JacketFlap connects you to the work of more than 200,000 authors, illustrators, publishers and other creators of books for Children and Young Adults. The site is updated daily with information about every book, author, illustrator, and publisher in the children's / young adult book industry. Members include published authors and illustrators, librarians, agents, editors, publicists, booksellers, publishers and fans. Join now (it's free).
Login or Register for free to create your own customized page of blog posts from your favorite blogs. You can also add blogs by clicking the "Add to MyJacketFlap" links next to the blog name in each post.
Blog Posts by Tag
In the past 7 days
Blog Posts by Date
Click days in this calendar to see posts by day or month
Viewing: Blog Posts Tagged with: epidemiology, Most Recent at Top [Help]
Results 1 - 13 of 13
How to use this Page
You are viewing the most recent posts tagged with the words: epidemiology in the JacketFlap blog reader. What is a tag? Think of a tag as a keyword or category label. Tags can both help you find posts on JacketFlap.com as well as provide an easy way for you to "remember" and classify posts for later recall. Try adding a tag yourself by clicking "Add a tag" below a post's header. Scroll down through the list of Recent Posts in the left column and click on a post title that sounds interesting. You can view all posts from a specific blog by clicking the Blog name in the right column, or you can click a 'More Posts from this Blog' link in any individual post.
Today is the 60th anniversary of the polio vaccine being declared safe to use. The poliovirus was a major health concern for much of the twentieth century, but in the last sixty years huge gains have been made that have almost resulted in its complete eradication. The condition polio is caused by a human enterovirus called the poliovirus.
Immigration is an inflammatory matter and probably always has been. Immigrant groups, with few exceptions, have to endure the brickbats of prejudice of the recipient population. Emigration, by contrast, hardly troubles people — but the departure of one’s people is not a trifling matter. I wonder why these differential responses occur. It seems to me that humans are highly territorial and territory signifies resources and power. Immigration usually means sharing of resources, at least in the short-term, while emigration means more for those left behind and brings hope of acquiring even more from overseas in the long term. This might explain why those most needy of settled immigrant status — asylum seekers, the persecuted or denigrated, and the poor — are most resisted while those least in need of immigration status, such as the rich, are often welcomed.
Notwithstanding, consternation about migration it is rapidly leading to diverse, multiethnic and multicultural nations across the world. Many people dislike the changes this brings but it is hard to see what they are to do except change themselves. The forces for migration are strong, for example, globalization of trade and education, increasing inequalities in wealth and employment opportunities, and changing demography whereby rich economies are needing younger migrants to keep them functioning.
Whether you are a migrant (like me) or the host to migrants it is wise to remember that migration is a fundamental human behavior that is instrumental to the success of the human species. Without migration Homo sapiens would be confined to East Africa, and other species (or variants of humans — all now extinct) would be enjoying the bounties of other continents. Surely, migration will continue to bring many benefits to humanity in the future.
My special research interest is in the comparative health of migrants and their offspring, who together comprise ethnic (or racial, as preferred in some countries) minority groups. There is a remarkable variation in the pattern of diseases (and the factors that cause diseases) among migrant and ethnic groups and very often the minorities are faring better than the recipient populations. Probing these patterns scientifically, especially in the discipline of epidemiology, which describes and interprets the occurrence of disease in large populations, helps in understanding the causes of disease. There are opportunities to apply such learning to improve the health of the whole population; migrants, minorities and settled majority populations alike.
Let me share with you three observations from my research areas that help illustrate this point, one concerns heart disease and diabetes, another colorectal cancer, and the third smoking in pregnancy. Coronary heart disease (CHD) and its major co-disease type 2 diabetes (DM2) have been studied intensively but still some mysteries remain. The white Scottish people are especially notorious for their tendency to CHD. Our studies in Scotland have shown that the recently settled Pakistani origin population has much higher CHD rates than white Scottish people. Amazingly, the recently settled Chinese origin population has much lower rates of CHD than the white Scottish people. These intriguing observations raise both scientific questions and give pointers to public health. If we could all enjoy the CHD rates of the Chinese in Scotland the public’s health would be hugely improved.
Intriguingly, although colorectal cancer, heart disease and diabetes share risk factors (especially high fat, low fibre diet) we found that Pakistani people in Scotland had much lower risks than the white Scottish Group. This makes us re-think what we know about the causes of this cancer. In our scientific paper we put forward the idea that Pakistani people may be protected by their comparatively low consumption of processed meats (fresh meat is commonly eaten).
Might the high risk of CHD in Pakistani populations in Scotland be a result of heavier tobacco use? The evidence shows that while the smoking prevalence in Pakistani men is about the same as in white men, the prevalence in Pakistani women is very low. Smoking in white Scottish woman, even in pregnancy, is about 25% but it is close to nil in pregnant Pakistani women. This raises interesting questions about the cultural and environmental circumstances that maintain high or low use of tobacco in populations. These observations raise public health challenges of a high order — how can we maintain the cultures that lead to low tobacco use in some ethnic groups while altering the cultures that lead to high tobacco use in others?
The intermingling of migrants and settled populations creates new societies that provide innumerable opportunities for learning and advancement. While my examples are from the health arena, the same is true for other fields: education, entrepreneurship, social capital, crime, and child rearing to name a few. This historical perspective on human migration, evolution and advancement can benefit our health, as well as providing a foundation to contextualize the challenges and changes we face.
Heading image: People migrating to Italy on a boat in the Mediterranean Sea by Vito Manzari from Martina Franca (TA), Italy (Immigrati Lampedusa). CC-BY-2.0 via Wikimedia Commons.
If a “revolution” in our field or area of knowledge was ongoing, would we feel it and recognize it? And if so, how?
I think a methodological “revolution” is probably going on in the science of epidemiology, but I’m not totally sure. Of course, in science not being sure is part of our normal state. And we mostly like it. I had the feeling that a revolution was ongoing in epidemiology many times. While reading scientific articles, for example. And I saw signs of it, which I think are clear, when reading the latest draft of the forthcoming book Causal Inference by M.A. Hernán and J.M. Robins from Harvard (Chapman & Hall / CRC, 2015). I think the “revolution” — or should we just call it a “renewal”? — is deeply changing how epidemiological and clinical research is conceived, how causal inferences are made, and how we assess the validity and relevance of epidemiological findings. I suspect it may be having an immense impact on the production of scientific evidence in the health, life, and social sciences. If this were so, then the impact would also be large on most policies, programs, services, and products in which such evidence is used. And it would be affecting thousands of institutions, organizations and companies, millions of people.
One example: at present, in clinical and epidemiological research, every week “paradoxes” are being deconstructed. Apparent paradoxes that have long been observed, and whose causal interpretation was at best dubious, are now shown to have little or no causal significance. For example, while obesity is a well-established risk factor for type 2 diabetes (T2D), among people who already developed T2D the obese fare better than T2D individuals with normal weight. Obese diabetics appear to survive longer and to have a milder clinical course than non-obese diabetics. But it is now being shown that the observation lacks causal significance. (Yes, indeed, an observation may be real and yet lack causal meaning.) The demonstration comes from physicians, epidemiologists, and mathematicians like Robins, Hernán, and colleagues as diverse as S. Greenland, J. Pearl, A. Wilcox, C. Weinberg, S. Hernández-Díaz, N. Pearce, C. Poole, T. Lash , J. Ioannidis, P. Rosenbaum, D. Lawlor, J. Vandenbroucke, G. Davey Smith, T. VanderWeele, or E. Tchetgen, among others. They are building methodological knowledge upon knowledge and methods generated by graph theory, computer science, or artificial intelligence. Perhaps one way to explain the main reason to argue that observations as the mentioned “obesity paradox” lack causal significance, is that “conditioning on a collider” (in our example, focusing only on individuals who developed T2D) creates a spurious association between obesity and survival.
Influenza virus research by James Gathany for CDC. Public domain via Wikimedia Commons.
The “revolution” is partly founded on complex mathematics, and concepts as “counterfactuals,” as well as on attractive “causal diagrams” like Directed Acyclic Graphs (DAGs). Causal diagrams are a simple way to encode our subject-matter knowledge, and our assumptions, about the qualitative causal structure of a problem. Causal diagrams also encode information about potential associations between the variables in the causal network. DAGs must be drawn following rules much more strict than the informal, heuristic graphs that we all use intuitively. Amazingly, but not surprisingly, the new approaches provide insights that are beyond most methods in current use. In particular, the new methods go far deeper and beyond the methods of “modern epidemiology,” a methodological, conceptual, and partly ideological current whose main eclosion took place in the 1980s lead by statisticians and epidemiologists as O. Miettinen, B. MacMahon, K. Rothman, S. Greenland, S. Lemeshow, D. Hosmer, P. Armitage, J. Fleiss, D. Clayton, M. Susser, D. Rubin, G. Guyatt, D. Altman, J. Kalbfleisch, R. Prentice, N. Breslow, N. Day, D. Kleinbaum, and others.
We live exciting days of paradox deconstruction. It is probably part of a wider cultural phenomenon, if you think of the “deconstruction of the Spanish omelette” authored by Ferran Adrià when he was the world-famous chef at the elBulli restaurant. Yes, just kidding.
Right now I cannot find a better or easier way to document the possible “revolution” in epidemiological and clinical research. Worse, I cannot find a firm way to assess whether my impressions are true. No doubt this is partly due to my ignorance in the social sciences. Actually, I don’t know much about social studies of science, epistemic communities, or knowledge construction. Maybe this is why I claimed that a sociology of epidemiology is much needed. A sociology of epidemiology would apply the scientific principles and methods of sociology to the science, discipline, and profession of epidemiology in order to improve understanding of the wider social causes and consequences of epidemiologists’ professional and scientific organization, patterns of practice, ideas, knowledge, and cultures (e.g., institutional arrangements, academic norms, scientific discourses, defense of identity, and epistemic authority). It could also address the patterns of interaction of epidemiologists with other branches of science and professions (e.g. clinical medicine, public health, the other health, life, and social sciences), and with social agents, organizations, and systems (e.g. the economic, political, and legal systems). I believe the tradition of sociology in epidemiology is rich, while the sociology of epidemiology is virtually uncharted (in the sense of not mapped neither surveyed) and unchartered (i.e. not furnished with a charter or constitution).
Another way I can suggest to look at what may be happening with clinical and epidemiological research methods is to read the changes that we are witnessing in the definitions of basic concepts as risk, rate, risk ratio, attributable fraction, bias, selection bias, confounding, residual confounding, interaction, cumulative and density sampling, open population, test hypothesis, null hypothesis, causal null, causal inference, Berkson’s bias, Simpson’s paradox, frequentist statistics, generalizability, representativeness, missing data, standardization, or overadjustment. The possible existence of a “revolution” might also be assessed in recent and new terms as collider, M-bias, causal diagram, backdoor (biasing path), instrumental variable, negative controls, inverse probability weighting, identifiability, transportability, positivity, ignorability, collapsibility, exchangeable, g-estimation, marginal structural models, risk set, immortal time bias, Mendelian randomization, nonmonotonic, counterfactual outcome, potential outcome, sample space, or false discovery rate.
You may say: “And what about textbooks? Are they changing dramatically? Has one changed the rules?” Well, the new generation of textbooks is just emerging, and very few people have yet read them. Two good examples are the already mentioned text by Hernán and Robins, and the soon to be published by T. VanderWeele, Explanation in causal inference: Methods for mediation and interaction (Oxford University Press, 2015). Clues can also be found in widely used textbooks by K. Rothman et al. (Modern Epidemiology, Lippincott-Raven, 2008), M. Szklo and J Nieto (Epidemiology: Beyond the Basics, Jones & Bartlett, 2014), or L. Gordis (Epidemiology, Elsevier, 2009).
Finally, another good way to assess what might be changing is to read what gets published in top journals as Epidemiology, the International Journal of Epidemiology, the American Journal of Epidemiology, or the Journal of Clinical Epidemiology. Pick up any issue of the main epidemiologic journals and you will find several examples of what I suspect is going on. If you feel like it, look for the DAGs. I recently saw a tweet saying “A DAG in The Lancet!”. It was a surprise: major clinical journals are lagging behind. But they will soon follow and adopt the new methods: the clinical relevance of the latter is huge. Or is it not such a big deal? If no “revolution” is going on, how are we to know?
Occupational epidemiology is one of those fascinating areas which spans important areas of human life: health, disease, work, law, public policy, the economy. Work is fundamental to any society and the importance society attaches to the health of its workers varies over time and between countries. Because of the lessons to be learned by looking at other countries as well as one’s own, occupational epidemiology is a truly global discipline. Emerging economies often prioritize productivity over other issues, but also can learn from the long history of improvement in working conditions which has taken place in developed countries. Looking the other way, the West can learn from fresh insights gained in studies set in low and middle-income countries.
Exposures are usually higher in emerging economies and epidemiological methods are an important tool in detecting and quantifying outbreaks of occupational disease which may have been controlled in the West. A recent study of digestive cancer in a Chinese asbestos mining and milling cohort provides additional evidence that stomach cancer may be associated with high levels of exposure to chrostile asbestos, for example. This was a collaborative study between researchers in China, Hong Kong, Japan, and the United States, and illustrates the way that studying an “old” disease in a new context can provide results which are of global benefit.
Issues in occupational epidemiology are never static. Work exposures change along with materials and processes. The ubiquitous printing industry, for example, is always developing new inks, cleaning agents, and processes. A cluster of cases of the rare liver cancer, cholangiocarcinoma, was noted in Japanese printers and this finding was replicated in the Nordic printing industry by using one of the large Nordic population-based databases. This replication is important because it shows that the association is unlikely to be due to a lifestyle factor specific to Japan.
“Big data” sharpens statistical power and there are now specific data pooling projects in occupational epidemiology, to supplement the use of existing large databases. The SYNERGY study, for example, pools lung cancer case-control studies with the aim of teasing out occupational effects from behind the masking effect of smoking, which remains by far the most important driver for lung cancer. A recent analysis with around 20,000 cases and controls was able to show that bakers are not at increased risk of lung cancer, whereas the many previous smaller studies had given inconsistent results.
The addition of systematic reviews to the toolkit has strengthened the evidence base in occupational epidemiology, allowing policy about occupational risks and their prevention to be made with confidence. Health economics, also, can be applied to findings from occupational epidemiology to clarify policy issues.
Development brings its own issues to which occupational epidemiology can be applied. We now live longer in the West, and we will have to work into old age, often while carrying chronic diseases. Despite frequently-expressed concerns about an ageing workforce, a recent study in an Australian smelter confirmed others in that the older workers maintained their ability to work safely and the highest injury rates were in young workers. Patients with previously fatal diseases survive into adult life and, potentially, the workforce; a survey of patients with cystic fibrosis, for example, found that disease severity was less important as a predictor of employment than social factors such as educational attainment and locality. A loss of heavy industry in the West, combined with cheap transport, means that many of us spend most of our waking hours sitting down, promoting obesity and its complications. A sample of UK office workers spent 65% of their work time sitting and did not compensate for this by being more active outside work. The economic downturn is a major political and social preoccupation, bringing uncertainty about future employment, which may fuel dysfunctional behaviour such as ‘presenteeism’. A Swedish study suggested that this may be associated with poor mental wellbeing.
Katherine M. Venables is a Reader in the Department of Public Health at the University of Oxford. Her research has always focused on aetiological epidemiology. At Oxford, she has worked on a cohort study of mortality and cancer incidence in military veterans exposed to low levels of chemical warfare agents, and also on the provision of occupational health services to university staff. She is editor of Current Topics in Occupational Epidemiology.
Subscribe to the OUPblog via email or RSS.
Subscribe to only science and medicine articles on the OUPblog via email or RSS.
Image: Woman smoking a cigarette by Oxfordian Kissuth. CC-BY-SA-3.0 via Wikimedia Commons.
My card-carrying North London media brother, Ben, describes himself on his Twitter feed as a ‘recovering Northerner’.
In my case the disease is almost certainly incurable. Despite spending a good deal of last year in cosmopolitan London — beautiful, exciting and diverse as it is — I found myself on occasions near tears of joy as my feet hit the platform at King’s Cross.
“I need to know I can be at the coast or in miles of open countryside within 20 minutes,” I told Ben.
“I need to know I can get Vietnamese food at 3.00 a.m.,” he replied.
While mine is clearly the healthier individual craving, the gulf in population health outcomes between the North and South of England, or, perhaps more accurately, between the provinces and the capital and its South Eastern sprawl, remains as wide as ever.
On examining the distribution of age-standardised mortality for Nomenclature of Territorial Units for Statistics regions, the United Kingdom remains the most starkly unequal of European nations. This is starkly illustrated in our new analyses of the North South divide in England, when compared with the experience of East and West Germany following the fall of the Berlin Wall. After that great political upheaval, notably for women, life expectancy in East Germany began to climb rapidly. Twenty years on, it is indistinguishable from that of the former West Germany.
In contrast, the gap between the North East of England and London, which in 1990 was similar to that between East and West Germany, remains just as wide in the most recent figures. Of course, life expectancy has risen markedly in both countries and their regions; modern North East English life expectancy is significantly higher than that which obtained in 1990 for West Germany. But the English failure to narrow its inequality gap despite overt national efforts signals that those efforts are simply too light-touch to be effective.
“it did not address the most relevant entry-points, did not use effective policies and was not delivered at a large enough scale for achieving population-wide impacts. Health inequalities can only be reduced substantially if governments have a democratic mandate to make the necessary policy changes, if demonstrably effective policies can be developed, and if these policies are implemented on the scale needed to reach the overall targets.”
Of course, fundamental to this problem is economics. The wealth of London and the South East in comparison to, well just about anywhere else in the UK, is now extraordinarily stark. London now feels more alien to my Northern sensibilities than much of Europe, and the reason is not people but cash.
The difference is illustrated rather well by the contrasting artistic expectations of the South Bank Centre — close by the Waterloo offices of Public Health England, for whom I worked last year — and the Culture budget of the City of Newcastle — for whom I now work as Director of Public Health.
On consecutive days in 2013, the Guardian and BBC reported the Southbank Centre’s unveiling of its £100m redevelopment plans (6 March), having made a successful first stage bid for £20m from the Arts Council, and Newcastle City Council was reported (7 March) as having cut its £2.5m culture budget by 50%. This comparison could equally be drawn in many other ways: for transport and infrastructure, investment in business, development of academic institutions (why did the Crick Institute need to be in King’s Cross?). And it all matters because, despite the cleaner air and wide open spaces, the English provinces and in particular the North, are losing out — on culture, mobility, urban environment, jobs, and crucially on health.
The English North has many charms, both for its natives and many who come upon its joys by accident (see this delightful, recent New York Times piece). For too many, however, it remains a place of shorter and poorer lives. The German experience suggests that it need not be so.
Prof. Eugene Milne became Director of Public Health for Newcastle upon Tyne earlier this year, after working nationally for Public Health England as Director for Adult Health and Wellbeing. He is an Honorary Professor in Medicine and Health at the University of Durham, and joint-editor, with his colleague Prof. Ted Schrecker, of the Journal of Public Health. He has research interests in health improvement, inequalities and ageing.
The Journal of Public Health invites submission of papers on any aspect of public health research and practice. We welcome papers on the theory and practice of the whole spectrum of public health across the domains of health improvement, health protection and service improvement, with a particular focus on the translation of science into action. Papers on the role of public health ethics and law are welcome.
Subscribe to the OUPblog via email or RSS.
Subscribe to only health and medicine articles on the OUPblog via email or RSS.
Image credit: Angel of the North, Gateshead, by NickyHall5. CC-BY-SA-3.0 via Wikimedia Commons.
Oxford Scholarship Online (OSO) launched in 2003 with 700 titles. Now, on its tenth birthday, it’s the online home of over 9,000 titles from Oxford University Press’s distinguished academic list, and part of University Press Scholarship Online. To celebrate OSO turning ten, we’ve invited a host of people to reflect on the past ten years of online academic publishing, and what the next ten might bring.
By Nicola Wilson
When I was invited to develop two lists for Oxford Scholarship Online, I jumped at the chance. From the perspective of a commissioning editor, digital publishing has extended the “life” of our copyrights indefinitely, and we no longer need to hold a book in physical print for it to continue to be available to our readers.
The first module that I developed was “Public Health and Epidemiology,” back in 2008. The books contained in the module have been published by our medical department over the course of three decades, and many are now considered public health classics, such as Michael Marmot’s Social Determinants of Health, and Geoffrey Rose’s The Strategy of Preventative Medicine.
The books that we chose to include on Oxford Scholarship Online present research and analysis of global health issues, and insight into the impact of diseases and conditions on populations. Several of the projects in the module have directly influenced policy planning and clinical attitudes to disease prevention and management, transforming scientific investigation methods and treatment approaches worldwide.
The biggest challenge in developing the module was the time that it took to clear permission to reproduce the material online. Many of the contracts and agreements that we held for our older books long pre-dated electronic resources, and we had to ask the authors and editors to sign contract addendums to allow us to proceed with publishing the books online. In some instances, authors had died since the book was published with us, so we needed to contact authors’ estates and ask surviving relatives to grant us permission to reproduce the material online.
In other cases, we needed to trace the ownership of third-party copyrighted material which was included in the books, so I became a detective, trying to identify the current owners of defunct publishers, some of which had changed their ownership through multiple company mergers over a thirty-year period. What naively started out as a few hours of looking through dusty hard-copy records in our basement, turned into a few months of internet heavy investigation and phone calls to numerous publishers’ Rights departments.
The amount of work that clearing permissions created turned it into an “all hands on deck during evenings and weekends” project. Over half of the medical department pitched in extra hours over a four-month period to ensure that we hit the launch deadline that we had been set. (Never underestimate the power of food to complete a project on schedule.)
The trickiest book that we worked on was Nutrition for Developing Countries, which was originally published in 1993 before our copyright clearance rules were defined. It’s full of unique hand drawn illustrations of Tanzanian families, different types of food, and easy-to-read graphs. It was specifically presented in such a way that could be used as a “show and tell” book by doctors working with non-literate families in Africa. For example, they could point at the illustrations of healthy foods in the book and explain to nursing mothers how eating those foods would help their babies to grow strong and remain healthy.
However, our challenge was trying to find out who had drawn the pictures, and subsequently who owned the copyright for them. Many of the illustrations had been drawn by a friend of one of the editors, and given to the editor as a wedding present. Did this mean that the copyright was held by the editor, or was it held by the artist? No copyright permission had ever been signed to state either way, and we had no contact details for the artist to enquire with them directly. We contacted the book editor, but they were often working in areas of Africa where Internet access was non-existent, so it took around four months to liaise with the editor and the artist (whom the editor contacted on our behalf), and acquire permission from both of them (to cover all legal bases) to use the illustrations in a digital form.
A major benefit of putting books online is the global availability of the information they contain; practitioners and academics can access and use these books online wherever they are in world. It’s wonderful that public health and epidemiology books attract a global readership, and through their availability online, they will have an even broader reach, and continue to help develop and improve research and treatment for many years to come.
Nicola Wilson is Commissioning Editor for the “Palliative Care” and “Public Health and Epidemiology” modules on Oxford Scholarship Online.
Subscribe to the OUPblog via email or RSS.
Subscribe to only education articles on the OUPblog via email or RSS.
Since their introduction in the United States in the 1940s, artificial fluoridation programmes have been credited with reducing tooth decay, particularly in deprived areas. They are acknowledged by the US Centers for Disease Control and Prevention as one of the ten great public health achievements of the 20th century (alongside vaccination and the recognition of tobacco use as a health hazard). Such plaudits however, have only gone on to fuel what is an extremely polarised ‘water fight’. Those opposed to artificial fluoridation continue to claim it causes a range of health conditions and diseases such as reduced IQ in children, reduced thyroid function, and increased risk of bone cancer. Regardless of the controversy, the one thing that everyone agrees upon is that little or no high quality research is available to confirm or refute any public concerns. The York systematic review of water fluoridation has previously highlighted the weakness of the evidence base by acknowledging the quality of the research included in the review was low to moderate.
Fluoride changes the structure of tooth enamel making it more resistant to acid attack and can reduce the incidence of tooth decay. This is why it is added to drinking water as part of artificial fluoridation programmes. The aim is to dose naturally occurring fluoride to a level that provides optimum benefit for the prevention of dental caries. The optimum range can depend on temperature but falls within the range of 0.7-1.2 parts per million (ppm) for Great Britain. Levels lower than 0.7ppm are considered to provide little or no benefit. Drinking water standards are set so that the level of fluoride must not exceed 1.5ppm in accordance with national regulations that come directly from EU law.
Severn Trent Water, Northumbrian Water, South Staffordshire Water, United Utilities, and Anglian Water are the only water companies in Great Britain that artificially fluoridate their water supply to a target level of 1 ppm. The legal agreements to fluoridate currently sit with the Secretary of State, acting through Public Health England, although local authorities are the ultimate decision makers when it comes to establishing, maintaining, adjusting or terminating artificial fluoridation programmes. As a programme dedicated to improving oral health, all of the associated costs come from the public health budget. Therefore, it is important to know that the money is being spent in the most effective way.
Our study has, for the first time, enabled an in-depth examination of the relationship between the incidence of two of the most common types of bone cancer that are found in children and young adults, osteosarcoma and Ewing sarcoma, and fluoride levels in drinking water across the whole of Great Britain. We have combined case data from population based cancer registries, fluoride monitoring data from water companies and census data within a computerised geographic information system, to enable us to carry out sophisticated geo-statistical analyses.
The study found no evidence of an association between fluoride in drinking water and osteosarcoma or Ewing sarcoma. The study also found no evidence that those who lived in an area of Great Britain with artificially fluoridated drinking water, or who were supplied with drinking water containing naturally occurring fluoride at a level within the optimal range, were at an increased risk of osteosarcoma or Ewing sarcoma.
It is important to note that finding no evidence of an association between the geographical occurrences of osteosarcoma or Ewing sarcoma and fluoride levels in drinking water, does not necessarily mean there is no association. Indeed, intake of fluids and food products that contain fluoride will not be the same for everyone and not taking this variation into consideration is one of the limitations of our study. Nevertheless, the methodologies we have developed could be used in the future to examine fluoride exposure over time and take other risk factors into consideration at an individual level. Such an approach could help the controversy surrounding artificial fluoridation ebb rather than flow.
Another important, although unexpected, finding arose from our use of fluoride monitoring data. We found that the fluoridation levels of approximately one third of the artificially fluoridated water supply zones were below 0.7ppm (the minimum limit of the optimum range). This finding reinforces that it is incorrect to assume an artificially fluoridated area is dosed up to 1ppm. In reality, it may be a lot less. A number of previous studies have mistakenly made this assumption making their conclusions unreliable. Our study shows that you cannot guarantee that fluoride levels in all artificially fluoridated water supply zones are close to the target level of 1ppm. Assuming that water fluoridation is a safe practice and evidence surrounding calculation of recommended dosage is reliable, this finding has economic implications in terms of public health. If public money is paying for artificial fluoridation shouldn’t the water supply zones be dosed up to a level that will provide the greatest benefit? If they aren’t then could it be that public money is merely being thrown down the drain?
The International Journal of Epidemiology is an essential requirement for anyone who needs to keep up to date with epidemiological advances and new developments throughout the world. It encourages communication among those engaged in the research, teaching, and application of epidemiology of both communicable and non-communicable disease, including research into health services and medical care.
Subscribe to the OUPblog via email or RSS.
Subscribe to only health and medicine articles on the OUPblog via email or RSS.
Image credit: Glass half full. By Jenny Downing. CC-BY-2.0 via Wikimedia Commons
Depression in old age occurs frequently, places a severe burden on patients and relatives, and increases the utilization of medical services and health care costs. Although the association between age and depression has received considerable attention, very little is known about the incidence of depression among those 75 years of age and older. Studies that treat the group 65+ as one entity are often heavily weighted towards the age group 65-75. Therefore, the prediction of depression in the very old is uncertain, since many community-based studies lack adequate samples over the age of 75.
With the demographic change in the forthcoming decades, more emphasis should be put on epidemiological studies of the older old, since in many countries the increase in this age group will be particularly high. To study the older old is also important, since some crucial risk factors such as bereavement, social isolation, somatic diseases, and functional impairment become more common with increasing age. These factors may exert different effects in the younger old compared to the older old. Knowledge of risk factors is a prerequisite to designing tailored interventions, either to tackle the factors themselves or to define high-risk groups, since depression is treatable in most cases.
In our recent study, over 3,000 patients recruited by GPs in Germany were assessed by means of structured clinical interviews conducted by trained physicians and psychologists during visits to the participants’ homes. Inclusion criteria for GP patients were an age of 75 years and over, the absence of dementia in the GP’s view, and at least one contact with the GP within the last 12 months. The two follow-up examinations were done, on average, one and a half and then three years after the initial interview.
Depressive symptoms were ascertained using the 15-item version of the Geriatric Depression Scale (GDS). We found that the risk for incident depression was significantly higher for subjects
85 years and older
with mobility impairment and vision impairment
with mild cognitive impairment and subjective memory impairment
who were current smokers.
It revealed that the incidence of late-life depression in Germany and other industrialized countries is substantial, and neither educational level, marital status, living situation nor presence of chronic diseases contributed to the incidence of depression. Impairments of mobility and vision are much more likely to cause incidents of depression than individual somatic illnesses such as diabetes mellitus and coronary heart disease. As such, it is vital that more attention is paid to the oldest old, functional impairment, cognitive impairment, and smoking, when designing depression prevention programs.
GP practices offers ample opportunity to treat mental health problems such as depression occurring in relation to physical disability. If functional impairment causes greater likelihood of depression, GPs should focus on encouraging older patients to maintain physical health, whether by changing in personal health habits, advocating exercise, correcting or compensating functional deficits by means of medical and surgical treatments, or encouraging use of walking aids. Additionally, cognitive and memory training could prevent the onset of depressive symptoms, as could smoking cessation. If these steps are taken, the burden of old age depression could be significantly reduced.
Siegfried Weyerer is professor of epidemiology at the Central Institute of Mental Health in Mannheim, Germany. He has conducted several national and international studies on the epidemiology of dementia, depression and substance use disorders at different care levels. He is also an expert in health/nursing services research. He is one of the authors of the paper ‘Incidence and predictors of depression in non-demented primary care attenders aged 75 years and older: results from a 3-year follow-up study’, which appears in the journal Age and Ageing. You can read the paper in full here.
Age and Ageing is an international journal publishing refereed original articles and commissioned reviews on geriatric medicine and gerontology. Its range includes research on ageing and clinical, epidemiological, and psychological aspects of later life.
Do vascular risk factors such as high blood pressure and smoking make us forgetful?
As our bodies start to show the signs of ageing, our brain is naturally ageing too. But some older people can become forgetful and have trouble remembering common words or organising daily activities more than others. There are few proven interventions to prevent this kind of cognitive decline in older adults, although treating modifiable risk factors for vascular disease and stroke, such as cholesterol and body mass index (BMI), has been suggested as a promising approach to preventing or delaying cognitive impairment for a growing UK population of older adults. So is there a link between high blood pressure and forgetfulness?
Despite much recent interest, studies to date have reported inconsistent relationships between blood pressure and cognitive functioning. Evidence suggests that people diagnosed with high blood pressure levels tend to perform more poorly on most domains of cognitive functioning, including memory, learning, attention, and reasoning. However, clinical trials have so far failed to demonstrate that antihypertensive drugs used to lower or control high blood pressure levels are effective in preventing cognitive decline in older adults. This inconsistent evidence poses a challenge when developing recommendations for the prevention of cognitive ageing.
Cognitive ageing, such as symptoms of forgetfulness, is increasingly seen as the result of the joint effect of several vascular disease risk factors, including high blood pressure, BMI, cholesterol levels, and smoking. However, the combined influence of these on cognitive decline is less commonly explored among older adults at increased risk of both cardiovascular disease and cognitive decline.
In a recent paper, we looked at Framingham stroke and cardiovascular risk scores (a measure used to assess an individual’s probability of developing stroke or cardiovascular disease over a 10-years period) and investigated their association with cognitive decline in older adults. The study included over 8,000 adults aged 50+ living in private households in England. Participants with the highest risk of future stroke or cardiovascular events, based on their risk factors values, were found to perform more poorly on tests of memory and executive functioning after a four year period. This adds weight to the theory that the combined effects of risk factors for vascular disease and stroke may be associated with more rapid cognitive decline in older adults. In other words, those at greater risk of cardiovascular problems were likely to experience a more rapid onset of symptoms associated with cognitive decline, such as forgetfulness.
We believe that these findings support the need for a multifaceted approach when seeking to prevent cognitive decline. The main implication of this is the need for addressing the combined effect of multiple risk factors, including lowering high blood pressure and high cholesterol levels, weight loss, and stopping smoking. Thus, healthcare professionals should encourage older people to adopt healthy lifestyles that would include stopping smoking and increased exercise (as well as improved diet not investigated here) and taking prescribed medicines aimed at controlling high blood pressure and high cholesterol levels. Such recommendations could potentially prevent or delay future declining memory or reasoning capacities in older adults, particularly those in higher risk groups.
The results also suggest that a harmful effect of high blood pressure on memory or reasoning abilities may develop over a prolonged period of time. This may be one reason why short-term trials have failed to show a consistent benefit from antihypertensive treatment on cognitive decline. For instance, since the negative impact of high blood pressure on memory or reasoning abilities takes place over a prolonged period of time, short-term treatment may not be sufficient to reverse or delay its adverse influence. Therefore, we would expect that any potential cognitive benefits from lowering blood pressure may only be observed over substantial periods of time.
These new results suggest that attention to the combined effects of multiple vascular risk factors may hold some promise as a strategy to prevent cognitive decline in older adults.
Dr Alex Dregan is a Lecturer in Translational Epidemiology within the NIHR Biomedical Research Centre at the Guy’s and St Thomas’ NHS Trust and King’s College London. He trained in Public health at the Institute of Education, University of London. His research interests are in translational epidemiology research as applied to public health. He is co-author of the paper Cardiovascular risk factors and cognitive decline in adults aged 50 and over: a population-based cohort study for the Age and Ageing journal, and this has been made freely available for a limited time.
Age and Ageing is an international journal publishing refereed original articles and commissioned reviews on geriatric medicine and gerontology. Its range includes research on ageing and clinical, epidemiological, and psychological aspects of later life.
Subscribe to the OUPblog via email or RSS.
Subscribe to only health and medicines articles on the OUPblog via email or RSS.
Epidemiology, a well established cornerstone of medical research, is a group level discipline that aims to decipher the distribution and causes of diseases in populations. Epigenetics, perceived by many as the most fashionable research arena in which to be involved, is a mechanism of gene regulation. What brings these perhaps unlikely partners together?
Epigenetic processes are key features in gene regulation. Epigenetic patterns are laid down in early development and are moulded through in utero and early postnatal life and continue to show some degree of plasticity across the lifecourse. Many environmental, behavioural, nutritional and lifestyle factors are believed to influence epigenetic patterns and in some case the evidence base is substantial. What is less clear is the role of this environmentally modifiable ‘epigenome’ on disease risk in populations. This is where epidemiology can help. A good starting point for an epidemiological engagement with epigenetics is clearly identified by Nessa Carey, in her recent popular science book The Epigenetics Revolution:
“The majority of non-infectious diseases that afflict most people take a long time to develop, and then remain as a problem for many years if there is no cure available. The stimuli from the environment could theoretically be acting on the genes all the time in the cells that are acting abnormally, leading to disease. But this seems unlikely, especially because most of the chronic diseases probably involve the interaction of multiple stimuli with multiple genes. It’s hard to imagine that all these stimuli would be present for decades at a time. The alternative is that there is a mechanism that keeps the disease-associated cells in an abnormal state, i.e. expressing genes inappropriately. In the absence of any substantial evidence for a role for somatic mutation, epigenetics seems like a strong candidate for this mechanism”.
Recent literature points to a role for epigenetic variation in a range of diseases including neurological disease, cardiovascular disease, osteoarthritis and obesity but in most instances these are correlations without robust evidence of causality. Indeed, epigenetics is often proffered as the answer to many unresolved causes of disease. The enthusiasm for establishing whether epigenetic mechanisms link the environment with disease development must be tempered by the knowledge that the epigenome is dynamic and has as much potential to respond to disease as respond to the environment. Therefore it is very difficult to disentangle cause from consequence when studying epigenetic variation and disease.
This is just one of the many challenges that face researchers interested in understanding the role of epigenetics in common complex disease. Other challenges include the differences in interpretation of the term ‘epigenetics’ itself – in a field that attracts cell, developmental and evolutionary biologists, epidemiologists and bioinformaticians, amongst others, it is unsurprising that epigenetics means different things to different people and discussions of its relevance to disease can sometimes suffer misinterpretation.
The methods at our disposal to accurately measure epigenetic variation and in turn assess the impact this has upon disease risk are still being developed and there is much to do in this arena with respect to when, where and how to look at the epigenome. The complexity and interplay of multiple factors in determining d
0 Comments on Epidemiology and epigenetics – a marriage made in heaven? as of 1/1/1900
In her novel, Prodigal Summer, Barbara Kingsolver celebrates the lush fecundity of nature. The main character marvels at the way her ovulation dependably comes with the full moon.
It’s a poetic image – but is there any evidence for it?
Actually, no. It’s true that the length of the average menstrual cycle is close to the length of the lunar cycle. But like so many notions about fertility, an effect of the moon on ovulation is just a nice story. The menstrual cycle is remarkably variable, even among women who say their cycles are “regular.” This is not surprising – unlike the movement of stars and planets, biology is full of variation. The day of ovulation is unpredictable, and there is no evidence (even in remote tribal cultures) that ovulation is related to phases of the moon or other outside events.
We humans are susceptible to myths about our fertility and pregnancy. These myths also invade science. One scientific “fact” you may have heard is that women who live in close quarters synchronize their menstrual cycles. The paper that launched this idea was published forty years ago in the prestigious journal Nature1. Efforts to replicate those findings have been wobbly at best – but the idea still persists.
Another scientific myth is the notion that sperm carrying the Y male chromosome swim faster than sperm carrying the X female chromosome. It’s true that the Y chromosome is smaller than the X. But there is no evidence that this very small addition of genetic cargo slows down the X-carrying sperm. As often as this idea is debunked, it continues to appear in scientific literature – and especially the literature suggesting that couples can tilt the odds towards having a baby of a particular sex.
Choosing your baby’s sex
Many couples have a definite preference for the sex of their baby. The baby’s sex is established at conception, which has led to a lot of advice on things to do around the time of conception to favor one sex or the other. Recommendations include advice on timing of sex in relation to ovulation, position during sex, frequency of sex, foods to eat or avoid, etc. The good thing about every one of these techniques is that they work 50% of the time. (This is good enough to produce many sincere on-line testimonials.) Despite what you may read, there is no scientific evidence that any of these methods improves your chances for one sex or the other, even slightly. The solution? Relax and enjoy what you get.
When will the baby arrive?
Everyone knows that pregnancies last nine months – but do they? Doctors routinely assign pregnant women a “due-date,” estimated from the day of her last menstrual period before getting pregnant. The due-date is set at 40 weeks after the last menstrual period. You might think the due-date is based on scientific evidence, but in fact, 40 weeks was proposed in 1709 for a rather flaky reason: since the average menstrual period is four weeks, it seemed “harmonious” for pregnancy to last the equivalent of ten menstrual cycles.
So what are a woman’s chances of actually delivering on her due date? Fifty percent? Twenty percent?
Try four percent. Just like the length of menstrual cycles (and every other aspect of human biology), there is lots of variation in the natural length of pregnancy. If the due-date is useful at all, it is as the median length of pregnancy – in other words, about half of women will deliver before their due-date, and about half after. So don’t cancel your appointments on the due-date just because you think it’s The Day – there’s a 96% chance the baby will arrive some other time.
1. McClintock MK. Menstrual synchorony and suppression.
0 Comments on Fertility and the full moon as of 1/1/1900
Making a difference to the health of populations, however small, is what most people in public health hope they are doing. Epidemiologists are no exception. But often caught up in the minutiae of our day-to-day work, it is easy to lose sight of the bigger picture. Is health improving, mortality declining, are things moving in a positive direction? Getting out and taking in the view (metaphorically as well as literally) can have a salutary effect. It broadens our perspectives and challenges our assumptions. Looking at recent trends in European life expectancy is a case in point.
Since 1950 estimated life expectancy at birth of the world’s population has been increasing. Initially, this was accompanied by a convergence in mortality experience across the globe—with gains in all regions. However, in the final 15 years of the 20th century, convergence was replaced with divergence, in part due to declines in life expectancy in sub-Saharan Africa. However, this global divergence was also the result of declining life expectancy in Europe. Home to 1 in 10 of the world’s population, and mainly comprised of industrialized, high-income countries, Europe has over 50 states. These include Sweden and Iceland that have consistently been ranked among the countries with the highest life expectancies in the world. But while for the past 60 years all Western European countries have shown increases in life expectancy, the countries of Central and Eastern Europe (CEE), Russia and other parts of the former Soviet Union have had a very different, and altogether more negative experience.
Trends in life expectancy between 1970 and the latest year available are shown in the Figure 1 for an illustrative selection of countries. These data were taken from one of two open sources : (i) the WHO Health for All Database or (ii) the Human Mortality Database, depending on which one had the longest time series. Differences between the sources are minimal for the purposes of this editorial. It is important to emphasize at the outset, that with one exception (discussed below), the trends shown in the Figure 1 are overwhelmingly driven by changes in mortality in adult life, not in infancy or childhood and are not the result of artefact.
Former communist countries of Eastern Europe
Between 1970 and the end of the 1980s, life expectancy at birth in the former communist countries of CEE (Czech Republic, Hungary, Poland and Slovakia), Russia and the Baltic states (Estonia, Latvia and Lithuania) stagnated or declined (Figure 1). This led to an increasing gap between them and Western European countries as the latter steadily improved. However, within a few years of the collapse of the Berlin wall in 1989, life expectancy started to steadily increase in the countries of CEE. This vividly illustrates that mortality can decline rapidly in response to political, social and economic change. Interestingly, once underway, the post-1989 increase in life expectancy in these countries has continued at a steady rate that is very similar to Western Europe. These parallel trajectories mean that the East–West gap, measured in terms of absolute differences in years of life expectancy, is proving very difficult to eliminate, despite earnest hopes to the contrary.
The trajectories of Russia and other Soviet countries, including the three Baltic States in the Figure 1, were strikingly different to those of the CEE countries. The anti-alcohol
0 Comments on Trends in European life expectancy: a salutary view as of 1/1/1900
You already know where babies come from – the business about sperm and eggs, and getting them together. You also know something about birth control – after all, people spend most of their reproductive years trying NOT to get pregnant.
But there comes a time for many women when they ready to have a baby. That’s when some interesting questions arise.
- Once you stop using birth control, how long does it take to get pregnant?
- Is there something women should do to increase their chances of getting pregnant?
- What can a woman do to help make sure her baby will be healthy?
Let’s start with the last question first. The most important thing a woman can do before getting pregnant is to start taking daily multivitamins with folic acid. Folic acid helps prevent serious birth defects of the brain and spine (neural tube defects) and probably other defects as well. These defects happen very early in the baby’s development – waiting until you think you are pregnant can be too late.
Another thing you can do, if you are a smoker, is to quit smoking. Smoking puts a damper on women’s fertility (although apparently not on the fertility of men – life is not fair). Smoking also increases the small chance of fetal death later in pregnancy. Do yourself (and your baby) a favor, and give up the cigarettes.
Besides that, what should you do (besides the obvious)?
Nothing.
Really, nothing. You already have a lot going for you. Consider the benefits of your family history – not a single one of your ancestors was infertile. If you are a reasonably healthy person with no history of reproductive problems, and if you are having unprotected sex at least weekly, biology is on your side.
Some useful facts
There is a spectrum of fertility, ranging from very low to very high. You won’t know where you are on that spectrum until you actually try to conceive. On average, your chance of getting pregnant in the first month is 25%. For a few unlucky couples, the chances are zero – they are sterile. Other couples may have a 50% or 75% chance of getting pregnant in their very first month of trying. For couples as a whole, about half will be pregnant after three months. That goes up to two-thirds of couples after six months, and more than 90% after a year. Even if you don’t conceive in the first year, you still have a 50% chance in the next year or so. Only about 5% or so of couples are unable to conceive at all by natural means.
Probably the biggest predictor of fertility is woman’s age. Women are at their reproductive peak during their twenties. As they move through their thirties, their fertility begins to decline. This is relevant because many women (for lots of good reasons) delay their childbearing until they are in their 30s or even older. If a woman is not so fertile to start with, this delay can cause problems. Unfortunately, there is no medical test to tell women in advance how fertile they are.
The fertility window
Let’s get down to the biology. Pregnancy happens when couples have sex during the five days before ovulation and the day of ovulation itself. (In other words, sperm can survive up to five days in the woman’s reproductive tract.) This six-day fertility window gives you a fairly wide span of days in each cycle for intercourse that can produce pregnancy.
But there is a catch. Most women don’t know
0 Comments on How to Get Pregnant (so your baby can be born on 11-11-11!) as of 1/1/1900
“Big data” sharpens statistical power and there are now specific data pooling projects in occupational epidemiology, to supplement the use of existing large databases. The SYNERGY study, for example, pools lung cancer case-control studies with the aim of teasing out occupational effects from behind the masking effect of smoking, which remains by far the most important driver for lung cancer. A recent analysis with around 20,000 cases and controls was able to show that bakers are not at increased risk of lung cancer, whereas the many previous smaller studies had given inconsistent results.
The first module that I developed was “Public Health and Epidemiology,” back in 2008. The books contained in the module have been published by our medical department over the course of three decades, and many are now considered public health classics, such as Michael Marmot’s Social Determinants of Health, and Geoffrey Rose’s The Strategy of Preventative Medicine.
