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Health News from NHS Choices

Constantly updated health news across a range of subjects.

NHS Choices News

  • Healthy older adults carry leukaemia mutations

    BBC News reports that, according to researchers, “It is ‘almost inevitable’ that your blood will take the first steps towards leukaemia as you age”.

    Researchers analysed the blood of 4,219 people, looking for DNA errors (mutations) linked to blood cancers (leukaemia).

    The number of mutations in healthy older people without the disease was higher than expected. The research focused on 15 genetic hotspots of leukaemia-linked mutations and found them in 0.8% of individuals aged under 60, and 19.5% of those aged 90 or older. 

    The media quoted figures suggesting that more than 70% of people in their 90s would have some form of leukaemia-associated mutation. This was based on predictions of the prevalence of other mutations outside of the 15 tested. 

    The good news is that this form of age-related leukaemia is highly unlikely to kill you. The bad news is you are far more likely to die of something else before the mutations trigger the onset of leukaemia.

    Still, as some are predicting that average lifespans will rise dramatically in the decades ahead, the results of this study could become more of an issue for future generations, and might also apply to other cancer types.

     

    Where did the story come from?

    The study was carried out by researchers from Wellcome Trust Sanger Institute, Cambridge (UK), and was funded by the Wellcome Trust, Leukaemia Lymphoma Research, the Kay Kendal Leukaemia Fund and the Spanish Ministerio de Economía y Competitividad  Subprograma Ramón y Cajal.

    The study was published in the peer-reviewed medical journal Cell Reports. It is open-access, so is free to read and download online.

    Generally, the media reported the story accurately. The Independent quoted Dr Vassiliou, senior author of the study, reassuring readers that: “These mutations will be harmless for the majority of people, but for a few unlucky carriers, they will take the body on a journey towards leukaemia. We are now beginning to understand the major landmarks on that journey”.

    One small gripe is with the choice of figures used. The main study result was that leukaemia-linked mutations were found in 0.8% of under-60s and 19.5% of over 90s. This was based on studying 15 leukaemia-linked hotspots. 

    Both the Independent and the BBC quoted figures suggesting that 20% of 50 to 60 year olds, and over 70% of over 90s, had dormant leukaemia-linked mutations. These much higher figures come from the study discussion and were not directly tested in the current research. They were figures based on assumptions about combining results from the 15 hotspots with other non-hotspot mutations from previous studies. We are not able to appraise the non-hotspot mutations studies, so we don’t know how accurate these figures are.

     

    What kind of research was this?

    This was a genetic study investigating how common small, leukaemia-linked DNA changes were in cancer-free adults.

    Cancers, including leukaemia, develop through the combined action of mutations that are acquired over time. The researchers say that leukaemia-associated DNA mutations can occur without evidence of the disease. They wanted to find out how common these were in healthy people, and how common they were as people got older.

     

    What did the research involve?

    The researchers analysed DNA samples at 15 pre-defined leukaemia-associated mutation hotspots, using highly sensitive tests. They analysed the DNA of 4,219 people aged 17 and over.

    The majority of DNA tests were on healthy people, but for comparison, they analysed the genes of a number of blood cells from people with myeloid leukaemia.

    The production of the range of different types of mature white blood cells starts with a small number of stem cells. More specialised cells develop from these, like tree branches. The stem cells replicate themselves, producing clones. Some of these clones receive signals from the body, causing them to replicate and develop (differentiate) into more specialised white blood cells. Different signals produce different types of cells. The researchers were looking at what stage in the production process the mutations were occurring. If the mutations happened early in the differentiation process, they would be found in many downstream white cell types. If they occurred later, then they would be found in fewer cell types.

     

    What were the basic results?

    The main results were that age-related leukaemia-linked mutations were much more common than previously predicted.

    Using only the 15 hotspots studied, they identified leukaemia-linked mutations in 0.8% of individuals under 60, rising to 19.5% of those aged 90 years and over. Coupling these estimates with other mutation rates from previous studies (outside of the 15 hotspots tested) they came up with much higher estimates. They predicted that more than 70% of people aged 90 or older would have some form of leukaemia-associated mutation. The 70% figure made it into the media coverage; the 19.5% was not mentioned.

    On closer inspection, they found that mutations DNMT3A-R882 were most common and, although their prevalence increased with age, were found in individuals as young as 25. By contrast, mutations affecting spliceosome genes SF3B1 and SRSF2, closely associated with the myelodysplastic syndromes, were identified only in those aged over 70 years, with several individuals harbouring more than one mutation.

    Myelodysplastic syndrome is an uncommon condition of unknown cause, that can lead to a drop in the number of healthy blood cells being produced. In some cases, it can progress into acute myeloid leukaemia.

    Mutations in gene NPM1 were not seen in the group. This gene is thought to act as a “gatekeeper” to leukaemia. If it goes wrong, your risk of leukaemia rises considerably. As the group were symptom-free, it is not surprising that this gene was not affected in most people.

     

    How did the researchers interpret the results?

    The study group said: “individuals without overt features of a haematological [blood] disorder may harbor hemopoietic cell clones [blood stem cells] carrying leukemia-associated mutations” and that accumulating these mutations “is an almost inevitable consequence of aging in humans”

     

    Conclusion

    This study estimated that 0.8% of individuals under 60, and 19.5% of those aged 90 years and over, had leukaemia-linked mutations. These mutations caused no immediate harm and the people didn’t have leukaemia. The mutations were lurking in the background, but could have the potential to contribute to leukaemia in the future.

    The research primarily focused on 15 genetic hotspots of leukaemia-linked mutations.

    However, in their discussion, they predicted that more than 70% of people aged 90 or older would have some form of leukaemia-associated mutation. This formed the basis of their comment that these mutations seem an inevitable part of ageing. It is important to realise that this much higher estimate was not directly tested in the study. That is not to say it is not true, but we can’t confirm or refute it either way. Further research could confirm this prediction.

    Scientists know that cancer is caused by the accumulation of genetic mutations over many years. This is why most cancers occur in older people, and the risk of cancer increases with age. What is surprising about this study is the relatively high prevalence of leukaemia-linked background mutations in healthy adults. The implication is that if people were to live a lot longer, say 150 years, they might expect to get leukaemia. In theory, this could also apply to some other types of cancer.

    This is all largely theoretical. The impact on the average person is minimal, though if lifespans continue to increase, it could be a potential problem for your grandchildren.

    It’s important to remember that we can all reduce our risk of cancer by making some simple changes to our lifestyle.

    For example, healthy eating, taking regular exercise and stopping smoking will help to lower your risk.

    Read more about how a healthy lifestyle can help to reduce your chances of developing cancer

    Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

    Links To The Headlines

    DNA develops to acquire genetic mutations linked with cancer as you get older, says study. The Independent, February 26 2015

    Leukaemia mutations 'almost inevitable', researchers say. BBC News, February 27 2015

    Links To Science

    McKerrell T, Park N, Moreno T, et al. Leukemia-Associated Somatic Mutations Drive Distinct Patterns of Age-Related Clonal Hemopoiesis. Cell Reports. February 26 2014



  • Does deadly diet drug DNP defeat diabetes?

    "A chemical [DNP] which caused munitions factory workers to lose weight inexplicably in the First World War could cure diabetes," The Daily Telegraph reports. The banned weight loss drug looked effective and safe when given in a modified form to rats bred to have diabetes.

    The potential benefits of DNP surfaced in WW1 munitions workers who lost a lot of weight after being exposed to it. DNP sped up their metabolism, leading to rapid weight loss. After being made into a weight loss drug in the 1930s, it was quickly withdrawn, as it was proven highly toxic.

    The problem was that it sped up the metabolism to a dangerously high rate, causing a range of serious side effects, and some deaths. Illegal sales of the drug have caused a number of deaths in the UK in recent years.

    Researchers at Yale University wanted to see if it was possible to harness DNP’s metabolic properties, while removing the toxic effects.

    They created a slow-release version of DNP, called CRMP, which improved the way the liver processed fat and improved other measures linked to type 2 diabetes risk in rats. As it delivered DNP at a much lower dose over time, there were no toxic effects.

    This is encouraging research that should lead to further studies.

    The version of DNP that is available through illegal sales, typically via the internet, is toxic, even in tiny amounts. Do not take it under any circumstances.

     

    Where did the story come from?

    The study was carried out by researchers from Yale University and was funded by United States National Institutes of Health and Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Denmark.

    Yale University has applied for a patent-related to the use of CRMP and things working in a similar way for the treatment of metabolic diseases, including non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes.

    The study was published in the peer-reviewed journal Science Express.

    The Daily Telegraph’s coverage was factually accurate. They made it clear the research was in rats, but also explained how: "the [research] team is confident that the research would translate to humans and are keen to start trials".

     

    What kind of research was this?

    This was an animal study investigating potential new uses for the banned chemical DNP for non-alcoholic fatty liver disease, which in turn, is a major risk factor for type 2 diabetes. Alternatively, both conditions can develop in tandem.

    DNP has a murky past. Starting life as an ingredient of explosives in WW1, its potential use as a weight loss drug was recognised in workers handling the agent. They sweated profusely, had sky-high temperatures and lost a lot of weight. In the 1930s, it was sold as a wonder weight loss drug. However, it was quickly withdrawn, because it was highly toxic, causing side effects and, in some cases, death. 

    DNP was also linked to deaths in 2013, after a resurgence among bodybuilders. This lead to the Food Standards Agency issuing a public warning about the risks of DNP, saying that: “DNP is an industrial chemical that is extremely dangerous to human health.” 
     
    NAFLD is the term used when there is a build-up of fat within the liver cells that is not caused by alcohol intake. It is usually seen in people who are overweight or obese, and is associated with metabolic syndrome. A healthy liver should contain little or no fat. Most people with NAFLD do not develop serious liver problems and just have stage 1 of the disease (simple fatty liver). The most important thing that people with NAFLD can do is to go on a gradual weight loss programme and exercise regularly.

    It is known that DNP has benefits on NAFLD, obesity and regulating blood glucose, but is usually too toxic to be used as a treatment. The chemical targets the mitochondria in cells. These are the little "batteries" responsible for making energy in cells, which is essential for life.

    DNP speeds up the metabolism; however, our metabolic system operates at the rate it does for a reason – it is safe. Speeding up the metabolism may help burn off fat, but it can also trigger a number of dangerous side effects and potentially cause death.

    This research team tried to devise a way to harness the benefits of DNP, while minimising its toxic side effects. All their experiments were in rats. This is the usual approach when testing chemicals to treat diseases, particularly dangerous ones. People and rats, both mammals, share lots of common biology, but there are differences.

     

    What did the research involve?

    The researchers gave groups of rats low levels of DNP and monitored its effect on fat content in the liver and other measures linked to a higher risk of type 2 diabetes. They were looking to confirm the benefits reported in previous studies.

    After encouraging results, they modified DNP to create CRMP (controlled-release mitochondrial protonophore). They fed this to rats in small amounts of peanut butter to see whether it had the same benefits, with fewer side effects.

    The benefits and side effects of DNP were compared with CRMP in a range of experiments lasting up to six weeks. During the experiments, rats were fed a high-fat diet and the researchers paid particular attention to changes in the function of the liver in dealing with this fat.

     

    What were the basic results?

    The main result was that CRMP caused fewer side effects than raw DNP, while maintaining similar benefits, including burning lots of fat, improved glucose tolerance and lower insulin levels.

    When testing for specific effects, CRMP prevented the development of the rat version of NAFLD in rats fed a high-fat diet for two weeks. Similarly, it seemed to improve blood glucose regulation when given to rats with diabetes for two weeks, also improving their blood fat levels.

    CRMP released the DNP-active chemical at a more gradual rate, and over a longer period, than giving straight DNP. This meant the levels in the blood did not spike as much and were lower overall. This seems to be the key to avoiding some of the worst side effects.

    One of the biggest side effects of DNP was that it caused a potentially fatal very high temperature. The researchers were able to find a dose of CRMP that was beneficial to the liver, without causing a huge rise in temperature.

     

    How did the researchers interpret the results?

    The researchers said: "we have shown that altering the pharmacokinetics of DNP to promote a low sustained systemic release can increase the therapeutic window of this agent by more than 500-fold. Daily CRMP administration reversed NAFLD, insulin resistance, T2D [type 2 diabetes], and liver fibrosis in rats without detectable toxicity".

    They added: "These data support the potential utility of mitochondrial protonophores and other mitochondrial uncoupling agents for the treatment of the related epidemics of NASH, metabolic syndrome and T2D."

     

    Conclusion

    This study created a slow release version of DNP, called CRMP, that improved the way the liver processed fat and improved other measures linked to type 2 diabetes risk in rats. It did this when given for up to six weeks without the toxic side effects known to be associated with unmodified DNP.

    This is encouraging research, which appears to have partially tamed some of the toxic effects of DNP, while protecting its benefits. Researchers will build on this in further studies in rats and possibly people, if these results are confirmed in more studies.

    However, the current version of DNP that is available for sale illegally online is toxic to humans, even in tiny amounts, and has been linked to a number of deaths. Do not take it under any circumstances.

    The study used a chemically-modified version of DNP, called CRMP, in rats. DNP on its own remains as dangerous as ever to people. CRMP’s safety in humans has not yet been tested.

    This study showed proof of the concept that DNP can be modified to make it safer in rats, while maintaining its benefits. This has not yet been proven in humans.

    The authors are planning further safety studies, reporting in the Telegraph that: "Given these promising results in animal models of fatty liver disease and type 2 diabetes, we are pursuing additional preclinical safety studies to take this approach to the clinic."

    Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

    Links To The Headlines

    First World War explosive could reverse diabetes, says Yale University. The Daily Telegraph, February 26 2015

    Links To Science

    Perry RJ, Zhang D, Zhang X, et al. Controlled-release mitochondrial protonophore reverses diabetes and steatohepatitis in rats. Science. Published online February 26 2015



  • Over two hours screen time a day may raise a child’s blood pressure

    "Watching TV for more than two hours a day increases the risk of raised blood pressure in children," The Daily Telegraph reports.

    A large study, involving more than 5,000 children who were followed up over two years, found a link between time sitting in front of a screen and an increase in blood pressure rates.

    It found that a worryingly high number of children – more than one in 10 – developed high blood pressure, a major risk factor for cardiovascular diseases (CVDs) in later life. CVDs are conditions that can damage the heart and blood vessels, such as a stroke.

    Children who spent more than two hours a day on “screen time” over the two years were at increased risk, as were those with low levels of physical activity.

    This study supports previous evidence that a sedentary lifestyle and low levels of physical activity are associated with high blood pressure, although it does not prove that the former causes the latter.

    There are many factors that can affect blood pressure, including genetics, development in the womb, socioeconomic status and weight.

    That said, the more time your child spends watching TV or playing on their PlayStation 4, the less time they are physically active.

    In the UK, children aged five to 18 are advised to do at least 60 minutes of physical activity a day.

     

    Where did the story come from?

    The study was carried out by researchers from several academic centres worldwide, including the University of Glasgow in the UK. It was funded by the European Community Sixth Research, Technological Development and Demonstration Framework Programme.

    The study was published in the peer-reviewed medical journal International Journal of Cardiology.

    Both The Daily Telegraph’s and the Daily Mail’s reporting was fair, although neither paper included comment from independent experts, and they failed to explain the fact that this kind of study cannot prove cause and effect.

     

    What kind of research was this?

    This was an observational cohort study looking at the incidence of pre-high blood pressure and high blood pressure in children in Europe and any association between blood pressure, levels of physical activity and sedentary behaviour.

    The study’s authors say high blood pressure is one of the most important factors for cardiovascular disease, and studies have shown that blood pressure levels in children and adolescents are linked to high blood pressure in adulthood. However, little is known about the risk factors for high blood pressure in childhood. Their hypothesis is that low levels of physical activity (and high levels of sedentary behaviour may contribute to the development of high blood pressure.

    Sedentary behaviour was classified as the amount of time parents reported their children spending in front of a screen – whether watching TV, videos or playing computer games. It did not include other kinds of sedentary activity – such as reading.

    Blood pressure is measured in millimetres of mercury (mmHg) and is recorded as two figures:

    • systolic pressure – the pressure of the blood when your heart beats to pump blood out
    • diastolic pressure – the pressure of the blood when your heart rests in between beats, which reflects how strongly your arteries are resisting blood flow

    In children, high blood pressure is defined as blood pressure greater than the 95th percentile for their age, height and gender.

     

    What did the research involve?

    The researchers used data from a study of 16,224 children from eight European countries (Spain, Germany, Hungary, Italy, Cyprus, Estonia, Sweden and Belgium) looking at the effects of diet and lifestyle on health. The current analysis was based on 5,221 children who were between two and 10 years old at the start of the study, for whom all data was available. Of these, 5,061 children were re-examined two years later.

    The children had their systolic and diastolic blood pressure measured at the start of the study and at two years follow-up. Pre-high blood pressure was defined as systolic or diastolic blood pressure from the 90th to 95th percentile for their age and height; and high blood pressure was defined as systolic or diastolic blood pressure above the 95th percentile for age and height.

    Physical activity in the children was measured using an accelerometer – an electronic device which measures the intensity of exercise. The unit had to be worn for at least six hours a day, for at least three days during one week (two weekdays and one weekend day).

    From this, the researchers calculated the time children spent in moderate physical activity and in vigorous physical activity. Moderate activity includes activities such as cycling, while vigorous activity includes running, football and energetic dancing.

    The children were classified into two groups – those who met current physical activity guidelines – doing at least 60 minutes of physical activity daily – and those who did not meet the guidelines. They were further classified as to whether changes in physical activity levels had taken place over the two years.

    The children’s parents were asked to fill in a questionnaire on their children’s sedentary behaviour, as measured by hours of TV/DVD/video viewing and computer/games-console use for both typical weekdays and weekend days. Researchers used this information to calculate the children’s “total screen time” per day. Participants were classified into two groups – those who met (US) guidelines on total screen time (two hours or less a day) and those who did not. Researchers also calculated changes in sedentary behaviour at two years.

    They also included a range of potential confounders, including season, sex, age, parental education and waist circumference.

    Researchers estimated the relationship between physical activity levels, reported screen time and the risk of developing high blood pressure or pre-high blood pressure. 

     

    What were the basic results?

    • Researchers found that the yearly incidence of pre-high blood pressure was 121 per 1,000 children, and high blood pressure was 110 per 1,000 children.
    • Children who maintained sedentary behaviour of more than two hours a day during the two year follow-up had a 28% higher risk of having  high blood pressure (relative risk (RR) 1.28, 95% confidence interval (CI) 1.03 to 1.60).
    • Children not performing the recommended amount of physical activity (60 minutes a day) at the start of the study had a 53% higher risk of high blood pressure (RR 1.53, 95% CI 1.12 to 2.09).
    • There was no association between pre- high blood pressure and children’s behaviours.

     

    How did the researchers interpret the results?

    The researchers say that the incidence of pre-high blood pressure and  high blood pressure is high in European children, with those doing less than 60 minutes of physical activity daily or spending two hours or more per day in front of a screen at higher risk. They say that the results suggest regular physical activity should be promoted and sedentary behaviour discouraged in children to prevent high blood pressure and its consequences in adulthood.

     

    Conclusion

    The study found a worryingly high incidence of high blood pressure in children of just over 10%, instead of the expected 5%. It also found that low levels of physical activity and high levels of “screen time” raised the risk.

    Although researchers adjusted their analysis for a range of other factors which might affect blood pressure (called confounders), it is always possible that other unmeasured factors could have affected the results. In addition, the study was reliant on parental estimates of the amount of sedentary behaviour their children had per day, which may be an over- or underestimate. Wearing the accelerometer may also have influenced the amount of physical activity that was performed on those days, which could also affect the results.

    It’s generally agreed that many of today’s children spend too much time in front of a screen – and too little on physical activity. The real question is – what can we do about it?  

    Children are more likely to accept changes to their lifestyle if they involve the whole family.  Read more about getting healthy as a family.

    Also, evidence has shown that placing limits on the use of any type of screen equipment in the hours before bedtime can improve the quality of their sleep. This could then help them improve their energy and activity levels during the day.

    Read more about how TVs, phones and screens impair kids' sleep.

    Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

    Links To The Headlines

    Too much TV could raise a child’s blood pressure: Watching more than two hours a day ‘makes them 30% more likely to have condition’. Mail Online, February 26 2015

    Children who watch TV for more than two hours a day 'at greater risk of high blood pressure'. The Daily Telegraph, February 26 2015

    Links To Science

    de Moraes ACF, Carvalho HB, Siani A, et al. Incidence of high blood pressure in children — Effects of physical activity and sedentary behaviors: The IDEFICS study: High blood pressure, lifestyle and children. International Journal of Cardiology. Published online November 26 2014



  • Longer sleep linked to stroke

    “Too much sleep could kill you,” is the baseless and needlessly alarmist headline on the front cover of today’s Daily Express.

    The study it is reporting on actually showed that people who sleep for more than eight hours a night had a 46% increased risk of stroke over the following 10 years, compared with people sleeping six to eight hours.

    While these results certainly warrant further investigation, it does not show that the increased sleep caused strokes, let alone death.

    The researchers assessed the usual sleep patterns of nearly 10,000 adults in 1998 and again in 2002, looking for associations between the amount of sleep and the number of people having a stroke over the next 10 years.

    They also pooled the results from similar studies. These also showed a 45% increased risk for people who sleep more than eight hours.

    When the results were analysed by sex, the link was statistically significant for women, but not men. This wasn’t made clear in the UK media coverage. Women’s risk was 80% higher, which is almost double the 46% risk when the sexes were combined.

    The study took into account cardiovascular risk factors such as high blood pressure and cholesterol, but not other illnesses. Without accounting for other illnesses, it is not clear what association the length of sleep has with risk of stroke from these studies. As that widely used, though valid, scientific cliché goes: “further research is needed”.

     

    Where did the story come from?

    The study was carried out by researchers from the University of Cambridge and the University of Warwick. It was funded by the Medical Research Council and Cancer Research UK.

    The study was published in the peer-reviewed medical journal Neurology. The study was published on an open-access basis, meaning that anyone can read and download it for free online. There is also a related editorial.

    The quality of the UK media's reporting of the study was mixed. The Independent and The Daily Telegraph took a measured approach, making clear the uncertainties of the study.

    The Daily Mirror somewhat contradicted itself, saying first that: “Shock study reveals sleeping for longer than eight hours 'could cause a stroke'.” Whereas later on, it correctly says: “Importantly, the study only found an association between sleep length and risk of stroke. It did not find that sleeping for too long actually causes stroke.”

    The Daily Express and the Metro said that increased sleep causes strokes, when this is not actually what the study found.

    At most, the study found that increased sleep is associated with an increased risk of stroke in women, but it did not take illnesses other than diabetes, high blood pressure and previous stroke into account, which could have affected the results.

    A lot of the media carried a useful quote from Yue Leng, from the University of Cambridge, saying: “It’s apparent both from our own participants and the wealth of international data that there’s a link between sleeping longer than average and a greater risk of stroke. What is far less clear, however, is the direction of this link. Whether longer sleep is a symptom, an early marker or a cause of cardiovascular problems.”

     

    What kind of research was this?

    This was a cohort study, which aimed to see if there was an association between sleep duration and risk of stroke. The researchers also performed a systematic review to find other relevant research, and pooled all the results in a meta-analysis.

    A cohort study is the most appropriate type of study when looking at the long-term effect of sleep patterns, as it would not be feasible or ethical to conduct a randomised controlled trial over a long time period. Combining the results with other similar studies in a meta-analysis increases the strength of the evidence. However, due to the nature of the study types, they can only show an association between sleep duration and risk of stroke – they cannot prove that sleep duration causes a stroke.

     

    What did the research involve?

    The researchers assessed the regular sleep patterns of nearly 10,000 adults, looking for links between the amount of sleep they got and the number of people who had a stroke over the next 10 years. They systematically searched for similar studies and pooled their own results with these others in a meta-analysis.

    The researchers recruited 9,692 participants from a larger longstanding study called the European Prospective Investigation of Cancer-Norfolk cohort, EPIC-Norfolk. They were given a questionnaire in 1998-2000, and again in 2002 to 2004, asking how much sleep they usually have over a 24-hour period, with the following options:

    • less than four hours
    • four to six hours
    • six to eight hours
    • eight to 10 hours
    • 10 to 12 hours
    • more than 12 hours

    They were also asked if they sleep well, to which they could respond “yes” or “no”.

    Participants were excluded from the study if they had already had a stroke. The researchers then obtained all cases of stroke from the National Health Services district database and the UK Office of National Statistics up until March 2009.

    They analysed the results according to the average sleep duration, or the change in sleep duration between the two questionnaires. They also took into account all of the following potential confounding factors:

    • age
    • sex
    • social class
    • education
    • marital status
    • smoking
    • alcohol intake
    • hypnotic drug use (sedatives and “sleeping tablets”)
    • family history of stroke
    • physical activity
    • major depressive disorder in the previous year
    • previous heart attack
    • diabetes
    • use of blood pressure medication
    • body mass index (BMI)
    • blood pressure
    • cholesterol

    Finally, they performed the systematic review and meta-analysis using all available trials up until May 2014.

     

    What were the basic results?

    The average age of the participants at the start of the study was 62, and ranged from 42 to 81 years. Most of them slept between six and eight hours per day (69%), with 10% sleeping for more than eight hours. In total, 346 people had a stroke during the 9.5-year follow-up period.

    After adjusting for all of the confounding factors listed above, sleep of more than eight hours:

    • increased the risk of stroke by 46% (hazard ratio (HR) 1.46, 95% confidence interval (CI) 1.08 to 1.98)
    • increased the risk of stroke in women by 80% (HR 1.80, 95% CI 1.13 to 2.85)
    • was not associated with stroke in men

    There was no statistically significant association between sleep of less than six hours and stroke.

    The systematic review identified 11 relevant studies, including 559,252 participants from seven countries. They were followed up for between 7.5 and 35 years. The pooled relative risks for sleep duration and stroke were:

    • increased risk of 15% for sleep of less than six hours (relative risk (RR) 1.15, 95% CI 1.07 to 1.24)
    • increased risk of 45% for sleep of more than eight hours (RR 1.45, 95% CI 1.30 to 1.62)

     

    How did the researchers interpret the results?

    The researchers concluded that this study, “suggested a significant increase in stroke risk among long sleepers and a modest increase among short sleepers”. They say that, “the underlying mechanism needs further investigation”.

     

    Conclusion

    This cohort study found that, overall, people who sleep for more than eight hours have a 46% increased risk of stroke. When analysed separately, there was no statistically significant association for men, but a much higher increased risk for women, of 80%.

    A major strength of the study is the number of potential confounding factors that the researchers tried to account for, including many cardiovascular risk factors. However, it did not account for other illnesses such as sleep apnoea or cancer, which may have had an effect on the amount of sleep and risk of stroke.

    In addition, the study is reliant on the information provided in the questionnaires, which may not be entirely accurate:

    • alcohol intake is famously under-reported
    • perception of sleep duration and actual duration may be different and could be affected by illness and memory problems

    The results of the meta-analysis were in line with the results of this study, though they also found an increased risk for people who have less than six hours sleep.

    Professor Kay-Tee Khaw, senior author on the study, said in the Mirror that: “We need to understand the reasons behind the link between sleep and stroke risk”. She added that, “With further research, we may find that excessive sleep proves to be an early indicator of increased stroke risk, particularly among older people.”

    In conclusion, without accounting for other illnesses, it is not clear what association the length of sleep has with risk of stroke from these studies. Known modifiable risk factors that can reduce your risk of stroke are to stop smoking, eat healthily, do physical exercise, and keep blood pressure and cholesterol within normal limits through lifestyle and use of medication where required.

    If you are concerned that your normal sleep patterns have changed for no apparent reason, visit your GP.

    Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

    Links To The Headlines

    Weekend lie-in danger: Sleeping for eight hours can increase the risk of a stroke - especially for women over 63. Mail Online, February 26 2015

    People who sleep more than eight hours are more likely to have a stroke, research shows. The Independent, February 25 2015

    Sleeping more than eight hours raises stroke risk, Cambridge University warns. The Daily Telegraph, February 25 2015

    Shock study reveals sleeping for longer than eight hours 'could cause a stroke'. Daily Mirror, February 25 2015

    Sleeping too much ‘increases your risk of having a stroke’, study reveals. Metro, February 25 2015

    Too MUCH sleep could KILL YOU: More than eight hours a night can double risk of stroke. Daily Express, February 26 2015

    Links To Science

    Leng Y, Cappuccio FP, Wainwright NWJ, et al. Sleep duration and risk of fatal and nonfatal stroke. Neurology. Published online February 25 2015



  • 'Game changer' HIV drug cuts infection risk by 86%

    "Scientists hail discovery of 'game-changer' that cuts the risk of infection among gay men by 86%," The Independent reports. The drug, Truvada, has proved very successful in a "real-world" trial involving 545 participants.

    Truvada is currently used as part of a treatment plan for people with HIV. It stops the virus from replicating, which helps protect the immune system.

    Researchers wanted to see if it could also prevent the infection taking hold in the first place and have now presented initial results at a conference.

    They recruited gay men, other men who have sex with men (MSM) and transgender women who were HIV negative and at high risk of HIV infection from 13 sexual health clinics in England. They randomly assigned them to either immediately start taking Truvada each day, or to wait and start taking it 12 months later.

    The researchers also wanted to see if taking the medication made people more likely to increase their sexual risk-taking behaviour because they thought they were protected.

    It is reported that both groups had the same rate of other sexually transmitted infections (STIs), an indication that sexual risk-taking did not change. The incidence of HIV infection in their first year of the study was much smaller in the Truvada group, at three people compared to 19 in the group who had to wait for a year before starting taking Truvada.

    The researchers plan to submit the study to a peer-reviewed journal in April and are working with a range of stakeholders to determine whether a Truvada service could be commissioned across the NHS for high-risk individuals.

     

    Where did the story come from?

    The study was carried out by researchers from the Medical Research Council Clinical Trials Unit at University College London, Public Health England and 12 NHS trusts across England. It was co-funded by the Medical Research Council and Public Health England.

    The results of the study were presented at the Conference on Retroviruses and Opportunistic Infections in Seattle, Washington. The study has not yet been published, so has not gone through external peer review to ensure the methodology and findings are reliable. The Medical Research Council reports that the study will be submitted to a peer-reviewed journal in April.

    As the study has not yet been published, this article is based on the information so far released from the Medical Research Council and Public Health England.

    Most of the UK media’s reporting of the study is accurate. An exception to this is the headline from The Daily Telegraph – "HIV drug taken before and after sex cuts risk by 86pc", which is misleading as it implies that Truvada could be taken like a morning after pill, but this has not been tested.

    It is highly likely that taking it in this manner would not be effective.

     

    What kind of research was this?

    This was a randomised controlled trial that aimed to see if Truvada was effective in reducing the incidence of HIV infection in gay and other MSM, and trans-women.

    The use of drugs such as Truvada to prevent infection, rather than treat infection, is known as Pre-Exposure Prophylaxes (PrEP). Truvada is an anti-retroviral (anti-HIV) drug, which is usually used to treat HIV. It contains two antiviral compounds called emtricitabine and tenofovir disoproxil fumarate. The drug is taken once a day. Anti-retrovirals work by stopping the virus replicating in the body, allowing the immune system to repair itself and preventing further damage. They have proved very successful, though resistance can be a problem, so people with HIV are usually required to take a combination of drugs.

    Truvada has already been shown to be effective in reducing the incidence of HIV infection compared to placebo (dummy pill). The purpose of this study was to see if taking Truvada changed sexual risk-taking behaviour, by making people feel that they were less likely to be infected and thus increasing their exposure to HIV.

    This kind of research is important because among gay men, MSM, and trans-women in the UK the rate of HIV infection remains high at 2,800 in 2013.

     

    What did the research involve?

    The researchers recruited 545 gay men, MSM, and trans-women who were HIV negative into the PROUD study (Pre-exposure Option for reducing HIV in the UK: immediate or Deferred). The participants were randomly assigned to have Truvada immediately (N=276) or to wait and have it after 12 months (N=269).

    The participants were recruited from 13 sexual health clinics in England between November 2012 and April 2014. People were eligible to be included in the study if they had reported having anal sex without a condom in the previous three months and planned to do so again in the near future. This put them in the very high risk category.

    Participants in both groups were advised to continue other risk prevention strategies such as condom use. They were also asked to keep a short diary, fill out a monthly questionnaire and attend a clinic appointment every three months.

     

    What were the basic results?

    Those taking Truvada were 86% less likely to be infected with HIV:

    • HIV infection occurred in three people taking Truvada compared to 19 in the group who had to wait for a year.
    • The infection rate in the Truvada group was 1.3 people infected per 100 people followed up for one year (100 person-years).
    • The infection rate in the waiting group was 8.9 per 100 person-years.

    Sexual risk-taking behaviour was judged not to have increased in the Truvada group as there was no difference between the groups in terms of the number of participants who had a sexually transmitted infection (STI).

    No results were provided from the diaries or questionnaires.

     

    How did the researchers interpret the results?

    The chief investigator of the study, Sheena McCormack, is reported to have said: "These results are extremely exciting and show PrEP is highly effective at preventing HIV infection in the real world." They are now working with a range of stakeholders to determine whether a PrEP service could be commissioned across the NHS.

     

    Conclusion

    The results of this unpublished study were presented at a conference in Seattle and have been reported by the Medical Research Council, who helped fund it. As it has not been published, some important details are not yet known, such as:

    • The researchers report that there was "high adherence" to taking the medication, but it is not known how regularly it was taken, or how many people stopped taking it and why.
    • No details have been provided about any side effects experienced on the medication.
    • The incidence of STIs was used to determine whether taking Truvada changed sexual risk-taking behaviour. It is currently unclear which STIs were compared between the two groups. Three common STIs are viral (genital herpes, genital warts and human papilloma virus), so it is possible that the Truvada reduced their incidence in addition to HIV. This could be an added bonus, but we will need to await publication of the study to look at this.

    A limitation of the study is the amount of contact the participants had with the sexual health clinics. They were asked to fill out monthly questionnaires and attend a clinic every three months. It is possible this frequent contact with services caused this particular group to be more aware of the risks of HIV infection.

    The researchers plan to submit the study to a peer-reviewed journal in April. In the meantime, they are working with a range of stakeholders to determine whether a PrEP service could be commissioned across the NHS. It has been suggested that men may wish to take PrEP during periods in their life when their sexual risk is highest, rather than continuously. This will no doubt be among the many considerations that will be taken into account.

    In conclusion, the researchers report that PrEP reduced HIV infection by 86% in this very high risk group when it was taken on a daily basis. Full publication of this study, and any further developments, are awaited.

    The most effective method of reducing your risk of HIV if you are sexually active – and whether you are gay, bisexual, trans or straight, is to always use a condom.

    Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

    Links To The Headlines

    HIV pill: Scientists hail discovery of 'game-changer' that cuts the risk of infection among gay men by 86%. The Independent, February 24 2015

    Daily pill Truvada cuts spread of HIV by 86%, study shows. The Guardian, February 24 2015

    'Give HIV drugs to healthy gay men'. BBC News, February 24 2015

    HIV Drug: 'Game Changer' Hopes For Gay Men. Sky News, February 25 2015

    Healthy gay men should be given HIV treatment to PREVENT infection, 'game-changing' trial suggests. Mail Online, February 24 2015

    Healthy gay men 'should be offered HIV drugs'. ITV News, February 25 2015

    HIV drug taken before and after sex cuts risk by 86pc. The Daily Telegraph, February 25 2015