated with ageing to the threats posed by rapidly mutating micro-organisms. http://www. The MRC Epidemiology Unit is a department at the University of Cambridge. It studies the genetic, developmental and environmental factors that cause obesity, type 2 diabetes and related metabolic disorders. The outcomes from these studies are then used to develop strategies for the prevention of these diseases in the general population. http://www.


News Article | November 15, 2016
Site: www.sciencedaily.com

A large-scale genetic study has provided strong evidence that the development of insulin resistance -- a risk factor for type 2 diabetes and heart attacks and one of the key adverse consequences of obesity -- results from the failure to safely store excess fat in the body. Overeating and lack of physical activity worldwide has led to rising levels of obesity and a global epidemic of diseases such as heart disease, stroke and type 2 diabetes. A key process in the development of these diseases is the progressive resistance of the body to the actions of insulin, a hormone that controls the levels of blood sugar. When the body becomes resistant to insulin, levels of blood sugars and lipids rise, increasing the risk of diabetes and heart disease. However, it is not clear in most cases how insulin resistance arises and why some people become resistant, particularly when overweight, while others do not. An international team led by researchers at the University of Cambridge studied over two million genetic variants in almost 200,000 people to look for links to insulin resistance. In an article published today in Nature Genetics, they report 53 regions of the genome associated with insulin resistance and higher risk of diabetes and heart disease; only 10 of these regions have previously been linked to insulin resistance. The researchers then carried out a follow-up study with over 12,000 participants in the Fenland and EPIC-Norfolk studies, each of whom underwent a body scan that shows fat deposits in different regions of the body. They found that having a greater number of the 53 genetic variants for insulin resistance was associated with having lower amounts of fat under the skin, particularly in the lower half of the body. The team also found a link between having a higher number of the 53 genetic risk variants and a severe form of insulin resistance characterized by loss of fat tissue in the arms and legs, known as familial partial lipodystrophy type 1. Patients with lipodystrophy are unable to adequately develop fat tissue when eating too much, and often develop diabetes and heart disease as a result. In follow-up experiments in mouse cells, the researchers were also able to show that suppression of several of the identified genes (including CCDC92, DNAH10 and L3MBTL3) results in an impaired ability to develop mature fat cells. "Our study provides compelling evidence that a genetically-determined inability to store fat under the skin in the lower half of the body is linked to a higher risk of conditions such as diabetes and heart disease," says Dr Luca Lotta from the Medical Research Council (MRC) Epidemiology Unit at the University of Cambridge. "Our results highlight the important biological role of peripheral fat tissue as a deposit of the surplus of energy due to overeating and lack of physical exercise." "We've long suspected that problems with fat storage might lead to its accumulation in other organs such as the liver, pancreas and muscles, where it causes insulin resistance and eventually diabetes, but the evidence for this has mostly come from rare forms of human lipodystrophy," adds Professor Sir Stephen O'Rahilly from the MRC Metabolic Diseases Unit and Metabolic Research Laboratories at the University of Cambridge. "Our study suggests that these processes also take place in the general population." Overeating and being physically inactive leads to excess energy, which is stored as fat tissue. This new study suggests that among individuals who have similar levels of eating and physical exercise, those who are less able store the surplus energy as fat in the peripheral body, such as the legs, are at a higher risk of developing insulin resistance, diabetes and cardiovascular disease than those who are able to do so. "People who carry the genetic risk variants that we've identified store less fat in peripheral areas," says Professor Nick Wareham, also from the MRC Epidemiology Unit. "But this does not mean that they are free from risk of disease, because when their energy intake exceeds expenditure, excess fat is more likely to be stored in unhealthy deposits. The key to avoiding the adverse effects is the maintenance of energy balance by limiting energy intake and maximising expenditure through physical activity." These new findings may lead to future improvements in the way we prevent and treat insulin resistance and its complications. The researchers are now collaborating with other academic as well as industry partners with the aim of finding drugs that may reduce the risk of diabetes and heart attack by targeting the identified pathways.


News Article | November 14, 2016
Site: www.chromatographytechniques.com

A large-scale genetic study has provided strong evidence that the development of insulin resistance - a risk factor for type 2 diabetes and heart attacks and one of the key adverse consequences of obesity - results from the failure to safely store excess fat in the body. Overeating and lack of physical activity worldwide has led to rising levels of obesity and a global epidemic of diseases such as heart disease, stroke and type 2 diabetes. A key process in the development of these diseases is the progressive resistance of the body to the actions of insulin, a hormone that controls the levels of blood sugar. When the body becomes resistant to insulin, levels of blood sugars and lipids rise, increasing the risk of diabetes and heart disease. However, it is not clear in most cases how insulin resistance arises and why some people become resistant, particularly when overweight, while others do not. An international team led by researchers at the University of Cambridge studied over 2 million genetic variants in almost 200,000 people to look for links to insulin resistance. In an article published today in Nature Genetics, they report 53 regions of the genome associated with insulin resistance and higher risk of diabetes and heart disease; only 10 of these regions have previously been linked to insulin resistance. The researchers then carried out a follow-up study with over 12,000 participants in the Fenland and EPIC-Norfolk studies, each of whom underwent a body scan that shows fat deposits in different regions of the body. They found that having a greater number of the 53 genetic variants for insulin resistance was associated with having lower amounts of fat under the skin, particularly in the lower half of the body. The team also found a link between having a higher number of the 53 genetic risk variants and a severe form of insulin resistance characterized by loss of fat tissue in the arms and legs, known as familial partial lipodystrophy type 1. Patients with lipodystrophy are unable to adequately develop fat tissue when eating too much, and often develop diabetes and heart disease as a result. In follow-up experiments in mouse cells, the researchers were also able to show that suppression of several of the identified genes (including CCDC92, DNAH10 and L3MBTL3) results in an impaired ability to develop mature fat cells. "Our study provides compelling evidence that a genetically-determined inability to store fat under the skin in the lower half of the body is linked to a higher risk of conditions such as diabetes and heart disease," says Luca Lotta from the Medical Research Council (MRC) Epidemiology Unit at the University of Cambridge. "Our results highlight the important biological role of peripheral fat tissue as a deposit of the surplus of energy due to overeating and lack of physical exercise." "We've long suspected that problems with fat storage might lead to its accumulation in other organs such as the liver, pancreas and muscles, where it causes insulin resistance and eventually diabetes, but the evidence for this has mostly come from rare forms of human lipodystrophy," adds Stephen O'Rahilly from the MRC Metabolic Diseases Unit and Metabolic Research Laboratories at the University of Cambridge. "Our study suggests that these processes also take place in the general population." Overeating and being physically inactive leads to excess energy, which is stored as fat tissue. This new study suggests that among individuals who have similar levels of eating and physical exercise, those who are less able store the surplus energy as fat in the peripheral body, such as the legs, are at a higher risk of developing insulin resistance, diabetes and cardiovascular disease than those who are able to do so. "People who carry the genetic risk variants that we've identified store less fat in peripheral areas," says Professor Nick Wareham, also from the MRC Epidemiology Unit. "But this does not mean that they are free from risk of disease, because when their energy intake exceeds expenditure, excess fat is more likely to be stored in unhealthy deposits. The key to avoiding the adverse effects is the maintenance of energy balance by limiting energy intake and maximising expenditure through physical activity." These new findings may lead to future improvements in the way we prevent and treat insulin resistance and its complications. The researchers are now collaborating with other academic as well as industry partners with the aim of finding drugs that may reduce the risk of diabetes and heart attack by targeting the identified pathways.


News Article | November 14, 2016
Site: www.eurekalert.org

A large-scale genetic study has provided strong evidence that the development of insulin resistance - a risk factor for type 2 diabetes and heart attacks and one of the key adverse consequences of obesity - results from the failure to safely store excess fat in the body. Overeating and lack of physical activity worldwide has led to rising levels of obesity and a global epidemic of diseases such as heart disease, stroke and type 2 diabetes. A key process in the development of these diseases is the progressive resistance of the body to the actions of insulin, a hormone that controls the levels of blood sugar. When the body becomes resistant to insulin, levels of blood sugars and lipids rise, increasing the risk of diabetes and heart disease. However, it is not clear in most cases how insulin resistance arises and why some people become resistant, particularly when overweight, while others do not. An international team led by researchers at the University of Cambridge studied over two million genetic variants in almost 200,000 people to look for links to insulin resistance. In an article published today in Nature Genetics, they report 53 regions of the genome associated with insulin resistance and higher risk of diabetes and heart disease; only 10 of these regions have previously been linked to insulin resistance. The researchers then carried out a follow-up study with over 12,000 participants in the Fenland and EPIC-Norfolk studies, each of whom underwent a body scan that shows fat deposits in different regions of the body. They found that having a greater number of the 53 genetic variants for insulin resistance was associated with having lower amounts of fat under the skin, particularly in the lower half of the body. The team also found a link between having a higher number of the 53 genetic risk variants and a severe form of insulin resistance characterized by loss of fat tissue in the arms and legs, known as familial partial lipodystrophy type 1. Patients with lipodystrophy are unable to adequately develop fat tissue when eating too much, and often develop diabetes and heart disease as a result. In follow-up experiments in mouse cells, the researchers were also able to show that suppression of several of the identified genes (including CCDC92, DNAH10 and L3MBTL3) results in an impaired ability to develop mature fat cells. "Our study provides compelling evidence that a genetically-determined inability to store fat under the skin in the lower half of the body is linked to a higher risk of conditions such as diabetes and heart disease," says Dr Luca Lotta from the Medical Research Council (MRC) Epidemiology Unit at the University of Cambridge. "Our results highlight the important biological role of peripheral fat tissue as a deposit of the surplus of energy due to overeating and lack of physical exercise." "We've long suspected that problems with fat storage might lead to its accumulation in other organs such as the liver, pancreas and muscles, where it causes insulin resistance and eventually diabetes, but the evidence for this has mostly come from rare forms of human lipodystrophy," adds Professor Sir Stephen O'Rahilly from the MRC Metabolic Diseases Unit and Metabolic Research Laboratories at the University of Cambridge. "Our study suggests that these processes also take place in the general population." Overeating and being physically inactive leads to excess energy, which is stored as fat tissue. This new study suggests that among individuals who have similar levels of eating and physical exercise, those who are less able store the surplus energy as fat in the peripheral body, such as the legs, are at a higher risk of developing insulin resistance, diabetes and cardiovascular disease than those who are able to do so. "People who carry the genetic risk variants that we've identified store less fat in peripheral areas," says Professor Nick Wareham, also from the MRC Epidemiology Unit. "But this does not mean that they are free from risk of disease, because when their energy intake exceeds expenditure, excess fat is more likely to be stored in unhealthy deposits. The key to avoiding the adverse effects is the maintenance of energy balance by limiting energy intake and maximising expenditure through physical activity." These new findings may lead to future improvements in the way we prevent and treat insulin resistance and its complications. The researchers are now collaborating with other academic as well as industry partners with the aim of finding drugs that may reduce the risk of diabetes and heart attack by targeting the identified pathways. The research was mainly funded by the Medical Research Council, with additional support from the Wellcome Trust. Lotta, LA et al. Integrative genomic analysis implicates limited peripheral adipose storage capacity in the pathogenesis of human insulin resistance. Nature Genetics; 14 Nov 2016; DOI: 10.1038/ng.3714


Black J.A.,MRC Epidemiology Unit | White B.,University College London | Viner R.M.,University College London | Simmons R.K.,MRC Epidemiology Unit
Obesity Reviews | Year: 2013

The number of obese young people continues to rise, with a corresponding increase in extreme obesity and paediatric-adolescent bariatric surgery. We aimed to (i) systematically review the literature on bariatric surgery in children and adolescents; (ii) meta-analyse change in body mass index (BMI) 1-year post-surgery and (iii) report complications, co-morbidity resolution and health-related quality of life (HRQoL). A systematic literature search (1955-2013) was performed to examine adjustable gastric band, sleeve gastrectomy, Roux-en-Y gastric bypass or biliopancreatic diversions operations among obese children and adolescents. Change in BMI a year after surgery was meta-analysed using a random effects model. In total, 637 patients from 23 studies were included in the meta-analysis. There were significant decreases in BMI at 1 year (average weighted mean BMI difference: -13.5kgm-2; 95% confidence interval [CI] -14.1 to -11.9). Complications were inconsistently reported. There was some evidence of co-morbidity resolution and improvements in HRQol post-surgery. Bariatric surgery leads to significant short-term weight loss in obese children and adolescents. However, the risks of complications are not well defined in the literature. Long-term, prospectively designed studies, with clear reporting of complications and co-morbidity resolution, alongside measures of HRQol, are needed to firmly establish the harms and benefits of bariatric surgery in children and adolescents. © 2013 International Association for the Study of Obesity.


Grant
Agency: GTR | Branch: MRC | Program: | Phase: Intramural | Award Amount: 2.50M | Year: 2013

Abstracts are not currently available in GtR for all funded research. This is normally because the abstract was not required at the time of proposal submission, but may be because it included sensitive information such as personal details.


Grant
Agency: GTR | Branch: MRC | Program: | Phase: Intramural | Award Amount: 382.75K | Year: 2012

Physical activity is important for young people’s current and future health. However, it appears that many young people are not active enough to enjoy these health benefits. We also know that children do less physical activity when they become older, particularly during teenage years. Identifying ways to maintain and promote young people’s levels of physical activity is therefore important for public health. Physical activity behaviour is complex, not just consisting of sports activities but including behaviours such as walking the dog, cycling to school, playing in the playground and physical education lessons. How active young people are is influenced by many factors, such as their preference for physical activity, the provision of footpaths in the neighbourhood, weather and how much their parents support them in being physically active. How these factors work together in promoting physical activity and how to use this knowledge to promote increases in physical activity is still largely unknown. The Behavioural Epidemiology of Physical Activity Group therefore aims to improve the long-term health of young people by: - developing and evaluating interventions to increase physical activity in young people - increasing our understanding of where, when and how physical activity interventions in young people may be applied

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