Epidemiology Unit

Reggio nell'Emilia, Italy

Epidemiology Unit

Reggio nell'Emilia, Italy
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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 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


Baraliakos X.,Ruhr University Bochum | Baraliakos X.,Epidemiology Unit | Baraliakos X.,Universitair Ziekenhuis Ghent | Baraliakos X.,University of Versailles | And 2 more authors.
Annals of the rheumatic diseases | Year: 2014

OBJECTIVE: To study the relationship of spinal inflammation and fatty degeneration (FD) as detected by MRI and new bone formation seen on conventional radiographs (CRs) in ankylosing spondylitis (AS).METHODS: CRs at baseline, 2 years and 5 years and spinal MRIs at baseline and 2 years of 73 AS patients treated with infliximab in European AS Infliximab Cohort were available. Relative risks (RR) were calculated with a general linear model after adjustment for within-patient variation.RESULTS: In a total of 1466 vertebral edges (VEs) without baseline syndesmophytes, 61 syndesmophytes developed at 5 years, the majority of which (57.4%) had no corresponding detectable MRI lesions at baseline. VEs with both inflammation and FD at baseline had the highest risk (RR 3.3, p=0.009) for syndesmophyte formation at 5 years, followed by VEs that developed new FD or did not resolve FD at 2 years (RR=2.3, p=0.034), while inflammation at baseline with no FD at 2 years had the lowest risk for syndesmophyte formation at 5 years (RR=0.8). Of the VEs with inflammation at baseline, >70% resolved completely, 28.8% turned into FD after 2 years, but only 1 syndesmophyte developed within 5 years.CONCLUSIONS: Parallel occurrence of inflammation and FD at baseline and development of FD without prior inflammation after 2 years were significantly associated with syndesmophyte formation after 5 years of anti-tumour necrosis factor (TNF) therapy. However, the sequence 'inflammation-FD-new bone formation' was rarely observed, an argument against the TNF-brake hypothesis. Whether an early suppression of inflammation leads to a decrease of the risk for new bone formation remains to be demonstrated. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.


Baraliakos X.,Ruhr University Bochum | Haibel H.,Franklin University | Listing J.,Epidemiology Unit | Sieper J.,Epidemiology Unit | Braun J.,Ruhr University Bochum
Annals of the Rheumatic Diseases | Year: 2014

Objective: Compare the radiographic progression of ankylosing spondylitis (AS) patients treated with infliximab (INF) versus historical controls (Herne cohort, HC) never treated with tumour necrosis factor (TNF)-blockers over 8 years. Methods: Patients were selected based on the availability of lateral cervical and lumbar radiographs at baseline (BL) and after 8 years. Radiographs were scored by two blinded readers using modified Stokes AS spinal score (mSASSS). Mixed linear models were applied to compare radiographic progression between cohorts after adjustment for baseline status. Results: Patients in INF (n=22) and HC (n=34) did not differ in the mSASSS status: 13.2±17.6 in INF versus 14.2±13.8 in HC (p=0.254). Both showed progression at 8 years: mean mSASSS 20.2±21.4 in INF and 25.9 ±17.8 in HC. After adjustment for baseline damage the mean mSASSS (SEM) at 8 years was 21.0 (1.4) in INF and 25.5 (1.1) HC (p=0.047). The mean mSASSS difference was similar in the groups between baseline and 4 years but was more pronounced in HC between 4 and 8 years (p=0.03 between groups). The mean number of syndesmophytes, although similar at baseline, differed significantly at 8 years: 1.0±0.6 new syndesmophytes/patient in INF versus 2.7±0.8 in HC (p=0.007). Adjustment for age, symptom duration, HLA-B27, Bath AS disease activity index and Bath AS function index at baseline had no influence. Conclusions: Despite limitations of patient numbers and retrospective study design, these data show increase in new bone formation in both patients treated with anti-TNF and those who did not. However, since there was even less bone formation in the INF treated group after 8 years, these data argue against a major role for the TNF-brake hypothesis.


News Article | March 7, 2016
Site: www.biosciencetechnology.com

An analysis of data from two long-term epidemiologic studies has found that regular use of aspirin significantly reduces the overall risk of cancer, an effect that primarily reflects a lower risk of colorectal cancer and other tumors of the gastrointestinal tract. The findings, published in JAMA Oncology, suggest that the use of aspirin may complement, but not replace, the preventive benefits of colonoscopy and other methods of cancer screening, according to the study authors. “We now can recommend that many individuals consider taking aspirin to reduce their risk of colorectal cancer — particularly those with other reasons for regular use, such as heart disease prevention — but we are not at a point where we can make a general recommendation for overall cancer prevention,” said senior author Andrew Chan, a Harvard Medical School associate professor and chief of the Clinical and Translational Epidemiology Unit in the Division of Gastroenterology at Massachusetts General Hospital. “Our findings imply that aspirin use would be expected to prevent a significant number of colorectal cancers above and beyond those that would be prevented by screening and may have even greater benefit in settings in which the resources to devote to cancer screening are lacking.” A large number of studies have linked regular aspirin use to a lower risk of colorectal cancer, but without clarifying aspirin’s effects on overall cancer risk. To investigate that question, the researchers analyzed 32 years’ worth of data from almost 136,000 participants in the Nurses’ Health Study and the Health Professionals Follow-up Study. They found that participants who reported regular aspirin use — defined as a standard or a low-dose aspirin tablet at least twice a week — had a 3 percent absolute lower risk of any type of cancer than did those not reporting regular aspirin use. Regular aspirin use reduced the risk of colorectal cancer by 19 percent and the risk of any gastrointestinal cancer by 15 percent. No effect was seen in the risk of breast, prostate, or lung cancer. The protective benefit appeared after five years of continuous use at dosages ranging from 0.5 to 1.5 standard tablets a week or one low-dose tablet a day. The researchers estimate that regular aspirin use could prevent close to 30,000 gastrointestinal tract tumors in the United States each year. “At this point, it would be very reasonable for individuals to discuss with their physicians the advisability of taking aspirin to prevent gastrointestinal cancer, particularly if they have risk factors such as a family history,” said Chan. “But this should be done with the caveat that patients be well informed about the potential side effects of regular aspirin treatment and continue their regular screening tests. Furthermore, aspirin should not be viewed as a substitute for colonoscopy or other cancer screening tests.”


Kelly H.A.,Epidemiology Unit
Medical Journal of Australia | Year: 2010

• From the recognition of the swine flu pandemic in late April 2009, health professionals, politicians and the public needed to know how serious pandemic (H1N1) 2009 influenza (swine flu) was in relation to other seasonal strains of influenza. • The Victorian experience suggests that the circulation of pandemic (H1N1) 2009 influenza in the community was at most like influenza circulation in a season of moderate seasonal activity. • We have no estimate of the total case count, but we know most infections have been mild. However, while disease in the community appears mild, and the risk of hospitalisation is low, a high proportion of patients hospitalised with swine flu required intensive care. • Deaths from swine flu have not been as numerous as the modelled deaths from seasonal influenza, although people dying from swine flu are younger. • Because we do not understand the laboratory-confirmed burden of disease due to seasonal influenza (as opposed to the modelled burden of disease), we could not base our response to the pandemic on an informed comparison of seasonal and pandemic influenza. • We may not have needed a pandemic response to a disease that, although it has a different footprint, has been predominantly of seasonal intensity. • It is critical to accumulate quality evidence about laboratory-confirmed influenza to guide our intervention policies for both seasonal and pandemic influenza.

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