"Low-fat diet bad for your health and cutting back on meat, dairy and eggs a disastrous mistake," the Daily Mirror reports.
That is the main message of a controversial report attacking official UK guidelines on diet and weight loss.
The report suggests it doesn't matter how much saturated fat we eat, and doesn't recommend counting calories.
Critics have pointed out there were no agreed criteria about what evidence would be considered in the report, leaving it open to accusations of cherry-picking.
This means the report's authors may have promoted evidence supporting their argument while ignoring evidence they saw as unhelpful.
Dr Mike Knapton, associate medical director at the British Heart Foundation (BHF), said: "This report is full of ideas and opinion.
"However, it does not offer the robust and comprehensive review of evidence that would be required for the BHF, as the UK's largest heart research charity, to take it seriously."
Who produced the report?
The report was published by the Public Health Collaboration, a not-for-profit organisation described as being dedicated to informing the public and implementing healthy decisions.
The report is said to follow decades of work and experience that founding and advisory board members have gathered through working with thousands of patients to improve their health.
The listed advisory board members are named health professionals, including dietitians, GPs, a cardiologist, a diabetes specialist and a psychiatrist. They also list a number of patrons.
It is unclear where Public Health Collaboration's funding comes from. Nor is it clear who wrote the report.
No author or authors are named, and it does not appear to have been peer-reviewed by independent experts.
The aim of the report is said to be to raise concerns about the government's current recommendations about healthy eating and weight loss, and also provide new evidence-based solutions to help people obtain healthy lifestyles and improve public health.
What does the report say?
The report states the current prevalence of obesity in the UK is 25%, costing the economy £47 billion a year.
It summarises the recommendations of the current Eatwell Guide for healthy eating, saying it has three main concerns with this guidance:
- the avoidance of foods because of their saturated fat content
- the dietary reference value of no more than 35% total fat
- the quality and quantity of carbohydrates
The researchers say current recommendations given on NHS Choices are to opt for low-fat dairy options, as high saturated fat can increase the risk of heart disease.
They highlight a large US cohort study from 2010 that concluded saturated fat intake was not associated with risk of cardiovascular disease.
They quote several other observational studies that supported the notion that high-fat dairy was not linked to obesity or cardiovascular and diabetes risk.
The researchers say: "In retrospect, there was never any strong evidence to recommend reducing total and saturated fat consumption, and in the 30 years since, the deteriorating health of the UK population suggests such advice may have been a dire mistake, however well intentioned."
They consider that if people had been opting for foods in the natural form, rather than manufactured low-fat foods, we wouldn't have the obesity problem we do today.
The Public Health Collaboration concludes the UK should stop recommending the avoidance of high saturated fat foods and focus on consuming food in its natural form – however much saturated fat it contains.No more than 35% total fat
The authors question recommendations that too much fat in your diet raises the risk of heart disease and makes you overweight, saying this is not backed by scientific evidence.
They reference a trial published this year, which found people on low-carb diets experienced more weight loss than people on low-fat diets, and say how recent US dietary guidelines have removed their previous 30% total fat limit and no longer place any restriction on fat.
They conclude the UK should remove the recommendation to eat no more than 35% total calorie intake from fat and instead focus on the health benefits of eating food in its natural form – regardless of fat content.Quality and quantity of carbohydrates
As the authors say, good blood glucose control is important to maintain health and reduce the risk of developing diabetes or pre-diabetes conditions.
However, they say eating lots of foods that raise blood glucose and promote the release of insulin are factors likely to increase this risk – and high carbohydrates do just that.
They discuss the glycaemic index (GI) of different foods, and say the UK's Eatwell Guide "illogically" recommends high-GI foods, advising people to "base meals on potatoes, bread, rice, pasta or other starchy carbohydrates".
They suggest that such recommendations are behind the increase in rates of type 2 diabetes and obesity.
The Public Health Collaboration concludes people should avoid foods that have a high carbohydrate density, and instead focus on food and drink that has a carb density of less than 25%. Such foods are usually in their natural form."Real food" lifestyle
The Collaboration sets out a new form of the Eatwell Guide called "The Real Food Lifestyle", which has a 50:50 split of fats and proteins against carbohydrates, but all food and drinks on the wheel are in their natural form.
They emphasise carbs with a density less than 25% and a minimum of 1g protein per 1kg bodyweight per day.
They also emphasise eating "real" foods that will fill you and avoiding processed "fake foods", which won't.
For example, they recommend natural oils and butter, including coconut oil, ghee, lard and cold-pressed olive oil – the "fake" ones are rapeseed, sunflower and corn oil – and no juices or processed sugar products.
If you were being critical you could argue that the division between “real food” and “fake food” is scientifically meaningless.
The report is presented in the form of a narrative, where individual pieces of evidence are cited as coming from particular studies. A list of references is then provided at the end.
However, the report does not provide any information about how the authors identified and selected the research reviewed.
As such, it is not possible to say this was a systematic review, and we cannot know for sure this is a balanced report that has reviewed all evidence relevant to diet and nutrition.
The standard warnings about cherry-picking – evidence that is inconvenient may be ignored – apply.
Also, without reviewing the individual studies referenced, it is not possible to appraise the quality and strength of this evidence. However, many are observational.
There is potential for various sources of confounding and bias to influence associations between self-reported diet and health outcomes, such as inaccurate recall on food questionnaires or the potential influence of other unmeasured health and lifestyle factors.
It can be difficult to know to what extent a particular outcome can be directly attributed to a particular food – or the absence of it.
The report further says it "clearly and concisely provides an insight into the decades of work and experience that our founding members and advisory board have accumulated from working with thousands of patients".
But it's not known what sort of experience or data from patients has contributed to informing this.
We also don't know, for example, whether the recommendations on fat and carbohydrate intake would be applicable to all stages in life, or whether there might be different advice for children.
The report makes much of the fact that in spite of UK dietary guidelines, the number of people with obesity and type 2 diabetes has grown in recent decades. However, this does not prove that the guidelines are to blame.What response has there been to the report?
The report has attracted quite considerable criticism.
Some professionals, such as the professor of diet and population health at the University of Oxford, note the lack of systematic review methods and accuse the report of potentially cherry-picking studies to support its viewpoint.
Other studies presenting contradictory findings do not seem to have been included, they say.
As a scientist from the University of Reading says: "As with any public health measure, it is important that any recommendations are based on solid evidence and take the wider implications of implementation into account. That doesn't seem to be the case in this instance."
Professor Tom Sanders, emeritus professor of nutrition and dietetics at King's College London, says statements such as "fat doesn't make you fat", "saturated fat doesn't cause heart disease", and "avoid 'low fat' " are potentially harmful and could mislead the public.
Other opinion is more mixed, with one professor saying the report has "good, bad and ugly elements in it". There are views that snacking and added sugar are to be avoided, but ideas that we should eat limitless fat and cut out sugar altogether are criticised.
BBC news quotes Dr Alison Tedstone, Public Health England's chief nutritionist, who says: "In the face of all the evidence, calling for people to eat more fat, cut out carbs and ignore calories is irresponsible."
She says thousands of scientific studies have been considered when making current UK health and nutrition recommendations.
"It's a risk to the nation's health when potentially influential voices suggest people should eat a high-fat diet, especially saturated fat," she says.
"Too much saturated fat in the diet increases the risk of raised cholesterol, a route to heart disease and possible death."
Links To The Headlines
Low fat diet bad for your health and cutting back on meat, dairy and eggs a disastrous mistake. Daily Mirror, May 23 2016
Public Health England: Advice to eat more fat 'irresponsible'. BBC News, May 23 2016
Official advice on low-fat diet and cholesterol is wrong, says health charity. The Guardian, May 23 2016
'Eat fat to get thin': Official diet advice is 'disastrous' for obesity fight, new report warns. The Daily Telegraph, May 23 2016
Eating full fat foods 'can lower chance of obesity'. The Independent, May 23 2016
Row over 'eat more fat' dietary advice. ITV News, May 22 2016
"Half of all cancer deaths could be avoided if people simply adopted a healthier lifestyle," the Daily Mail reports.
A new study adds to the weight of evidence that says combining simple lifestyle changes can dramatically cut cancer death rates.
More than 100,000 health professionals from the US were asked to complete questionnaires about their lifestyle and cancer status every two years, and diet every four years.
The researchers compared cancer rates between people with low- and high-risk lifestyle factors, and also compared rates in the low-risk group with the general white population in the US.
They found a large number of cancer cases and deaths could be attributed to a high-risk lifestyle, such as an individual being overweight, smoking, drinking heavily, or being physically inactive.
The researchers estimated between a quarter and a third of all cancer cases in this population group could be attributed to poor lifestyle factors.
These findings are in agreement with past research and the understanding that a healthier lifestyle may reduce the risk of various types of cancer.
But this study has limitations, including the population group, which only involved white American health professionals, and the possibility that the estimates are inaccurate.
The study would appear to confirm that any small lifestyle changes you can make, such as quitting smoking, could considerably reduce your risk of developing cancer. And the more of these small changes you can combine, the greater the effect.
Read more about how lifestyle changes can help prevent cancer.Where did the story come from?
The study was carried out by researchers from Harvard Medical School and was funded by the US National Institutes of Health.
It was published in the peer-reviewed journal, JAMA Oncology.
The Daily Mail reported on the study fairly accurately, but did not present any of its limitations.
It's nice to see that the article included clear recommendations from the research team about how a person can reduce their risk of cancer.
However, the headline figure of "half of all cancer deaths" seems a bit of a fudge, as the study presented a range of different results for specific cancer types.What kind of research was this?
This prospective cohort study followed a large population group over time, and assessed the incidence of cancer and related deaths.
The researchers looked at how these cancer outcomes were related to various lifestyle factors, and then estimated the proportion of cancers that could be attributed to these factors.
The observational nature of this type of study means it is not able to prove causation, but it can find links and potential risk factors.
This type of study has strengths in terms of being able to follow a large number of participants over a long period of time, but the number of people who become non-responsive to follow-up assessments may increase over the years.What did the research involve?
The researchers recruited participants from two cohort studies:
- The Nurses' Health Study – which started in 1976 and enrolled female nurses aged 30 to 55
- The Health Professionals Follow-up Study – which started in 1986 and enrolled male health professionals aged 40 to 75
Participants completed questionnaires about their medical history and lifestyle at the beginning of the study and every two years thereafter. Dietary information was collected every four years using a validated food frequency questionnaire.
The researchers split the participants into two groups according to the level of health risk associated with their lifestyle.
To be considered low risk, a participant had to meet the following requirements:
- have never smoked or be a past smoker more than five years ago
- drink no or a moderate amount of alcohol – no more than one drink a day for women and two for men
- have a body mass index (BMI) of at least 18.5 and lower than 27.5
- do at least 75 minutes of vigorous-intensity or 150 minutes of moderate-intensity aerobic physical activity a week
If all of these requirements were not met, the participant would be considered high risk.
The outcomes of interest were the incidence of total and major individual cancers and associated deaths. Cancer was self-reported in the questionnaires. Where a participant failed to respond, the National Death Index was used to identify deaths.
The researchers compared the cancer rates between the low- and high-risk groups. They then compared cancer rates in the low-risk group with cancer rates in the general population using national surveillance data.
They used this information to help them calculate population-attributable risk (PAR).
This is an estimate of the proportion of all cancer cases that can be attributed to poor lifestyle factors, or the number of cancers that would not occur in a population if the risk factor – in this case, a high-risk lifestyle – was eliminated.
For example, a PAR could be used to estimate how many people in a given population would not die of lung cancer if nobody in that population smoked.What were the basic results?
A total of 135,910 people were included in the study (89,571 women and 46,339 men). The low-risk group contained 21% of all participants (12% women and 9% men) with the remaining 79% classed as high risk (54% women and 25% men).
The incidence of cancer per 100,000 people was 463 for women and 283 for men in the low-risk groups, compared with 618 for women and 425 for men in the high-risk groups.
From this, the researchers estimated that 25% of cancers in women and 33% of cancers in men could be attributed to high-risk lifestyle factors. For cancer-related deaths, 48% of cancer deaths in women and 44% of cancer deaths in men could be attributed to a high-risk lifestyle.
For individual cancers, the proportion of cancers estimated to be caused by high-risk lifestyle factors were:
- lung – 82% for women, 78% for men
- bowel – 29% for women, 20% for men
- pancreas – 30% for women, 29% for men
- bladder – 36% for women, 44% for men
Estimates were similar for cancer death, though there were additional associations for some other sites, including breast (12%), womb (49%), kidney (48% in men), and oral and throat (75% in women and 57% in men) cancers.
The general US populations were at higher risk than the whole study population, meaning that the PARs for these cancers resulting from a poor lifestyle were even higher than the researchers' estimates – for example, the PAR for bowel cancer jumped to 50%.How did the researchers interpret the results?
The researchers concluded that, "In this cohort study of a portion of the US white population, about 20-40% of cancer cases and about half of cancer deaths can be potentially prevented through lifestyle modification.
"These figures increased to 40-70% when assessed with regard to the population of US whites, and the observations are potentially applicable to broader segments of the US population."Conclusion
This prospective cohort study assessed the number of cancer cases and related deaths associated with poor lifestyle factors in a sample of US health professionals.
As the findings demonstrate, a large number of cancer cases and deaths in both men and women can be attributed to a high-risk lifestyle, such as being overweight, smoking, drinking heavily, or being physically inactive.
Worryingly, a poor lifestyle was estimated to account for an even greater number of cancers in the general population.
These findings are in agreement with much research, which has found that a healthier lifestyle may reduce the risk of various cancers.
The study has both strengths and limitations to consider. It contained a large number of participants and excluded types of cancer where incidence may be related to environmental factors rather than lifestyle, both adding strength to the findings.
It did have limitations, however:
- The use of questionnaires for collecting information is prone to bias, either by people reporting what they think they should be doing rather than what they are doing, or because of difficulty recalling information over a period of time.
- Only medical professionals were included in the study. This group are potentially more health conscious, so may not be a good reflection of the whole population. This is supported by the fact that even the high-risk study group were healthier than the US population overall, and PAR estimates for cancer from poor lifestyle factors were higher in the general population.
- Only including a white population means these findings may not necessarily apply to other ethnicities.
- These results are only estimates: though informed by careful analysis of this population and their lifestyle factors and cancer rates, it's possible that the proportion of cancers attributed to poor lifestyle factors is inaccurate, particularly for wider populations.
Despite these limitations, it is well known that unhealthy lifestyle factors could increase your risk of developing cancer, as well as various other health problems. Any small changes you can make to your lifestyle could considerably reduce your risk.
Read more about how to prevent cancer.
Links To The Headlines
HALF of all cancer deaths could be avoided if we simply adopted a healthier lifestyle. Daily Mail, May 19 2016
Links To Science
Song M, Giovannucci E. Preventable Incidence and Mortality of Carcinoma Associated With Lifestyle Factors Among White Adults in the United States. JAMA Oncology. Published online May 19 2016
"Superbugs will kill someone every three seconds by 2050 unless the world acts now," BBC News reports.
A review commissioned by the UK government says wide-ranging action is required at a global level to prevent a post-antibiotic future.
The review panel, chaired by economist Jim O'Neill, warns that without global action, antibiotic resistance will become a "devastating problem" by 2050, responsible for an estimated 10 million deaths a year.
Surgery could also carry a much higher risk of complications because of the possibility of infection.What is antibiotic resistance?
Antibiotics are often used to treat bacterial infections and are a cornerstone of infectious disease care.
However, bacteria evolve in response to their environment. Over time, they can develop mechanisms to survive a course of antibiotic treatment.
This "resistance" to treatment starts as a random mutation in the bacteria's genetic code, or the transfer of small pieces of DNA between bacteria.
If the mutations are favourable to them, they are more likely to survive treatment and be able to replicate, and are therefore more likely to pass on their resistant nature to future generations of bacteria.
When taken correctly, antibiotics will kill most non-resistant bacteria, so these resistant strains can become the dominant strain of a bacterium. This means that when people become infected, existing treatments may be unable to stop the infections.What recommendations does the review make?
The review makes 10 recommendations, outlined below.Launch a massive global public awareness campaign
The issue of antibiotic resistance is still not fully appreciated, especially in the developing world, where antibiotics are often sold without prescription.
The review estimates that a successful global campaign could be mounted for around $40 to $100 million a year, a fraction of the advertising costs for products like pet food or chocolate.Improve hygiene and prevent the spread of infection
Improving access to clean water and sanitation, promoting best practice in hospital infection control, and simply encouraging people to wash their hands will all help prevent infection.Reduce unnecessary use of antibiotics in agriculture
The US Food and Drug Administration estimates 70% of medically useful antibiotics are actually sold for use in animals.
It argues that critically important antibiotics should be restricted from animal sales.Improve global surveillance of drug consumption and resistance
Governments need to share data on antibiotic consumption and levels of resistance, and the biological reasons underpinning the two. Poorer countries should be given assistance in gathering data.Promote new rapid diagnostic tests to reduce unnecessary use of antibiotics
Many antibiotics are prescribed in cases when a bacterial infection hasn't been confirmed, as a precaution. New types of tests could help prevent this.
The review hopes that by 2020, in wealthy countries antibiotics would only be prescribed if a bacterial infection had been confirmed through testing.Promote the development and use of vaccines and alternatives
Encouraging the take-up of existing vaccines, as well as providing incentives for the creation of new ones, should help reduce the demand for antibiotics.
There also may be alternative interventions that can help prevent infections occurring.Improve the number, pay and recognition of people working in infectious diseases
Infectious disease health professionals tend to be paid less than their peers working in other fields.
A similar pattern can be seen in both private and public sector workers involved in infection research.Establish a Global Innovation Fund for early-stage and non-commercial research
The review recommends that a Global Innovation Fund, endowed with $5 billion over the next five years, should be set up to fund "blue sky" research – research that may not have an immediate commercial application, but could lead to breakthroughs in the future.Better incentives to promote investment for new drugs and improve existing ones
There is currently not a great deal of profit in antibiotic research, so pharmaceutical companies should be encouraged by meaningful incentives, such as a reward for bringing a new drug to market.Build a global coalition for real action
Antibiotic resistance is a global problem, so it can only be tackled through global action. The review recommends that the G20 countries spearhead action via the United Nations.
Links To The Headlines
Global antibiotics 'revolution' needed. BBC News, May 19 2016
Blueprint To Tackle Growing Drug Resistance. Sky News, May 19 2016
Antibiotics will stop working at a 'terrible human cost', major report warns. The Independent, May 19 2016
Billion dollar rewards for new antibiotics called for to defeat catastrophic rise of superbugs. The Daily Telegraph, May 19 2016
No antibiotics without a test, says report on rising antimicrobial resistance. The Guardian, May 19 2016
Superbugs will kill 10m people a year without new antibiotics claims report. The Sun, May 19 2016
"People should consider taking aspirin immediately after a minor stroke," BBC News reports.
A review of existing evidence found people treated with aspirin after a mini stroke (transient ischaemic attack, or TIA) were less likely to experience a more serious follow-up stroke.
A TIA occurs when a blood clot temporarily blocks blood flow in the brain. It causes problems including numbness or weakness of the face, arms or legs, as well as dizziness and problems with speech and sight.
These usually pass quickly, but are a warning sign of the possibility of a second, more serious stroke in the next few weeks. If you have these symptoms or see someone with them, you should call 999 for an ambulance immediately.
The review found taking aspirin reduced the risk of having another stroke by about 60% in the first six weeks, and of having a disabling or fatal stroke by 70%.
The researchers also suggest people who have symptoms of a stroke should be advised to take aspirin straight away, while waiting for medical help.
But the possible risk of doing this is that if stroke symptoms are caused by bleeding inside the brain, taking an aspirin could make the situation much worse.
The transient symptoms of a TIA are most likely to be caused by a clot, but still, the advice on self-treatment needs to be considered by experts before we can recommend it. The key point is to get medical help immediately by dialling 999.
Where did the story come from?
The study was carried out by researchers from the University of Oxford, University Medical Centre Utrecht, University Duisburg-Essen and Lund University.
It was funded by the Wellcome Foundation and the National Institute of Health Research Biomedical Research Centre.
On the whole, UK media coverage was good, with accurate reporting of the research and the researcher's conclusions.What kind of research was this?
This analysis looked specifically at the effects of the treatment (aspirin) over the course of time.
The researchers wanted to see the effects of aspirin at particular times after a stroke – either a transient ischaemic attack (TIA) or a full stroke caused by a blood clot (ischaemic stroke).
While meta-analyses can provide reliable results, they are only as good as the studies they contain, and there may have been variability in the study design and assessments.What did the research involve?
Researchers analysed all RCTs that measured the effects of aspirin given after an ischaemic stroke or TIA to prevent a future stroke.
Because many of these trials did not start treatment straight away, they also looked at trials where aspirin was given to people being treated within 48 hours of having a stroke.
They measured the effects of aspirin on repeated stroke and the severity of repeat strokes at up to six weeks after the stroke, between 6 and 12 weeks, and more than 12 weeks.
Most of the studies that established the place of aspirin in the treatment and prevention of stroke were done in the 1980s and 1990s, so some of this research is quite old.
The researchers pooled individual patient data from the studies and stratified it into time periods.
They also looked at studies including the anti-clotting drug dipyramidole, which is sometimes used alongside or instead of aspirin, to see what effect the two drugs had at different time points.
The researchers also assessed the effects of the severity of the first stroke on the results.What were the basic results?
The risk of having a repeat stroke within six weeks of the initial TIA was cut by about 60% for people taking aspirin.
Just under 1% of people who took aspirin had a repeat stroke within six weeks, compared with 2.3% of people who did not take aspirin (hazard ratio [HR] 0.42, 95% confidence interval [CI] 0.32 to 0.55).
The risk of having a disabling or fatal stroke was cut even more, by about 70% (HR 0.26, 95% CI 0.2 to 0.42). People who'd had a TIA or minor stroke were more likely to benefit from aspirin treatment than those who'd had more severe strokes.
The risk of having a second stroke between 6 and 12 weeks later was also reduced for people taking aspirin.
But after 12 weeks, people who'd taken aspirin were as likely to have a stroke as those who hadn't taken aspirin.
This suggests the effects of aspirin are most important in the weeks immediately after a stroke or TIA, when the risk of another stroke is highest.
When the researchers looked at patients who'd been treated with aspirin immediately after an acute stroke, they again saw a drop in the risk of a repeat stroke, and found this drop in risk was biggest for patients who'd had less severe strokes.
In the trials that compared aspirin with dipyramidole, aspirin alone worked as well as aspirin with dipyramidole to reduce stroke risk in the first 12 weeks, but dipyramidole worked better after 12 weeks.How did the researchers interpret the results?
The researchers said their results show that the effects of aspirin in reducing the risk of stroke immediately after a first stroke or TIA have been underestimated.
They said that, "It is essential that aspirin is given to patients with suspected TIA or minor stroke immediately."
They went on to suggest that, "Consideration should be given to promoting self-administration [i.e. taking aspirin yourself] immediately after transient stroke-like neurological symptoms."
They also said it would be "prudent" to run a public education campaign to encourage people to seek medical help immediately after having symptoms of stroke, and also to take aspirin.Conclusion
The study supports current recommended practice that people with a TIA or ischaemic stroke caused by a blood clot are treated with aspirin as soon as possible.
NHS experts are considering whether to recommend that you take aspirin yourself while waiting for medical help.
The reason this isn't recommended at present is that some people will have had a haemorrhagic (bleeding) stroke, and aspirin can make the bleeding worse.
For people who've had a full stroke, an urgent brain scan is usually performed to exclude bleeding as a cause and check it's safe to proceed with anti-clotting treatment. The risk of transient symptoms being caused by bleeding is much smaller, but it is possible.
Until official guidelines are produced – NHS England are reportedly considering the report's findings – current advice still stands. If you are experiencing the symptoms of a stroke, the most important thing is to call for an ambulance immediately.
The new study included thousands of people from high-quality RCTs, so the results are likely to be reliable, although there are some limitations.
Most of the studies included were conducted 20 or 30 years ago, and the medical treatment of stroke has improved since then, so the results might be different if the trials were run again now.
People who have had a stroke nowadays are more likely to be treated urgently, although too many people with minor strokes or TIAs don't seek help quickly enough.
This analysis would be stronger if the studies included had more people randomised to aspirin treatment within hours or days of their stroke or mini stroke.
However, this would be likely only to strengthen the effects seen with aspirin, and it's unlikely that trials involving more people treated quickly would undermine the main results.
The key point is not to ignore the symptoms of a stroke or TIA, but to treat it as a medical emergency, as you would do a heart attack, and call 999 for help.
Links To The Headlines
'Immediate aspirin' advice for minor stroke. BBC News, May 19 2016
Taking aspirin quickly after minor stroke 'can cut risk of recurrence'. The Guardian, May 19 2016
Take aspirin immediately after a 'funny turn' to cut your risk of stroke. Daily Mail, May 19 2016
Immediate aspirin after mini-stroke substantially reduces risk of suffering a major stroke. The Daily Telegraph, May 18 2016
Taking an aspirin straight after a 'mini stroke' could save your life, say docs. The Sun, May 19 2016
Links To Science
Rothwell PM, Algra A, Chen Z, et al. Effects of aspirin on risk and severity of early recurrent stroke after transient ischaemic attack and ischaemic stroke: time-course analysis of randomised trials. The Lancet. Published online May 18 2016
"Magic mushrooms 'promising' in depression," BBC News reports. Magic mushrooms is an umbrella term for fungi that contain psilocybin, a psychoactive substance that can cause intense LSD-like hallucinations, as well as reported feelings of euphoria and "spiritual insight".
Researchers gave two doses of psilocybin to 12 volunteers, all of whom had moderate or severe depression that had not responded to other treatment. As this drug is controlled in the UK, permission from the Home Office was needed for the study, and the participants were closely monitored by psychiatrists.
The intention was to monitor the "intensity" of the experience, as reported by the volunteers, to see if it was feasible to use psilocybin to treat people with severe depression. The researchers also wanted to get an initial impression of its effects.
They found the 12 volunteers tolerated the drug, with minor side effects that did not last long. Eight of them had no symptoms of depression one week after treatment, and five were free from depression after three months.
But because of the type of study this is and its small size, we can't be sure if these results are the result of psilocybin.
The researchers warn that people should not try to treat themselves with mushrooms that contain psilocybin. Aside from their unpredictable effects, magic mushrooms are class A drugs that are illegal to possess – which can carry a seven-year jail sentence – or distribute, which can result in up to life imprisonment.Where did the story come from?
The study was carried out by researchers from Imperial College London, South London and Maudsley NHS Trust, King's College London, University College London, the Royal London Hospital, and the Beckley Foundation.
It was funded by the Medical Research Council.
While overall the UK media reporting was accurate, The Sun newspaper wins the most inappropriate headline of the month award (and is currently a leading contender for 2016).
Their headline, "Magic mushrooms make you a fun guy", manages to both trivialise the life-limiting and often horrible impact severe depression can have, while simplifying the complex results of this study.
The Sun also used a stock photo of a classic twentysomething cheesy raver with the caption: "Professor Nutt, who worked on the study, was previously sacked as the Government's chief drug adviser in 2009". The distinguished 65-year-old psychiatrist may be a little put out (or possibly amused) by this.
The Daily Mail was also overenthusiastic in its reporting, saying that "Hundreds of thousands of people could benefit from antidepressants derived from magic mushrooms", despite the limited nature of the study.
However, both The Guardian and The Independent give a more measured account of the study and its limitations.What kind of research was this?
This was an open-label feasibility study designed to test whether the drug psilocybin could be safely given to selected patients with depression, alongside psychological support.
Everyone in the study took the drug, meaning there was no comparison group and everyone knew that they were taking the drug.
That said, it is hard to imagine what could serve as a placebo for a drug (psilocybin) notorious for its hallucinogenic properties.
This type of early-stage trial cannot give us reliable information on efficacy – nor is it set up to do so.
Even if such a trial suggests possible effectiveness, it's hard to be sure whether the results are truly down to the drug or whether they could reflect an "expectation" effect, where people immediately felt better because that is what they expected.What did the research involve?
Researchers publicised their study, saying they wanted to recruit people with depression that had not responded to other treatments to test psilocybin. Only 12 of the 72 volunteers met the study requirements.
After physical and mental health tests – including checks to make sure the volunteers were not at high risk of psychosis – they were given two doses of psilocybin in hospital, one week apart.
The first was a low dose to check for unexpected reactions, while the second was a high dose aimed at treating depression. The day after treatment, people were asked about their experiences, including the intensity of psychedelic effects (on a scale of 0 to 1) and any unpleasant effects.
Everyone was followed up regularly, by telephone or email, from the day after the high-dose treatment until three months afterwards. Participants filled in questionnaires designed to monitor depression symptoms.
Researchers compared depression scores from before the study began, one week after treatment, and three months after treatment.What were the basic results?
On average, people rated the intensity of the experience as 0.5 for the low-dose and 0.75 for the high-dose treatment. Psychedelic effects typically appeared from 30 to 60 minutes after taking the dose, peaked after two to three hours, and were no longer detectable after six hours.
Nobody had to be sedated during the treatment. The main side effects were feeling anxious (which happened to everyone), confusion, nausea and headache. None of these side effects lasted. Average depression scores decreased at one week and remained lower at three months.
Because the study is so small, it may be more useful to look at what happened to the individuals, rather than average depression scores.
After one week, eight people responded to the medicine with reduced depression scores of at least half their previous score, suggesting a big improvement. Seven of them fell into the range that suggested they no longer had depression.
However, most people's depression scores increased over the next three months, and only five of the original 12 volunteers were still free from depression at the end of the study.
At the end of the study, six people had mild or moderate depression, and one person once again had severe depression.How did the researchers interpret the results?
The researchers said that: "Done with appropriate safeguards, [such as careful screening and therapeutic support] psilocybin can be safely administered" to patients with depression.
They admitted that the study design means "strong inferences cannot be made about the treatment’s therapeutic efficacy" – in other words, we can't be sure that it worked. They went on to say that: "The data do suggest that further research is warranted".
They pointed out that it is rare for people with severe depression to recover spontaneously without treatment, and most of their participants had lived with depression for many years.
They have called for a bigger randomised controlled trial to properly assess how well this treatment works.Conclusion
Depression is a disabling disease that affects many people in the UK. While antidepressants and therapy work for many people, some people don't fully respond to treatment.
A treatment for depression that uses a drug that works in a different way from existing antidepressants could be very helpful.
Having said that, this study doesn't tell us whether psilocybin is a useful drug for treating depression. This was a very small, early-stage trial that only aimed to see whether the drug was safe and has potential for use – the researchers did not set out to see if the drug is effective for treating severe depression.
Here are some points to consider:
- Ten of the recruits had referred themselves, rather than being referred by a doctor. This means they actively sought out treatment with psilocybin. Interestingly, five of the 12 had taken psilocybin before, which may mean they joined the study because they already thought the treatment worked for them.
- There was no control group and no placebo – everyone was given the treatment and knew they were taking the treatment. This means we don't know whether the treatment itself or another factor, such as the intensive therapeutic support from psychiatrists, might have caused the improved depression scores.
- The chart showing the depression scores for each individual shows that most people (not everyone) had a big initial drop in depression scores by one week after treatment, followed in many cases by a fairly sharp upswing in scores after that. This could mean that the experience of having the treatment has a short-term effect that wears off fairly quickly for most people.
Researchers and funders will review the results of the study and decide whether to build on this with a large randomised controlled trial.
This would give us a better indication of whether this treatment could work for people with depression who are not helped by current treatments – and, most importantly, whether it's safe for use.
The researchers warn that people should not try to treat themselves with mushrooms that contain psilocybin. Aside from their unpredictable effects, magic mushrooms are class A drugs that are illegal to possess or distribute.
We imagine that because of the ongoing political controversies around psychoactive drugs like psilocybin, ketamine and MDMA being used to treat mental health conditions, a larger follow-up phase II trial is not guaranteed to take place.
Links To The Headlines
Magic mushrooms 'promising' in depression. BBC News, May 17 2016
Magic mushrooms make you a fun guy: Tests show shrooms help fight depression. The Sun, May 17 2016
Magic mushrooms 'could help people tormented by incurable depression'. Daily Mail, May 17 2016
Magic mushrooms lift severe depression in clinical trial. The Guardian, May 17 2016
Magic mushrooms could be 'serious breakthrough' for depression treatment, claims drugs expert. The Independent, May 17 2016
Magic mushrooms lifts severe depression in trial. The Daily Telegraph, May 17 2016
Links To Science
Carhart-Harris RL, Bolstridge M, Rucker J, et al. Psilocybin with psychological support for treatment-resistant depression: an open-label feasibility study. The Lancet: Psychiatry. Published online May 17 2016
"Revealed, the five hidden killers that could send you to an early grave," the Daily Mail reports. These "hidden killers" include loneliness and poor sleep. But this is a simplistic take on complex research aiming to identify new ways of classifying health and wellbeing.
The research assessed the health and lifestyle of 3,000 US adults aged 57 to 85 years, then reassessed how many were incapacitated or had died five years later.
The researchers then compared two models to see which better categorised the participants' health status and risk.
The first mainly looked at the presence of diseases. The second model was more comprehensive, and included wider measures such as psychological wellbeing, mobility and health behaviours.
Overall, two-thirds of the sample was classed as being in "robust" good health when using the medical disease model, but many of these fell into more vulnerable risk groups when using a more comprehensive risk model.
The comprehensive model identified poor mental health, including depression, isolation and memory problems, and frailty and mobility problems as being predictive of mortality – "hidden killers" in newspaper speak – factors that would be largely overlooked if you only focused on physical diseases.
The findings suggest a comprehensive view of a person's health and wellbeing is needed when looking at their risk status and trying to target appropriate medical care and support.
Wellbeing and quality of life is not simply a case of whether or not someone has a physical illness.Where did the story come from?
The study was carried out by researchers from the University of Chicago, and was funded by the same institution and the US National Institute of Aging.
It was published in the peer-reviewed journal, PNAS, and the article is openly available for access.
The Daily Mail, The Sun and Metro articles are generally representative of the study's findings on loneliness, fractures and mobility problems.
But none of the papers grasped the point of the study – an attempt to create more complex and subtle models of wellbeing.What kind of research was this?
This cohort study aimed to look at the best way of defining population health.
The researchers explained how the World Health Organization (WHO) defines health as a "state of complete physical, mental and social wellbeing and not merely the absence of disease or infirmity".
However, despite this there has been little rigorous attempt to use this definition to measure and assess population health. More often, what is described as the "medical model" is used to measure health, which focuses solely on disease diagnoses.
The researchers propose a "comprehensive model" that also considers psychological wellbeing and function as being a better fit to the WHO classification.
The researchers applied both of these models to US survey data to see how population health was defined by the different methods.What did the research involve?
The research involved a large, nationally representative sample of 3,005 older US adults aged 57 to 85 years who lived in the community and were taking part in the National Social Life, Health and Aging Project (NSHAP).
The participants were interviewed and completed a questionnaire about their health and lifestyle, as well as having body measures taken.
The researchers then used two different models to categorise the state of a person's health.
The medical model looked at specific diseases:
- heart disease
- lung disease
- kidney disease
- liver disease
- high blood pressure
- thyroid disease
The comprehensive model also included 35 additional measures that encompassed five broad dimensions of health and wellbeing:
- health behaviour – smoking, exercise, sleep
- psychological health – depression, memory
- sensory abilities – vision, hearing
- neuroimmunity – chronic inflammation
- mobility or frailty – including fractures
The researchers followed these people up five years later. They then identified a few distinct health classes or categories within these models that encompassed several of the disease and wellbeing features, and most reliably indicated a person's health and mortality risk.What were the basic results?
The researchers identified five distinct health classes within the medical model that had significant and independent effects on mortality.
The first two classes were people who had undiagnosed high blood pressure (hypertension) and a single non-cardiovascular disease. These were the least vulnerable, or most "robust", health groups.
The intermediate (third) risk group were those with poorly controlled diabetes. The two most vulnerable groups (four and five) were those who had both cardiovascular disease and diabetes, or who had extensive medical illnesses.
People in the first two robust classes had around a 15% risk of being physically incapacitated or dead after five years, compared with 35% in the top extensive illness group.
In the comprehensive model, six distinct classes arose – again, the first two classes were the least vulnerable, or most robust; classes three and four had an intermediate risk; and five and six were the most vulnerable.
The six classes were:
- robust obese – obese but generally in good health
- one minor condition – stomach ulcer, thyroid problems, bladder problems
- broken bones – people with osteoporosis
- poor mental health – depression, poor memory and loneliness
- diabetes, hypertension and immobility
- extensive medical illnesses and frailty
Almost a quarter of this older US population (22%) were in the first robust obese group. These people often had undiagnosed hypertension as measured by a home device, but, other than this, few other diseases and only a 6% risk of dying after five years.
The second group were not obese and had a minor condition – one not considered to have high mortality risk – and a 16% risk of death.
The two middle classes of the comprehensive model – those with fractures or osteoporosis and poor mental health – included 28% of this US population, despite being, as the researchers say, "largely ignored" by the medical model.
The last two, most vulnerable, classes had the most compatibility with the vulnerable classes of the medical model, but still more people were reclassified as vulnerable when using the comprehensive model.
People in the most vulnerable sixth group had a 44% risk of dying within five years.
Overall, the medical model classified two-thirds of the older US population as being in robust health. Only half of these people went into the robust classes of the comprehensive model.
These findings suggest that factors such as poor mental health, bone fractures, and sensory and mobility problems are very important to consider when categorising vulnerability and mortality risk.How did the researchers interpret the results?
The researchers concluded that the comprehensive model identifies new classes of people with mortality risk, such as those with broken bones or poor mental health, who are largely overlooked by medical models that only focus on disease.
They said that: "This approach provides a method for broadly reconceptualising health, which may inform health policy", with implications for medical care, prevention and resource allocation.Conclusion
As the researchers say, the WHO definition of health encompasses physical, mental and social wellbeing – not just the presence or absence of disease.
But how often are these extra dimensions taken into account when assessing a person's health status?
In this sample of older adults, just looking at their disease status puts the majority of them into an apparently "robust" health group.
Yet when you consider the additional dimensions of psychological health and wellbeing, you seem to get a much better indication of those who were at higher or lower risk of dying or being incapacitated in the coming five years.
The "hidden killers" the media refer to are factors such as frailty and fractures, and depression and loneliness, which would be overlooked if you looked at disease diagnoses alone.
This suggests that a comprehensive view of a person's health and wellbeing is needed if you are looking at their risk status, and trying to target appropriate medical care and support.
But you can't say from the results of a study like this that these factors are being overlooked within healthcare.
For example, just because a medical risk model looking at physical diseases alone hasn't looked at these factors as a risk indicator doesn't necessarily mean that the people with these conditions have not been diagnosed in medical practice and are not receiving appropriate care and treatment.
The media term "hidden" in this context is therefore a bit misleading – as is the term "killer".
Of course, factors like loneliness and depression aren't necessarily going to lead to death directly, but could be associated with other poor health factors that together contribute to mortality risk.
Although this is a large, nationally representative sample, these are all older US adults. The six predictive classes the researchers identified to indicate robust, intermediate or vulnerable risk status may not be the same if people from another country were examined, or a population of middle-aged or younger adults.
It would be interesting and useful if researchers carried out a similar analysis on various groups within the UK population.
The study is a valuable contribution to how we define health and wellbeing. However, whether it has any direct implications in terms of health assessment, screening and diagnosis is unknown at this stage.
Links To The Headlines
Revealed: the five 'hidden killers' that could send you to an early grave. Daily Mail, May 16 2016
The 'hidden killers' that contribute to an early death. Metro, May 17 2016
Links To Science
McClintock MK, Dale W, Laumann EO, Waite L. Empirical redefinition of comprehensive health and well-being in the older adults of the United States (PDF, 984kb). PNAS. Published online May 16 2016
"Going to church could save your life," reports the Daily Mail, adding that, "Women who worship once a week are '25 per cent less likely to die early'."
Perhaps surprisingly, while the first part of the headline is overly simplistic, it may not technically be wrong – according to new research from the US, anyway. Whether or not divine providence is responsible for the increase in lifespan is still up for debate.
A large Harvard study showed that predominantly white Christian nurses who attended religious services more than once a week had a 33% lower relative risk of dying over a 16-year period compared with similar women who did not attend religious services.
A sizeable chunk of the link was explained by social support (23%), smoking rates (23%) and, to a lesser extent, optimism differences (9%) between attenders and non-attenders.
The study was very large, precise, and as robust to bias and confounding as you could reasonably expect, so it can be considered reliable. But the lifestyle and social differences between the groups can't go unnoticed.
It's therefore possible that the regular pattern of social interaction associated with being part of a religious community, and the benefits this brings, is mainly responsible for the outcome seen in this research, rather than any specific religious or spiritual aspects.
Atheists who regularly attend humanist gatherings, or just those who go to weekly bingo sessions, may also experience similar benefits.
Read more about the benefits of connecting with others.Where did the story come from?
The study was carried out by researchers from the Harvard T. H. Chan School of Public Health in the US.
It was funded by the John Templeton Foundation, which, according to its website, funds research on the "big questions of human purpose and ultimate reality". The foundation has a stated aim of using scientific methods to explore the alleged spiritual aspects of reality.
The study was published in the peer-reviewed Journal of the American Medical Association: Internal Medicine.
Generally, the media covered the story accurately, citing the possible reasons why attending religious services might be good for you in terms of boosting social support, happiness and optimism.
For example, The Independent reported advice from the researchers, who said: "Our results do not imply that healthcare professionals should prescribe attendance at religious services, but for those who already hold religious beliefs, attendance at services could be encouraged as a form of meaningful social participation."What kind of research was this?
This cohort study looked at the links between religious service attendance and subsequent death in female nurses.
This type of study is appropriate to investigate this link.
But many factors can influence death rates, and potentially also be linked to church attendance – for example, more resilient social networks can help people cope in times of hardship.
Teasing out any clear causal links from the vast mix of influencing factors is tricky.What did the research involve?
This study analysed self-reported religious service attendance information from 1996 to 2012 and linked death records from the same time period.
The researchers analysed information from 74,534 female US nurses who had been answering health and lifestyle questionnaires every two years from 1992 to 2012 as part of the Nurses' Health Study, a rich ongoing source of epidemiological research.
From 1992 and every four years thereafter, women were asked how often they go to religious meetings or services. Responses included more than once a week, once a week, one to three times a month, less than once a month, and never (or almost never).
The researchers' main analysis looked at the death rates of women with different frequency of religious attendance, comparing them with those who did not attend.
They adjusted for a lot of confounders to try to isolate the single effect of religious attendance, including:
- alcohol consumption
- physical exercise
- multivitamin use
- high blood pressure
- high cholesterol
- use of hormonal replacement therapy
- healthy eating scores
- smoking status
- body mass index
- husband's education level
- physical impairment
- social integration score – composite of marriage status, group participation, number of close friends or relatives
- living alone
- family income
- geographic region in the US
- depression in 1992
- religious attendance in 1992
The researchers also performed a "mediator" analysis, which helps understand how much each of the confounders is contributing to the main link of interest – in this case, religious service attendance and death.What were the basic results?
Most women were either Roman Catholic or belonged to other Christian denominations, and 97% or more were white. There was a small minority of Jewish women and no Hindu or Muslim women.
There was a consistent pattern between religious service attendance and lower rates of death from any cause, cardiovascular disease and cancer.
There were 13,537 deaths over the study period, giving a base rate of death of 18.1 %. Compared with women not attending religious services, women who attended a service more than once a week had 33% less risk of dying from any cause during the 16-year study (hazard ratio 0.67, 95% confidence interval [CI] 0.62 to 0.71).
Those attending regularly in both 1996 and 2000 – a sign of long-term, regular attendance – had an even lower relative risk at 45% (95% CI 0.52 to 0.59) less than non-attenders.
Looking at potential mediators, the researchers picked out depressive symptoms, smoking, less social support and optimism as the most important.
Social support explained the highest proportion of the link (23%), with smoking a close second (22%). Optimism accounted for around 9%.
The link appeared consistent over time, as well as for religion (although there wasn't much variety), geography and other potentially influential factors.How did the researchers interpret the results?
The researchers said that: "Frequent attendance at religious services was associated with significantly lower risk of all-cause, cardiovascular, and cancer mortality among women.
"Religion and spirituality may be an underappreciated resource that physicians could explore with their patients, as appropriate."Conclusion
This study showed that white Christian women who attended religious services more than once a week had a lower risk of dying from any cause, cancer, and cardiovascular disease specifically compared with similar women who did not attend religious services.
This link was at least partially explained by social support, smoking rates, and optimism differences between attenders and non-attenders.
As the study was very large, it gives precise estimates of relative risks. The researchers pointed out there are other factors that could potentially mediate the link that they couldn't measure in their study, like psychosocial resilience, religious coping mechanisms, a sense of a purpose in life, and self-discipline.
But their interesting stats also showed that biases from these or other sources would have to be very large to affect the result in a meaningful way, suggesting the study's conclusions are quite solid.
The study mainly involved white women who mostly identified as Christian, so we don't know if the same effects would be seen for men of a similar faith, or adults or children from other religions or with no religion.
Non-religious groups could argue having a purpose in life, self-discipline and many other aspects that potentially mediate the link are not the sole preserve of the religious, but there is no doubt that for many people this comes from practising a faith.
But it's possible the same effect could be achieved in other ways, too. While the researchers tried to account for social factors associated with religious attendance, there could well be other unmeasured, or possibly unconsidered, effects associated with regular social group interaction.
A similar study could have noted reduced mortality among people attending any community activity groups or societies, both for people of all faiths as well as people with none.
As we discussed last month, people with a history of cancer who regularly attended a choir session showed evidence of improved immune function.
Human beings are social animals, so enjoying regular social activities with others is probably a good way, among others, to improve both your physical and mental wellbeing.
Links To The Headlines
Women who go to church more than once a week live five months longer, Harvard study finds. The Independent, May 16 2016
Everlasting life? How going to church could help you live longer. The Daily Telegraph, May 16 2016
One religious step that could extend your life. Metro, May 16 2016
Links To Science
Li S, Stampfer MJ, Williams DR, VanderWeele TJ. Association of Religious Service Attendance With Mortality Among Women. JAMA Internal Medicine. Published online May 16 2016
"Men are being warned to become fathers by 40 or face a greater risk of having children with serious illnesses," the Daily Mail reports after a new review looked at some of the evidence about paternal influences on the risk of childhood diseases.
The review discusses several research findings found previously, including some reports that children born to fathers over the age of 40 have higher rates of conditions like autism spectrum disorder – and that stress, smoking and alcohol may also cause heritable changes.
But this is an opinion piece. We don't know how the researchers selected the evidence they reviewed, and it is possible that not all relevant research was considered.
The review should not be taken as firm evidence that there is such a thing as a "male biological clock" and fathers are putting their children at risk by delaying fatherhood until middle age.
Where did the story come from?
The study was carried out by researchers from Georgetown University Medical Centre in the US, and was funded by the US National Institutes of Health.
Neither the Daily Mail nor The Times recognise the important limitations of this review: namely, that is it is not a systematic review, so it carries far less weight in terms of evidence.
Also, the Mail talks about men being "warned" about delaying fatherhood – but, as far as we can tell, the only people actually issuing any warning based on this review is the Mail itself.What kind of research was this?
This appears to be a narrative review discussing whether how a man's age and environmental exposures may alter his genes and so be passed on to his offspring.
The article centred on epigenetics, the idea that, though a person's DNA sequence may not change, their exposures over the course of a lifetime may lead to changes in their gene activity and expression that can be passed on to their children.
This happens through mechanisms such as DNA methylation, where methyl groups (types of molecules) are added to the building blocks of the DNA, or where small RNA molecules (miRNA) are added to the DNA – both of which alter gene activity.
This review discusses how epigenetics in the father have an effect on the offspring, focusing on age and environmental exposures. The researchers discuss these theories, referencing various publications, but this does not appear to be a systematic review.
The research team did not provide any information about how they identified and selected the evidence they reviewed. As such, it is possible that not all relevant research has been examined and so this must largely be considered to be an opinion piece.What does the research say about a father's age?
The researchers say that past research has shown that a father's age has a significant effect on a child's characteristics and the likelihood of them having congenital abnormalities.
Some studies have linked increasing paternal age (over 40 or so years) with higher rates of conditions like autism and schizophrenia. Others have observed increased rates of birth abnormalities, such as heart defects, musculoskeletal abnormalities, and Down's syndrome.
Mouse studies also support this. Studies have shown that mice born to "old" fathers (over two years old) performed poorly on tests of learning and memory, and also had a reduced lifespan and less reproductive success themselves. Mice with slightly younger fathers (10 months old) were less social.
The researchers say that although the mechanism behind this is not established, most evidence points in the direction of DNA methylation. Animal studies have shown higher rates of DNA methylation in the sperm cells of older rats compared with younger rats.What does the research say about environmental exposure?
The effect of environmental exposures on offspring is less clear, although there is some evidence of this. Some studies have shown that people with little available food have demonstrated some changes that can be passed on to their children, though not necessarily bad ones.
It's reported that children born to fathers who had low food availability during pre-adolescence were less likely to die from cardiovascular disease. And those whose grandparents had little food were less likely to have diabetes.
Other studies have suggested stress induces DNA changes that could be passed on. Mouse fathers who were subject to the stress of food deprivation before mating had offspring with lower blood glucose levels.
Mice exposed to other psychological stressors – such as cage changes and fox smell – had offspring that displayed blunted stress responses, indicating some form of behavioural defect.
Smoking and alcohol may also have effects. Smoking has been shown to alter the DNA in sperm.
And three-quarters of babies with foetal alcohol syndrome – birth defects normally associated with maternal consumption of alcohol during pregnancy – are reported to have fathers with alcohol use problems.
Chronic alcohol use in the father is said to again affect DNA methylation. In rats, offspring from fathers given alcohol were more likely to have a low birthweight or spatial learning problems when put in a maze test.
Studies in mice also found those whose fathers were given alcohol were more likely to have cognitive and mobility problems.How did the researchers interpret the results?
The researchers say their review findings support the concept of the epigenetic inheritance of paternal experiences across generations.
They say their review highlights "the possible links between birth defects and paternal age, environmental factors, and alcohol consumption" and the need for future research in this area.Conclusion
This narrative review summarises past research on DNA changes that may occur as a result of a father's age and exposures that could be passed on to his children.
In particular, the review discusses animal and human studies that have linked changes in offspring with increasing paternal age, stress and substance use.
But this review must largely be considered to only be an opinion piece. We don't know how the researchers identified, appraised and selected the studies they discussed.
As such, there is a strong possibility that not all animal and human research relevant to the issue of paternal epigenetic inheritance will have been reviewed and discussed here.
There are also no clear methods or results provided for the studies that are discussed, with only a few brief sentences given for each study. We are not able to critique the quality and strength of evidence linking a father's age or any other exposure with the outcome reported.
For example, people would likely be concerned by reports that increased rates of autism or congenital defects have been observed in children born to fathers over the age of 40. But we have nothing more to go on than this – no firm risk figures are given.
And the observational studies themselves are likely to have been influenced by various unknown sources of bias and confounding, like the report that three-quarters of babies with foetal alcohol syndrome have a father with alcohol use problems.
This doesn't tell us anything about what the mother is doing. It could be that many of these babies had a mother who also had alcohol use problems – alongside her partner – and used alcohol during pregnancy, and has directly exposed the developing baby.
This study will add to the research on how parental exposures may be passed on to a child through epigenetics.
However, given the limitations of this review and the lack of methods given, this opinion piece should not be taken as firm evidence that fathers are putting their children at risk by delaying fatherhood.
These limitations aside, advice that men hoping to become fathers should avoid known bad lifestyle behaviours, such as smoking, drinking too much, not exercising and eating a poor diet seems sensible.
Read more about what both men and women can do to protect their fertility.
Links To The Headlines
Drinking dads can harm babies just as much as mums who drink alcohol. Metro, May 15 2016
Older fathers can raise risk of birth defect in children. The Times, May 16 2016 (subscription required)
Links To Science
Day J, Savani S, Krempley BD, et al. Influence of paternal preconception exposures on their offspring: through epigenetics to phenotype (PDF, 243kb). American Journal of Stem Cells. Published online May 15 2016
"Scientists have identified a new cause of devastating neurological conditions," the Mail Online reports – but this is entirely inaccurate.
A review of existing evidence makes the case that the innate immune system may be involved in neurodegenerative conditions, which are associated with progressive damage to brain cells, like Alzheimer's and Parkinson's. However, no new evidence was provided.
The innate immune system is designed to prevent the spread of infection by identifying foreign bodies such as viruses that may have infected cells and, if needs be, killing these cells so the infection doesn't spread.
The review argues that the innate immune system initially activates to eliminate a perceived threat of brain cell abnormality. But by remaining active over time, it causes low-level prolonged damage to normal brain cells, ultimately leading to their death.
The idea that immune responses may play a role in dementia is nothing new. A study published earlier this year tried using immunosuppressant drugs on rats with symptoms of dementia, with some degree of success.
This review doesn't pretend to be anything other than a collection of evidence supporting a hypothesis. It provides a useful range of evidence-based points exploring potential trigger molecules, genetic susceptibility, and how the underlying biology might work.
As any reputable scientist will tell you, a hypothesis needs to be tested by experimentation before it can advance into a credible theory.Where did the story come from?
The review was carried out by researchers from the University of Adelaide in Australia, and was funded by the Australian National Health and Medical Research Council, and a grant from the National Ataxia Foundation.
The Mail Online's headline, "Scientists discover new trigger for devastating brain diseases", is not accurate and the quality of its reporting is poor.
The study in question was a review, meaning it brought together research already published. There is no new laboratory or human study involved here, which isn't most people's idea of a "discovery".What kind of research was this?
This was a review of evidence to support the idea that a common disease-causing mechanism for neurodegenerative disease exists, and that "surveillance" by the innate immune system mediates cell death.
The innate immune system helps protect your body – inside and out – from threats like bacteria, viruses and cell damage. It's like a surveillance system keeping an eye on your body.
When foreign bacteria enters your blood, when you cut yourself and have dirt in your wound, or even if some of your cells are behaving abnormally, your innate immune system kicks in to attack and destroy the threat.
This often involves mobilising the immune system to trigger abnormal cells – those possibly infected by viruses or bacteria – to self-destruct, taking the bacteria or other offending organism with it. This process is called programme cell death or, in biological vernacular, apoptosis.
The immune system has innate and acquired components, which recruit different cells and processes to detect and neutralise health threats.
The innate immune system is largely what you are born with, whereas the acquired immune system varies from person to person, depending on what sorts of bacteria, viruses and other micro-organisms you come across in your life.What did the research involve?
The review reports no methods, only stating that the researchers intended to "present evidence to support the hypothesis that a common pathogenic mechanism for neurodegenerative disease exists, and is mediated by innate surveillance-cell death".
As such, we cannot assume they used systematic review methodology in their search for relevant material. This means some relevant evidence may have been missed.
The review openly looked for evidence in support of one theory, so was not concerned with alternative theories or the relative strength of evidence behind each study.What were the basic results?
The review itself describes the function of the innate immune system, how it triggers cell death and molecules for the immune system to attack, and different pathways whereby it can damage our bodies.
The researchers explain that many neurodegenerative diseases like Alzheimer's and Parkinson's diseases involve the gradual damage and death of brain cells called neurones.
But it isn't clear whether many disease-specific mechanisms are involved or whether they share a common disease-causing mechanism.
The review argues there is an increasing body of evidence that suggests the innate immune system is activated across a number of neurodegenerative conditions, so might be the obvious candidate for a common underlying mechanism.
Delving more into specifics, the researchers suggest that the innate immune system is initially activated to eliminate a perceived threat of brain cell abnormality in neurodegenerative diseases.
But it cannot remove the threat, meaning the immune system remains active, causing low-level prolonged damage and, ultimately, progressive brain cell death.
The review also identifies possible genetic susceptibility markers, identifying those more likely to have a larger innate immune response to brain cell damage in this way.
A lot of research on neurodegenerative diseases has focused on disease-specific features of the disease – in Alzheimer's, for example, the damaging bundles of amyloid protein that gather in the brain.
The review's authors argue that while these are important, we shouldn't ignore the possibility of a generic component across diseases, which in their view is driven by the innate immune system.How did the researchers interpret the results?
The researchers concluded that, "Here we have assembled evidence in favour of the hypothesis that neurodegenerative disease is the cumulative result of chronic activation of the innate surveillance pathway, triggered by endogenous or environmental danger or damage associated molecular patterns in a progressively expanding cascade of inflammation, tissue damage and cell death."Conclusion
This review presents evidence supporting the idea that the innate immune system is involved in a range of neurodegenerative conditions, such as Alzheimer's and Parkinson's.
Reviews like this are very useful at summarising the current state of science in an area, but may miss important research, unless they are systematic.
This review was openly one-sided, transparently exploring the evidence behind one hypothesis.
While there is nothing wrong with that, a more systematic and balanced review would add the extra value of being able to discuss alternative ideas and find out how much evidence stacks up behind each one, aiding comparisons.
Despite news coverage suggesting this is a radical new theory, the idea that the immune system might be involved in neurodegenerative conditions has been around for a while.
A study from earlier this year in mice tentatively suggested that inflammation might be involved in the progression of Alzheimer's disease, and can be reduced by targeting it.
Any potentially promising avenue of research into neurodegenerative diseases is worth exploring, and this review provides some interesting ideas that other researchers may want to follow up.
Links To The Headlines
Links To Science
Richards RI, Robertson SA, O'Keefe LV, et al. The Enemy within: Innate Surveillance-Mediated Cell Death, the Common Mechanism of Neurodegenerative Disease. Frontiers in Neuroscience. Published online May 10 2016
"Probiotic goods a 'waste of money' for healthy adults, research suggests," The Guardian reports. A new review of previously gathered data found no evidence that probiotics improved the balance of gut bacteria in healthy adults.
Probiotics are live bacteria and yeasts, often added to yoghurt or taken as a supplement, that are promoted as helping stimulate the growth of "friendly bacteria" in the gut.
Supporters claim they can help treat a wide range of conditions, from eczema to irritable bowel syndrome (IBS), but there's little evidence to support many of these claims.
It has also been claimed that healthy people should take probiotics to improve their digestive health, a claim assessed in this latest review.
The review found seven trials, all with vastly different designs, methods and assessment of outcomes. As such, trial results could not be pooled in any meaningful statistical way.
Four of the trials found the probiotic had no different effect on gut bacteria from inactive placebo. Three of the trials reported some effect, but the overall quality of reporting for all trials was poor.
Given the limitations of the studies – including the variety of probiotics examined – it is not possible to conclude with certainty that all probiotics are ineffective.
Absence of good-quality evidence is not evidence of there being no effect. Better-designed studies may yet find some benefit from taking probiotics.Where did the story come from?
The study was carried out by researchers from the University of Copenhagen and was funded by the Novo Nordisk Foundation.
It was published in the peer-reviewed journal, Genome Medicine.
The UK media's reporting takes a very black and white attitude towards the review, concluding that probiotics "don't work" and are "a waste of time".
But they would benefit from considering the limitations of the small number of diverse trials included in this study. It would have been more accurate to say that based on the current evidence, we don't know whether they work or not.
It should also be noted that photos of yoghurt drinks – including Tesco own-brand – are misleading. Only one of the seven trials assessed a milk-based drink and we don't know what brand it was. Considering these were all non-UK studies, though, it is very unlikely to have been a UK supermarket brand.What kind of research was this?
As the researchers say, in recent years the composition of bacteria in the human gut has received considerable attention as a possible modifiable risk factor for various digestive and metabolic diseases.
This has led to a surge in the use of probiotic supplements to try to boost the health of the gut, through ways such as improving the intestinal lining and introducing more "friendly" bacteria to compete against the "bad" bacteria.
However, the effect of probiotic supplements – particularly in healthy individuals – is poorly understood.
This review therefore aimed to compile the evidence, looking at RCTs that have compared supplements with inactive placebo and used molecular approaches to measure gut bacteria.
A systematic review is the best way of seeing if the evidence to date shows whether they are effective. But reviews are only as good as the studies they include.
Because of the vastly different designs of the various studies, the researchers were unable to perform a meta-analysis of the results.What did the research involve?
The researchers searched three literature databases up to August 2015 to identify RCTs of any duration that:
- included healthy adults only
- compared probiotics with placebo
- assessed gut bacteria composition using specific molecular techniques and reported this as the main outcome
They excluded studies where other interventions were combined with supplement use, such as antibiotics or other medications.
Two reviewers separately assessed trials for eligibility, and carried out quality assessment and data extraction from the trials included.
Seven trials met eligibility criteria: two from Italy, two from Denmark, and one trial each from the US, Germany and Finland.
All were conducted in healthy adults aged 19 to 88 years, and the sample size of the individual studies ranged from 21 to 81.
Most supplements included Lactobacillus, in one trial combined with Bifidobacterium, and one trial used Bacillus. These were provided as capsules in four trials or in biscuits, drinks or sachets in one trial each. The length of the trials was typically one to two months.
The main source of potential bias in the studies was the lack of blinding of researchers assessing outcomes.What were the basic results?
The results of the seven studies are not pooled and are only reported study by study.
Essentially, none of the studies provided evidence that probiotics had a beneficial effect on gut bacteria.
The results were as follows:
- Four studies reported no difference in the diversity of, composition of, or stability of bacteria between probiotic and placebo groups.
- One study reported that the probiotic reversed the age-related increase in certain disease-causing bacteria (such as C. difficile and Campylobacter), but did not compare between groups.
- One study reported some difference in the diversity of bacteria, with increased abundance of certain bacteria (such as Proteobacteria) in the probiotic group.
- One study also reported some differences in the abundance of certain bacteria, but did not directly compare between groups.
The researchers concluded that, "Overall, this systematic review demonstrates that there is no convincing evidence for consistent effects of probiotics on faecal microbiota composition in healthy adults."Conclusion
This review finds no evidence that probiotic supplements have beneficial effects on the composition of gut bacteria in healthy adults.
The review has strengths in that it pre-specified exactly which trials would be eligible – that is, only RCTs in healthy adults, comparing probiotics with placebo, that assessed changes in gut bacteria levels as the main outcome.
This should aim to reduce diversity between the trials and try to find a definitive answer on the effect in a specific population.
However, despite this, the seven trials were still highly variable in their methods and design, such as the type of probiotic given and how gut bacteria were assessed.
This variability is demonstrated by the fact they are only reported narratively and the results could not be pooled to give an overall quantitative effect, as would be the case in a meta-analysis.
The trials also contained several quality limitations. In most, the researchers were not blinded to the assigned group, which may have biased their assessment of outcomes.
Only one of the seven trials had calculated beforehand how many participants they would need to recruit to detect whether the treatment had a significant effect. This is a notable limitation, given that all had sample sizes of less than 100.
Also, several of the trials had not statistically assessed, or not clearly reported, whether there was a difference between the probiotic and placebo groups.
As the researchers say, future studies would benefit from clearly specifying the main outcome they're looking at, giving transparent results with statistical analyses, and clearly distinguishing within-group treatment effects – such as changes from study start to end – and between-group effects.
Further points to bear in mind:
- These trials only included healthy adults with no known diagnoses or conditions. This means the study can't tell us whether probiotics are effective in IBS or for "rebuilding" the gut bacteria in people who have had an illness. However, even though they were healthy adults, the trials included quite variable populations – for example, one was in elderly people, another specifically in postmenopausal women. We also do not know the effectiveness in children.
- There were only seven trials, and these used different probiotics containing different "friendly" bacteria, in different forms, from capsules to yoghurt drinks and biscuits. As such, there is not enough evidence to definitely conclude that all probiotics are ineffective, particularly given the limitations of the trials. It could be that certain bacteria in particular formulations could have different effects.
- None of the trials were from the UK, so the formulations used may differ from those on the UK market.
- The trials were only of a couple of months' duration, so we don't know what longer-term use might have.
- The trials only looked at direct effects on gut bacteria level. We don't know whether taking the probiotic increased the person's sense of health and wellbeing, for example. If probiotics help some people in this way, that can only be a good thing – even if it is just a placebo effect.
Overall, the current state of the evidence does not demonstrate that probiotics have any effect on gut bacteria in healthy people.
Given the limitations of these studies, that is not to say that all probiotics definitely have no effect. Further high-quality research in their use is needed.
Links To The Headlines
Probiotic goods a 'waste of money' for healthy adults, research suggests. The Guardian, May 10 2016
Probiotic drink 'myth': No evidence that yoghurt products boost healthy bacteria, say scientists. Daily Mail, May 10 2016
Healthy people who drink probiotic drinks full of 'good bacteria' wasting their time, according to report. Daily Mirror, May 10 2016
Links To Science
Kristensen NB, Bryrup T, Allin KH, et al. Alterations in fecal microbiota composition by probiotic supplementation in healthy adults: a systematic review of randomized controlled trials. Genome Medicine. Published online May 10 2016
"Pint of beer a day could protect you from heart attacks," The Independent reports. A new review on the alleged protective effects of moderate beer drinking has been warmly welcomed by the UK media – but nobody reported that it was funded by an Italian beer trade association.
Researchers reviewed the existing evidence about beer and health, including the effects on heart and circulation, cancer, liver disease, dementia and overall length of life. They say that much research has been done on the effects of wine on health, but less on beer.
The research team claims that, based on the result of their review, men who drink the equivalent of around two 330ml cans of beer a day, and women who drink one can, will receive "some benefit against cardiovascular disease".
This recommendation equates to around 2.5 units of alcohol a day for men and 1.25 for women, or 17.5 units a week for men and 8.75 units for women.
For men, this advice contradicts recent advice issued by UK Chief Medical Officers that "you are safest not regularly drinking more than 14 units per week".
So, who's right? Well, the methods the researchers used to identify and select the evidence are not clearly reported.
This means it's possible that this review may not have considered all relevant research and, playing devil's advocate, could have ignored evidence countering the researchers' hypothesis.
What we do know is that there are safer, well-validated methods to reduce your risk of cardiovascular disease.Where did the story come from?
The study was carried out by researchers from 10 research centres in Italy, Spain, Luxembourg and the US.
It was funded by the Italian Association of the Beer and Malt Industries, Assobira. The researchers say Assobira had no role in designing or writing the study.
Several of the researchers declared conflicts of interest in working for Assobira or other industry bodies linked to alcoholic drinks.
The study was published in the peer-reviewed journal Nutrition, Metabolism and Cardiovascular Diseases.
Disappointingly, not one single UK media outlet managed to report this arguably significant conflict of interest.
The study was met with enthusiasm by the UK media, although the quantities of alcohol recommended seemed to confuse some, and little mention was made of the downsides of this approach.
For example, The Daily Telegraph said, "drinking up to two 1.4 pints of beer a day for men and half of that for women" could benefit heart health.
However, the researchers define a healthy limit as "up to" one drink a day for women and two for men.
They say that one drink is approximately 330ml of 4% beer. That is equivalent to 0.58 of a pint – so the limit for men would be just over one pint, while the limit for women is just over half a pint.What kind of research was this?
This was a consensus document, which means a group of experts were brought together to review evidence on the topic and agree a statement outlining their conclusions.
It is not clear from the document who chose the experts in the group, or whether they used standard systematic review methods to review published evidence.
The problem with non-systematic evidence reviews is that researchers might cherry-pick the research that suits them and ignore anything that doesn't fit their theory. We're not saying that happened in this case, but it's unclear how the studies were chosen.What did the research involve?
A group of doctors were asked to review the evidence on the effect of the consumption of moderate amounts of beer on human health.
Each doctor carried out a search of the published literature before writing one section of the review, which was then shared for comments by other doctors. They arrived at a final version after meeting to discuss their findings.
While the study does tell us the search terms and the reasons for excluding studies from the review, it is unclear whether this was a formal systematic review.
The researchers did ask two external experts to review the manuscript as part of the process before meeting to prepare their final version.
They did not carry out a meta-analysis of their findings, but summarised the findings of the evidence they reviewed.What were the basic results?
Low to moderate consumption of beer seems to have the same effect of reducing the chances of cardiovascular disease as wine.
This was the clearest finding from the review, based on a meta-analysis published in 2011 that pooled the results of 16 studies in almost 290,000 healthy adults.
The maximum protection against cardiovascular disease observed in that study – a 33% risk reduction – was seen at a consumption level of 25g of alcohol a day (about one pint of beer).
As with all alcohol, beer increases the risk of cancer, even at low levels. The paper says that "most alcohol-related cancers (85-90%) are in fact due to heavy drinking", which they define as more than two drinks a day.
However, light and moderate drinking were linked to increased risk of breast, mouth and throat cancers.
Importantly, the chances of alcohol causing cancer seem higher in Asian people. This is said to possibly be because there are genetic differences in many people of Asian origin that mean they are less able to process the toxins produced by alcohol.
There was insufficient evidence to show the effect of beer on the liver, apart from the known effects of consuming too much alcohol, which increases the chance of liver disease.
It is unclear whether beer increased or decreased the chances of getting dementia, as the studies reviewed gave conflicting results.
The effects of beer on length of life are also unclear, although the report's authors say they are likely to be in line with the known effects of drinking any alcohol.
These show a "J-shaped curve", with non-drinkers being slightly more likely to die than those who drink a small or moderate amount of alcohol, but those who drink a large amount of alcohol being more likely to die.
As the authors said, "Heavy alcohol (and beer) consumption increases the risk of total mortality, ranking eighth place among the causes of attributable deaths all over the world."How did the researchers interpret the results?
The researchers said that, "Unless they are at high risk of alcohol-related cancers, there is no reason to discourage healthy adults who are already regular light-moderate beer consumers from continuing to follow the same pattern.
"On the other hand, we do not recommend that adult life-long abstainers begin drinking for health reasons as, up to now, there is no direct evidence that adult abstainers who start drinking beer or other alcoholic beverages (also in moderation) reduce their risk of chronic diseases."
In other words, if you don't drink beer, there's no reason to start – but if you're healthy and drink a small amount of beer, there's no need to stop.Conclusion
Perhaps the most important message from this study is that low to moderate drinking may have health benefits, but binge drinking or heavy drinking is very bad for your health. The other message seems to be that beer has similar effects to wine.
Whether wine is good or bad for us has been debated for many years. Some have pointed to a reduction in the risk of cardiovascular disease, perhaps because of the phenols produced by fermented grapes, or perhaps because of alcohol itself. It seems that any benefits from wine are also seen in beer – as long as this is in moderation.
However, even drinking in moderation raises the risk of some cancers. Overall mortality figures suggest that the benefits may outweigh harms at low to moderate levels of drinking.
The researchers included 150 papers for their review, which suggests they carried out a careful study of the evidence.
However, without knowing if the review was carried out systematically, it's hard to know how rigorous the evidence-gathering process was. It is possible that some research relevant to the issue has not been considered.
A review's findings are only as strong as the underlying studies. The consistent themes identified suggest these are likely to be true effects associated with low to moderate beer consumption.
However, the underlying studies are only observational, so introduce the possibility of many sources of bias and confounding. For example, there could be inaccurate recall of the type of alcohol consumed or its quantity.
It is also possible that other health and lifestyle factors are influencing the results. Several of the studies adjusted their analyses for common ones such as age, smoking and body mass index, but otherwise there was considerable inconsistency in the factors that were taken into account.
The study's conclusions – that there's no need to stop drinking moderate amounts of beer if you're healthy and already do so, but no need to start if you don't drink already – seem sensible. It's worth reiterating that pregnant women and those with certain conditions are advised to avoid alcohol altogether.
Because of this review's lack of rigour, we would recommend that you ignore the advice that if you are a man, you can safely drink 17.5 units a week, and stick to the recent official UK guidance that both men and women should drink no than 14 units a week.
This is equivalent to a bottle-and-a-half of wine or five pints of export-type lager (5% abv) over the course of a week.
Links To The Headlines
Pint of beer a day could protect you from heart attacks, scientists say. The Independent, May 11 2016
A beer a day keeps a heart attack at bay: Even one can reduces risk of disease by a quarter. Mail Online, May 11 2016
Beer is good for you! A pint a day could protect your heart. The Daily Telegraph, May 11 2016
Links To Science
de Gaetano G, Costanzo S, Di Castelnuovo A, et al. Effects of moderate beer consumption on health and disease: A consensus document. Nutrition, Metabolism and Cardiovascular Diseases. Published online March 30 2016
"Being overweight may not be as unhealthy as it was 40 years ago," BBC News reports.
New research has found a body mass index (BMI) of 27 is linked to the lowest rate of death – but someone with a BMI of 27 is currently classed as being overweight.
BMI is a score calculated by dividing your weight (usually in kilograms) by the square of your height (usually in metres and centimetres). Currently, a BMI of 25 to 25.9 is classified as being overweight.
Researchers looked at 120,528 people from Copenhagen, recruited from 1976 to 2013, and separately compared those recruited during the 1970s, 1990s and 2000s. They were followed up until they died, emigrated, or the study finished.
The BMI linked to the lowest risk of having died from any cause was 23.7 in the 1970s group, 24.6 in the 1990s group, and had further risen to 27 in the 2003-13 group.
But this is just an estimate based on averages – it doesn't mean that having a "healthy" BMI is bad for you. Similarly, it shouldn't be assumed that it's now best to be in the overweight category. People often gain weight as they age, so there is the risk you could move from being overweight to obese.Where did the story come from?
The study was carried out by researchers from Copenhagen University Hospital.
It was funded by the Danish Heart Foundation, the Danish Medical Research Council, Copenhagen County Foundation, Herlev and Gentofte Hospital, and Copenhagen University Hospital.
The study was published in the peer-reviewed Journal of the American Medical Association (JAMA).
The study was covered by the UK media with a certain amount of glee, with the Daily Mail suggesting that the BMI system was a "blunt instrument".
It also said this study showed that, "Millions of Britons who are currently classed as overweight, actually have the optimal BMI and the lowest chance of death."
However, the study was reported on accurately, and the reports included expert views saying that people still need to keep an eye on their weight.What kind of research was this?
This cohort study compared results from three large previous cohort studies in the same part of Denmark, starting at different times.
Researchers wanted to see if there had been a change over time in the optimal BMI score – that is, the BMI shared by people with the lowest rate of death from any cause.
While this type of study can show trends of this nature, it cannot explain why the changes happen.What did the research involve?
Groups of adults in Copenhagen had their height and weight measured as part of three studies carried out in the city in 1976-78, then 1991-94, and the final study in 2003-13.
Researchers followed them up, then looked to see at which BMI people had the lowest chance of dying. They compared the numbers for the three studies to see if that number changed over time.
The first two studies were linked. Participants for the first study were invited back for a second round of measurements over the period from 1991-94, although younger people were recruited to add to the numbers. People in the third study had not taken part in either of the first two.
As well as weight and height, researchers checked whether people smoked, how much exercise they did, whether they'd been diagnosed with any medical conditions, including cancer or heart disease, and how much alcohol they drank.
They carried out sensitivity checks by including or excluding people with different risk factors to see whether any of them explained the overall results.
The researchers also looked at whether length of follow-up made a difference. They did this by carrying out their calculations with a much shorter follow-up period to see if the longer follow-up from the older studies distorted the results.What were the basic results?
The average BMI at which fewest people in the studies died from any cause increased by three points over the three decades:
- 23.7 (95% confidence interval [CI] 23.4 to 24.3) in 1976-78
- 24.6 (95% CI 24 to 26.3) in 1991-94
- 27 (95% CI 26.5 to 27.6) in 2003-13
The results showed a similar shift when researchers looked at just deaths from cardiovascular disease for non-smokers who had not been diagnosed with diabetes, cardiovascular disease or cancer, as well as for shorter periods of follow-up. None of the sensitivity analyses explained the trend.
In addition, researchers found the increased risk of death linked to being obese – a BMI of 30 or above – compared with a "healthy" BMI has gradually decreased to zero.
In the 1970s obese people had a 31% increased risk of death. By the 1990s it had reduced to a 13% increased risk, and by 2003-13 there was no longer a statistically significant link (adjusted hazard ratio 0.99, 95% CI 0.92 to 1.07).How did the researchers interpret the results?
The researchers say their findings were "robust" and cannot be explained by confounding factors such as age, sex, smoking status and disease at the start of the study.
They said that, "If this finding is confirmed in other studies, it would indicate a need to revise the World Health Organization (WHO) categories presently used to define overweight."
They also said cohort studies cannot address the causes of the results, but speculated that their finding may reflect improvements in treatments for diseases affecting people with higher BMIs, such as heart disease and diabetes.
This would make it less risky to be overweight than in the 1970s, when more people died of these diseases. The reduction in smoking and increase in exercise they found could also have helped mitigate the effects of being overweight, they said.Conclusion
The link between weight and health is not straightforward. We've known for years that if you plot death rates against BMI categories on a graph, you get a U-shaped curve, where people who are very underweight or very overweight are at higher risk of dying, while people in the middle have a lower risk.
This makes sense: extremes of weight are linked to illness, both as a cause or result. Many people with cancer or lung disease, for example, are underweight, which is one reason why lower BMIs are linked to higher death rates. That's why doctors talk about people having a "healthy" BMI.
What this study seems to show is that the lowest point of that U-shaped curve has shifted to the right, towards higher BMIs. But it doesn't mean that slimmer people are at a higher risk of death.
The study shows that in the period 2003-13, there was no difference between the death rates of people with a BMI of 18.5 to 24.9 (healthy) and those with a BMI of 25 to 29.9 (overweight), which were 4 per 1,000 per year for both groups.
The rate for obese people was 5 per 1,000 per year, despite this being a non-significant increased risk of death. There's certainly no need to try to put on weight if you are already at a healthy weight for your height.
The potential reasons for the shift are interesting. It may be, as the researchers suggest, that the diseases which killed more overweight people in the 1970s are now better treated and controlled, meaning that the risks of being overweight are smaller than they once were.
It's possible that the risks associated with being underweight have not decreased in the same way, which would automatically shift the "optimal" point towards overweight.
Also, despite a general increase in the population's BMI over the decades, health awareness has improved. Though the results have taken smoking status into account in the analyses, other factors, such as improvements in physical activity and alcohol moderation, could be having an influence.
However, this study has some limitations. Importantly, it was only carried out among white Danish people, which means it may not apply to other ethnic groups.
We know that some groups, such as people of south Asian origin, are more likely to have problems such as diabetes at lower BMIs than white people, so this study might not apply to everyone. And the follow-up for the most recent group studied was, on average, four years, so we don't yet know if this is a long-term trend.
The criticisms of the BMI system are not unfounded, though. BMI doesn't take into account the increased weight of muscle compared with fat – some athletes have high BMIs, despite being very fit, for example.
Waist circumference and waist-to-hip ratio can give a good indication of body "fatness". Regardless of your height or BMI, you should try to lose weight if your waist is:
- 94cm (37in) or more for men
- 80cm (31.5in) or more for women
You are at very high risk and should contact your GP if your waist is:
- 102cm (40in) or more for men
- 88cm (34in) or more for women
Read more about why waist size is important.
Links To The Headlines
Being overweight 'may be less unhealthy'. BBC News, May 10 2016
Overweight people less likely to die early than the slim, study shows. The Daily Telegraph, May 10 2016
Links To Science
Afzal S, Tybjærg-Hansen A, Jensen GB, et al. Change in Body Mass Index Associated With Lowest Mortality in Denmark, 1976-2013. JAMA. Published online May 10 2016
"Thousands of heart victims killed by poor care," claims the Daily Mail.
A review of clinical data from the last 10 years in England and Wales looked at patients with a history of what are known as non-ST segment elevation myocardial infarction (NSTEMI) heart attacks.
NSTEMIs describe a class of heart attack that are serious enough to warrant hospitalisation, but don't pose as big a threat as typical heart attacks.
Data from almost 390,000 people who had an NSTEMI was included in the review. It found around 87% of patients did not receive one or more internationally agreed recommended interventions.
It has been estimated that if all patients had received all of the interventions recommended to them, 32,765 (28.9%) deaths may have been prevented over the 10-year period.
But an important consideration is that some of the interventions consisted of lifestyle advice, such as quitting smoking or changing diet. This means we cannot assume that all the people given such advice after a heart attack would follow it.
These findings are also limited by the possibility that data was missing or had been recorded incorrectly. The design of the study is not able to prove cause and effect, and there are a number of other factors beyond the recommended interventions that may have had an effect on survival.
The data is certainly worth considering – one preventable death is one too many – but it doesn't prove that "thousands of heart victims [were] killed by poor care", as reported by the media.
Where did the story come from?
The study was carried out by researchers from a number of institutions, including the University of Leeds and University College London.
Funding was provided by the British Heart Foundation and the National Institute for Health Research.
It was published in the peer-reviewed European Heart Journal: Acute Cardiovascular Care.
This study has been reported widely in the UK. And, while these reports have been accurate, none mention the inherent limitations of the study.
The Daily Mail and The Daily Telegraph both quote Professor Peter Weissberg, Medical Director at the British Heart Foundation, who said: "This study shows that many people in the UK are receiving suboptimal care after a heart attack and that lives are being lost as a consequence.
"Applying clinical guidelines in heart disease costs little, and in the long term saves money and, most importantly, saves lives."What kind of research was this?
This cohort study used data from the UK national heart attack register to see whether guidelines for the care of patients who have had a non-ST elevation myocardial infarction (NSTEMI) is being followed.
An NSTEMI is a type of heart attack where the person has the symptoms of a heart attack and associated blood test results (raised heart enzymes), but they don't have the typical signs of heart attack (ST elevation) on an ECG monitor.
Typically, in an NSTEMI the blood supply to the heart is only partially, rather than completely, blocked. As a result, a smaller section of the heart is damaged. However, NSTEMI is still regarded as a serious medical emergency.
They are managed slightly differently from a typical heart attack, usually with medications and a coronary angiography to identify any blocked blood vessels that may need treating.
This type of study is a good way of investigating whether the best care is being provided to people with this type of heart attack.
But as the data collected in this registry was not specifically for the study, it is possible that it is not entirely fit for purpose – not all relevant detail may have been recorded, for example – and so may introduce bias.What did the research involve?
The researchers used European Society of Cardiology guidelines for the management of NSTEMIs and mapped this to UK registry data to see whether guideline-indicated interventions were being followed.
The registry data included adults admitted to one of 247 hospitals in England and Wales with an NSTEMI attack between January 1 2003 and June 30 2013.
NSTEMI cases were identified using the recorded hospital discharge diagnosis. Exclusions were those who died in hospital, where pharmacological therapies were uncertain, or if there was missing data on death.
The data contained information corresponding to 13 interventions, some of which were:
- electrocardiogram (ECG)
- blood pressure medications – such as beta-blockers and ACE inhibitors
- anti-clotting medications – grouped as P2Y12 inhibitors in this study
- advice to quit smoking
- dietary advice
- cardiac rehabilitation programme
A total of 389,057 adults were included in the analysis, with an average age of 70.9 years. Researchers found 86.9% were not recorded as receiving one or more recommended interventions.
Some of the ones frequently missed were:
- advice to quit smoking (87.9%)
- dietary advice (68.1%)
- P2Y12 inhibitors (66.3%)
- coronary angiography (43.4%)
Of the missed interventions, the ones estimated to have the strongest effect on reducing survival were:
- coronary angiography
- cardiac rehabilitation
- advice to quit smoking
By modelling the collected data, it was found that if all eligible patients in the study had received all of the interventions recommended to them, 32,765 (28.9%) deaths may have been prevented during the 10-year period.How did the researchers interpret the results?
The researchers concluded that: "The majority of patients hospitalised with NSTEMI missed at least one guideline-indicated intervention for which they were eligible. This was significantly associated with excess mortality.
"Greater attention to the provision of guideline-indicated care for the management of NSTEMI will reduce premature cardiovascular deaths."Conclusion
This study aimed to investigate whether adults who have had a non-ST elevation (NSTEMI) heart attack were offered all of the guideline-recommended interventions they were eligible for.
The researchers used guidelines set out by the European Society of Cardiology and found almost 87% of patients were not recorded in the registry as receiving one or more of the 13 interventions reviewed.
This study has both strengths and a number of limitations. This is a large dataset that has been designed to assess the quality of care given for this type of heart attack in the UK.
But the findings are limited by a number of factors:
- Findings from data analysis studies are always limited by the possibility that the recording of data was not complete and there may be some misclassification. For example, interventions such as advice for stopping smoking or about diet may have been classified in the registry as cardiac rehabilitation rather than counselling.
- Reasons for not giving interventions such as contraindications for use or patient refusal were recorded in the registry. However, reasons were not given for those simply recorded as not having received the intervention.
- The researchers excluded more than 31,000 people who died in hospital because they had incomplete information on the medications they received, as well as more than 21,000 who had missing mortality data. The missing cases may have pushed the findings in either direction.
- The design of the study is not able to prove cause and effect. There are a number of other factors beyond the recommended interventions that may have an effect on survival.
- Improvements were seen in the interventions offered over the course of the study – if we are just considering present day data, the picture may therefore be quite different.
- Perhaps most importantly, it is unclear why the researchers compared UK practice against the European Society of Cardiology guidelines, rather than the guidelines on management of NSTEMI issued by the UK guideline body, the National Institute for Health and Care Excellence (NICE). This may have given slightly different results.
Guideline -ecommended interventions for managing heart attacks are usually backed by good-quality research. It is important that the best care is offered to all people, regardless of hospital trust or the severity of their illness.
If you have had this or another type of heart attack, you should take all medicines as prescribed and follow the advice given by your doctors.
Links To The Headlines
One third of heart attack deaths could be avoided. The Times, May 10 2016 (subscription required)
33,000 heart attack deaths could have been prevented if NHS had followed guidelines. The Daily Telegraph, May 10 2016
Heart attack care failings 'leading to tens of thousands of deaths'. ITV News, May 10 2016
33,000 heart attack victims killed by 'failings in care' study claims. Daily Mirror, May 10 2016
Heartbroke: 3,000 Brits die each year due to poor care after cardiac arrest. The Sun, May 10 2016
Links To Science
Dondo TB, Hall M, Timmis AD, et al. Excess mortality and guideline-indicated care following non-ST-elevation myocardial infarction. European Heart Journal: Acute Cardiovascular Care. Published online May 3 2016
"We are facing a global sleep crisis because we don't go to bed early enough, say scientists," the Mail Online reports.
The warning comes from a study produced by a research team using a smartphone app (Entrain) to track sleep patterns from around the world.
The findings reveal that as people age, they tend to go to sleep earlier and wake later, and women tend to sleep more than men.
The researchers also found the timing of sunrise and sunset does influence sleep, but less than you might think.
Worldwide, there is a lot of variability in people's bedtime and the researchers believe this is down to social influences.
The researchers warn of a "global sleep crisis", but it is difficult to assess exactly what evidence this warning is based on.
The big stumbling block for this research is it can't provide us with any conclusive answers. It may be that factors such as using technical devices are disrupting our sleep, but we can't say anything about that based on this research.
Another drawback is that people chose to download this app. It could be that people with troubled sleep patterns would be more motivated to download the app than people with healthy sleep patterns.
Signs you may not be getting enough sleep include irritability and problems with concentration and memory. Persistent lack of sleep can make you more prone to accidents and chronic diseases.
Read more about why lack of sleep can be bad for your health.Where did the story come from?
The study was carried out by researchers from the University of Michigan, and was funded by the Biomathematics Program at the Army Research Laboratory and the Human Frontier Science Program.
The Mail's headline, which says "we are facing a global sleep crisis", probably goes too far – the study provided no evidence to support the claims of an impending "sleep crisis". But, to be fair, this term was used in the study itself, but the researchers didn't elaborate on this.What kind of research was this?
This cross-sectional study aimed to validate the use of mobile technology to collect information on sleep patterns worldwide, and explore the possible influences that social pressures have on sleep.
Sleep is known to be driven by our internal body clock. Naturally, sunrise and sunset would regulate this rhythm, but our modern lives are controlled by social factors, work obligations and artificial lighting, meaning we can't follow this natural rhythm.
As the researchers say, understanding the factors that control how much sleep we get is important as this can have a direct effect on human health.
In 2014 the researchers released a free app for iOS and Android devices – Entrain – that recommends optimal lighting schedules for adjusting to new time zones.
Users input data on their normal sleeping times, home time zone and typical lighting, sleep schedules and experience of jetlag.
In this study, the researchers analysed sleep habits from those who submitted data.What did the research involve?
In 2014, the first year of the app's release, 8,070 users submitted data.
The researchers explained that when the app is loaded, the opening screen asks users their normal wake time and bedtime to the nearest hour, home time zone, and typical amount of light exposure.
The options for typical light were:
- low indoor (200 lux)
- bright indoor (500 lux)
- low outdoor (1,000 lux)
- bright outdoor (10,000 lux)
For the purposes of this study, the researchers combined the indoor categories into a single group and did the same for the outdoor ones.
Users were also asked to give data on age, gender and travel frequency (from several times a week to less than once a year). They could also record data on travel dates and experiences of jet lag.
The main countries contributing data were the US (45%), Australia (9%) and Canada (5%). The UK, France, Spain, the Netherlands, Denmark and Germany jointly contributed 15% of the data, and China, Japan and Singapore made up 5%.
The researchers excluded "outlier" data that was far from the norm: for example, those who woke before 3am or after 11am, who went to bed before 7pm or after 3am, or who had less than 4 or more than 12 hours' sleep a night. This means most shift workers would have been excluded.
They also excluded those aged under 18 or above 85. This left 5,450 people for analysis.What were the basic results?
The adults analysed (majority male) represented a wide range of time zones, and more commonly reported indoor rather than outdoor light.
The researchers observed a relationship between age and sleep schedule, where in general increasing age was associated with less sleep and earlier waking times.
They found age has the strongest influence on the timing of midpoint of sleep, while gender had the strongest influence on duration of sleep, with women getting more sleep at nearly all ages.
Prior mathematical models suggested a later sunset and sunrise influence both bedtime and wake time, and the app data supported this. Sunrise after 6.30am and later sunset were both associated with later wake time and bedtime.
Later sunset was also associated with more sleep, particularly in the group who reported spending more time in outdoor light.
In general, women, older people and those with more outdoor light exposure seemed more sensitive to changes in sunset and sunrise than men, younger people and those with mostly indoor light exposure.
However, sunset timing had a weaker effect on bedtime than models may have predicted. The researchers considered that solar cues do influence sleep but may be ignored in the real world, particularly around bedtime.
The country the person resided in had an influence on their bedtime, suggesting that people are more responsive to social cues at night.
And sleep duration goes down as bed time becomes later. While average bedtime varied across countries, average wake time remained fairly consistent.
No results are reported for the influence of travel and reports of jet lag.How did the researchers interpret the results?
The researchers noted that the trends they identified agree with previous large-scale surveys and laboratory studies, and validate the use of this mobile technology for assessing sleep.
They said that, "This work better defines and personalises 'normal' sleep, produces hypotheses for future testing in the laboratory, and suggests important ways to counteract the global sleep crisis."Conclusion
These findings show that the app works, and it is possible for people to input data on the timing and duration of their sleep for researchers to get a global picture of sleep patterns worldwide.
The researchers noticed a number of themes, including that age, gender and the amount of time we spend outdoors are factors that can influence the timing and duration of sleep.
Timing of sunrise and sunset do seem to have an influence on our sleep, but less than may be expected. Across countries worldwide there is most variability in the time we go to bed, and this directly influences our sleep duration.
The researchers also considered that social influences are causing us to go to bed later and ignore the natural influences of sunset.
However, this is the big stumbling block of this research – it can't provide us with any answers, and we can only speculate as to why this is the case.
It may be that factors such as late-night working, socialising or using technical devices are influencing our sleep, but we can't say anything about that based on this research.
Another limitation of the study is that excluding people with outlying sleep patterns – very late bed times or waking times – automatically excludes shift workers. This is often the group in which previous research has speculated disrupted sleep patterns could have an adverse effect on health.
There is also the potential for misclassification when people are asked to categorise their typical light exposure as indoor or outdoor. There is likely to be wide variation in the amount of natural daylight that people in these two broad categories are exposed to.
A final important limitation is that the population were self-selecting. People actively chose to download and use the application, meaning the study could be at risk of selection bias.
Arguably, people with sleep problems are more likely to download a sleep app than people without sleep problems, so the results may not be truly representative.
It is also worth noting that only a fraction of the data analysed comes from the UK, so the study can't give any great insight into this country's sleep patterns and influences.
Overall, the findings are undoubtedly of interest in furthering understanding of the world's sleep patterns. However, they raise more questions than answers on how our social and working lives are affecting our sleep and health.
Links To The Headlines
Global sleeping patterns revealed by app data. BBC News, May 7 2016
Scientists warn of 'global sleep crisis' from data collected on smartphone app. Daily Mirror, May 7 2016
Global sleeping study reveals women get more than men. The Independent, May 7 2016
Links To Science
Walch OJ, Cochran A, Forger DB. A global quantification of "normal" sleep schedules using smartphone data. Science Advances. Published online May 6 2016
"Mobile phones don't increase the risk of brain cancer, 30-year study concludes," the Mail Online reports.
The Australian study found the massive increase in mobile phone use over the past 30 years was not matched by a similar rise in brain cancer cases.
The first official mobile phone call in Oz took place in 1987 by the then Minister of Communication, Michael Duffy. Now, mobile phone ownership rates are estimated to be around 94%.
Despite the explosion in Australian mobile phone ownership, the researchers found no corresponding spike in brain cancer rates. They therefore concluded there was no evidence that mobile phones cause brain cancer.
But the researchers only had the number of Australians with mobile phone contracts to play with – they didn't have any individual data, for example, with information about how often or for how long people had their phones to their heads or, increasingly in the smartphone era, held over their faces.
The study tells us that at a population level, it's unlikely mobile phone ownership is responsible for any moderate or larger increase in brain cancer in Australia. But it doesn't tell us about individual risk patterns.
Despite this uncertainty, when it comes to other risk factors for cancer, such as smoking, poor diet, drinking too much alcohol and lack of exercise, mobile phone ownership is probably not a significant risk to your health.
If you are concerned, read more about the potential risks of mobile phone use.Where did the story come from?
The study was carried out by researchers from the University of Sydney and the University of New South Wales, Australia. No funding source was mentioned.
It was published in the peer-reviewed journal, Cancer Epidemiology.
The Mail Online coverage was accurate and contains a link to an article by the lead author, which may be of interest to those wanting more information about the background to the study and its possible implications.What kind of research was this?
This ecological study set out to look for a link between mobile phone ownership and brain cancer incidence since the first mobile phone call in Australia in 1987.
Since the 1980s, mobile phone use has rocketed in most countries, including Australia, where more than 90% of the adult population use them today.
But mobile phones have been dogged by consistent and high-profile concerns that the electromagnetic radiation they give off might cause or contribute to cancer.
The researchers reference several reports showing an alleged link between mobile phone radiation and cancer, but say they had problems with the methods used in these studies, which meant the results were inconsistent and hard to replicate, and so may be wrong.
In an attempt to clear up the controversy, they set out to do a large, long-term study assessing the alleged link, bypassing many of the methodological flaws of previous research.
This sort of study is the most appropriate type to uncover any link between mobile phone ownership and cancer at a country level.
But as it is an ecological study, we need to resist the natural temptation to apply the country-level findings to individuals. We are dealing with averages of large groups, not individual cases.What did the research involve?
All cases of cancer are recorded in Australia and have been for many decades. The percentage of Australians with mobile phone accounts was obtained from large mobile phone companies and governing bodies.
Putting these two pieces together, the researchers had mobile phone accounts dating between 1987 and 2014, and brain cancer diagnoses of 19,858 male and 14,222 females between 1982 and 2012.
Their analysis looked at whether the rise in mobile phone ownership was linked to a rise in new cases of brain cancer, and they did this separately for different age groups and genders.
The researchers then probed the alleged link in more detail. Assuming a 10-year lag between phone radiation exposure and resulting cancer, they calculated the number of cancer cases they would expect to see if phone radiation caused cancer in a 20-year period, using the best estimates of risk increase from recent studies.
Their assumption was that mobile phones raised the risk of brain cancer 1.5 times for "ever-users" – those who'd used a mobile phone at any point in their lives – and 2.5 times for "heavy users", defined as more than 896 hours of total life use, which represented around 19% of Australians. These risk estimates were informed by previous research.
Using these assumptions, they were able to calculate an expected number of brain cancer cases if mobile phones caused brain cancer and compare it with the number of cases actually observed.What were the basic results?
Mobile phone use in Australia rose from 0% in 1987 to 94% in 2014. Over a similar time period, 19,858 males and 14,222 females aged 20 to 84 were diagnosed with brain cancer from 1982 to 2012.
Age-adjusted brain cancer incidence rates over this time rose slightly in men but not at all in women. The rise in men was not attributed to mobile phone use.
Assuming mobile phones caused brain cancer, the researchers expected to see much higher rates of cancer than they did.
For example, the actual rate of brain cancer in men was 8.7 cases per 100,000 men, which should have been around 11.7 per 100,000 if the causal theory was true.
Combining men and women of all ages, they expected around 1,867 cases of brain cancer in 2012 if mobile phones were part of the cause (ever-users), but found significantly less: 1,434. The difference was even larger for heavy users: 2,038 expected compared with 1,434 actually observed.
One age group, 70 to 84 years, did show up as having similar expected and observed cases, but the rise in cases started in 1982, before the introduction of mobile phones, leading the researchers to conclude it couldn't be caused by mobiles.
They thought it was probably the result of more access to better cancer diagnosis over time – picking up more cancer cases than in the past – leading to higher rates of cancer overall.How did the researchers interpret the results?
The researchers concluded that: "After nearly 30 years of mobile phone use in Australia among millions of people, there is no evidence of any rise in any age group that could be plausibly attributed to mobile phones."Conclusion
This ecological study found an explosion in Australian mobile phone ownership since the 1980s coincided with relatively little change in brain cancer rates, suggesting mobile phone ownership is unlikely to cause brain cancer.
This conclusion is based on assuming there would be a 10-year lag between mobile phone use and cancer, and 1.5 and 2.5 times risk increases due to mobile phone use. Using different assumptions may lead to different conclusions.
The study has many strengths, including its large size, comprehensive information on brain cancer rates over many decades, and research-based assumptions when modelling the expected number of cancer cases – assuming mobile phones do raise the risk of cancer.
What might be less obvious is that the study was more about mobile phone ownership rather than use. While you'd expect the two to be closely linked, it's important to spot the difference.
The data the researchers had was about having a mobile phone contract – they didn't have individual patterns of use in terms of how often the phone was pressed up against users' heads emitting different strengths of radiation, for example.
As such, it's probably wise to use the term phone ownership, rather than phone use – used in the media – when talking about this study.
The study's conclusions are in line with other research quoted by this study, which showed no link between mobile phones and brain cancer.
The big problem with ecological studies are that they don't tell us about individual risk patterns, only about averages of large groups, in this case Australians. This is really useful for public health professionals who deal in population level issues, but less relevant for you and I.
For example, we can't infer from this study, however tempting, that mobile phone use doesn't contribute to brain cancer in some way, as the data simply isn't individualised or detailed enough to find out.
These caveats aside, it would be surprising, given the now massive ownership of mobile phones across the globe, if there was a strong cause and effect association, such as that between tobacco use and lung cancer.
If you are concerned, read more about the potential risks of mobile phone use.
Links To The Headlines
Mobile phones DON'T increase the risk of brain cancer, 30-year study concludes. Mail Online, May 6 2016
No link between mobile phones and brain cancer, according to 29-year study. Daily Mirror, May 6 2016
Links To Science
Chapman S, Azizi L, Luo Q, Sitas F. Has the incidence of brain cancer risen in Australia since the introduction of mobile phones 29 years ago? Cancer Epidemiology. Published online May 5 2016
"Why walking is good for you ... even in the smog. Health benefits of a stroll found to outweigh harm caused by chemicals and dust pumped out by traffic," says the Mail Online.
The report in question was carried out to see whether the harm caused by exposure to air pollution outweighs the benefit of doing exercise.
The study used computer modelling and found that the pollution level needed for the harms and benefits of exercise to become equal, the "tipping point", was only present in 1% of cities, according to the World Health Organization (WHO).
In an average city, physical exercise will remain beneficial for up to seven hours a day on a bicycle or walking for 16 hours. But in the most polluted cities, such as Delhi, this became as low as 30 minutes a day for cycling and 90 minutes of walking.
Although findings from these types of computer model studies have to be interpreted carefully, their findings can be quite accurate as long as the data used is accurate.
Keeping active can reduce your risk of illness such as heart disease, stroke and type 2 diabetes. This study suggests that in an urban environment you are unlikely to be putting your health at risk by exercising outdoors.Where did the story come from?
The study was carried out by researchers from a number of institutions including the Centre for Diet and Activity research at the University of Cambridge and the Centre for Environmental Policy at Imperial College London.
Funding was provided by the British Heart Foundation, Cancer Research UK, the Economic and Social Research Council, the Medical Research Council, the National Institute for Health Research, and the Wellcome Trust.
The study was published in the peer-reviewed journal: Preventative Medicine.
The results of the study were presented accurately in the media.What kind of research was this?
This was a health impact modelling study which assessed the risk-benefit balance between exposure to pollution through outdoor physical activity and the health benefits of exercise itself.
Previous work on the topic focused on high income countries with low pollution levels, but health risks are thought to rise with increased exposure to air pollution, this was investigated in the study.
Modelling studies are useful for investigating these scenarios, however as it is only a model it may never be true to life.What did the research involve?
The researchers carried out computer simulations, using data from epidemiological studies and meta-analyses, to assess exposure to air pollution through physical activity and the associated health risks around the world.
Walking and cycling were considered in the simulations and the concentration of pollution established that was required to reach the "tipping point", where the risk from pollution and the health benefit from exercise are equal, and the "break-even" point, beyond which any time spent exercising would cause adverse health effects.What were the basic results?
The researchers found that if cycling for 30 minutes, a pollution concentration (PM2.5) of 95 microgram/m3 (seen in less than 1% of cites according to the WHO Ambient Air Pollution Database) is required to meet the tipping point.
The breaking point is reached at a concentration of 160 microgram/m3.
For an average urban pollution concentration the tipping point would be reached after seven hours of cycling per day.
If walking for 30 minutes, the tipping and breaking points would be at a concentration above 200 microgram/m3, meaning in an average urban area, the tipping point would be reached after 16 hours of walking per day.
Highly polluted cities, such as Delhi, had low tipping and breaking points, these were 30 and 45 minutes of cycling per day.
Tipping points for the most polluted cities (44 microgram/m3 to 153 microgram/m3) varied between 30 and 120 minutes per day for cycling, and 90 minutes to 6 hours 15 minutes per day for walking.How did the researchers interpret the results?
The researchers conclude: "The benefits from active travel generally outweigh health risks from air pollution and therefore should be further encouraged.
"When weighing long-term health benefits from PA [physical activity] against possible risks from increased exposure to air pollution, our calculations show that promoting cycling and walking is justified in the vast majority of settings, and only in a small number of cities with the highest PM2.5 concentration in the world cycling could lead to increase in risk."Conclusion
This modelling study aimed to assess exposure to air pollution through physical activity and the associated health risks around the world.
The study found the background pollution level required to reach the tipping point is only present in less than 1% of cities, according to the WHO.
In an average city physical exercise will remain beneficial up to seven hours a day for cycling or 16 hours for walking.
In highly polluted areas this became as low as 30 minutes a day for cycling and 90 minutes of walking.
The main limitation of this study is that it is only a model and we do not know how true to life the findings are. But these studies can be quite accurate if representative data is used in the model.
The results will reassure those concerned about the effects of pollution on their health.
The study did not describe differences between children, adults and older adults or those with health conditions, as the tipping point may be different amongst these groups.
Keeping active can reduce your risk of illness such as heart disease, stroke and type 2 diabetes.
It is recommended that to stay healthy you should be active daily, this can be moderate activity for at least 150 minutes per week, 75 minutes of vigorous exercise or a mixture of both.
The findings of this study suggest that in an urban environment it is unlikely that you are putting your health at risk by exercising outdoors.
Links To The Headlines
Benefits of cycling and walking 'outweigh air pollution risk' in cities. The Guardian, 6 May 2016
Air pollution: Benefits of cycling and walking outweigh harms - study. Daily Mirror, 6 May 2016.
"Obesity could be contagious like superbug C diff, suggest scientists," The Daily Telegraph reports. This rather alarming headline follows a study that explored characteristics of bacteria living in the human gut.
The study did not, however, look at any link to obesity. There's no reason to think that you can "catch" obesity from spending time with people who are overweight.
The colony of bacteria in the human gut (known as the microbiome) affects how we digest food, our immune system, how our body temperature remains stable, and other bodily functions. Little is known about the hundreds of species of bacteria living in our guts, because they were thought to be difficult to culture in the laboratory.
In this study researchers showed that about 40% of the gut bacteria known to scientists could be cultured. Further investigation found some can live and be transferred outside the body by producing spores, which are germinated by gut acids when they reach a new host – in this case another human. The superbug Clostridium difficile (C diff), which causes diarrhoea, is known to spread from person to person in this way.
Researchers did not find (or look for) any bacteria that might be linked with obesity. But in their press release, they speculated that bowel conditions such as inflammatory bowel disease, or obesity, could be caused by an imbalance of gut bacteria.Where did the story come from?
The study was carried out by researchers from the Wellcome Trust Sanger Institute in the UK, Hudson Institute of Medical Research and Monash University in Australia. It was funded by the Wellcome Trust, the UK Medical Research Council, the Australian National Health and Medical Research Council, and the Victorian Government.
The Telegraph and Daily Mail both jump on the suggestion that obesity could be caused by gut bacteria and could be spread like an infection from person to person, even though the study does not look at obesity. We don't know the effects of the bacteria identified and cultured in the study.
It would be sad if this study led to obese people being labelled as "contagious", as the headlines might suggest.
The Wellcome Trust Sanger Institute's press release says: "Imbalances in our gut microbiome can contribute to complex conditions and diseases such as obesity, Inflammatory Bowel Disease, Irritable Bowel Syndrome and allergies." However, it does not suggest these imbalances are contagious.What kind of research was this?
This was a laboratory-based study using samples of faeces from six healthy people. Researchers used genetic profiling techniques and worked with cultures on agar plates to investigate the types of bacteria found in the samples.What did the research involve?
Researchers took stool samples from six healthy people and used gene sequencing combined with bacterial culturing to grow cultures of bacteria and identify the species found. They treated samples with ethanol, to separate out those bacteria (like C diff) which were resistant to ethanol because they formed spores.
They then looked to see how long the bacteria lived outside the human body. Most gut bacteria live in conditions with no oxygen, so they don't live long when exposed to oxygen. The researchers exposed the bacteria to acids produced in the body's bile duct, to see whether this induced the spores to "germinate", in the way that temperature and moisture induces germination in the seeds of plants.
Finally, the researchers used metagenomic sequencing (the study of genetic material) to work out what proportion of bacterial colonies in the gut are likely to be spore-forming.What were the basic results?
The researchers said they had been able to culture 39% of bacteria identified in a database of known gut bacteria, and 73.5% of the bacteria identified in the samples in this study. They also identified new species.
They found about one third of the bacteria from their samples formed spores, and that these spores could last at least 21 days (the length of the study) of exposure to oxygen, while most non-spore forming bacteria lived for only two to six days.
When researchers exposed the bacteria to bile acids (which form part of our digestive system), the spore-forming bacteria germinated, enabling the bacteria to be cultured, while the non-spore forming bacteria were not affected.How did the researchers interpret the results?
The researchers said they had shown that spore-formation among gut bacteria was "widespread" and that these bacteria shared characteristics with C diff, which could make them "highly transmissible for long periods" outside the body, and "have the potential to spread rapidly over long distances".
They say their research "unlocks the human intestinal microbiota" for further investigation. In their press release, they suggest they could develop treatments for conditions such as C diff infection, by creating pills with mixtures of desirable gut bacteria to compete with the bacteria causing problems.Conclusion
The human microbiome is a fascinating field of research, and we are just beginning to learn how this colony of bacteria in our guts affects our health. This research widens our knowledge of these bacteria, and suggests ways they may survive and spread from person to person.
It also shows that many bacterial spores are resistant to ethanol, the main ingredient of hygienic hand gels. This reinforces the importance of using soap to wash your hands and not to rely on hand gels, especially in hospitals.
Because of the headlines in some newspapers, it's important to be clear about what the research hasn't found. It hasn't found bacteria in the gut that are responsible for causing obesity, or a link between obesity and C diff. It also hasn't found evidence that obesity spreads from person to person by bacterial transfer.
The study has simply found that about 30% of bacteria in our guts are likely to be capable of spreading from person to person. We don't know what effect that has, because we don't yet understand what role these bacteria play in the gut.
If you are worried about your weight, take a look at our weight loss guide; you can find out what weight is healthy for your height, and get advice on how to lose weight sensibly if you need to.
Links To The Headlines
Obesity could be contagious like superbug C. diff, suggest scientists. Daily Telegraph, May 5 2016.
Is obesity CONTAGIOUS? Spores of bacteria from guts of fat people 'could spread to healthy individuals'. Mail Online, May 5 2016.
Links To Science
Browne HP, Forster SC, Blessing O, et al. Culturing of 'unculturable' human microbiota reveals novel taxa and extensive sporulation. Nature. Published online May 4 2016
"Scientists have revealed which fruit can stop toddlers crying due to stomach pains," says the Daily Mirror, missing the point of the study it reports on.
When children get diarrhoea or vomiting, the main danger is that they will lose too much fluid (become dehydrated). Severe dehydration can be life-threatening and can happen quickly in young children.
To prevent this, doctors often recommend giving them specially made rehydration drinks, with a mixture of salts and sugars designed to keep fluid levels stable. However, the drinks are expensive and some children don't like the taste.
The researchers wanted to see if rehydration drinks were actually better, or if drinking diluted apple juice followed by children's usual preferred drinks would work just as well for children aged over six months.
The study found that children given apple juice were less likely to need additional treatments – possibly because they were happier with the taste and more willing to drink the juice.
However, this may not work for all children, as the study didn't include any babies under six months, children with more serious stomach upsets or other conditions, and those who were already severely dehydrated.
The advice from the National Institute for Health and Care Excellence (NICE) is still to give your child rehydration solution if you're worried they may become dehydrated and to seek medical advice if they don't get better. Fruit juice could make their diarrhoea worse and the current advice is that it should be avoided.Where did the story come from?
The study was carried out by researchers from the University of Calgary, the University of Toronto and the Hospital for Sick Children and Child Health Evaluative Services in Toronto, all in Canada. It was funded by the Physician Services Incorporated Foundation.
No apple juice producers were involved in the funding of this study and the authors reported no conflict of interests.
The study seems to have confused the UK media. The Daily Express says "an apple a day" might cure children's tummy aches, the Daily Mirror says apples "could stop toddlers crying", while the Daily Mail says apples "could keep tummy bugs at bay".
All the headlines miss the point that the apple juice was tested as a treatment to prevent dehydration when a child has a bug, not to prevent stomach aches or infections. There's no evidence in the study to back up these headline claims.What kind of research was this?
Researchers carried out a single-blind randomised controlled trial (RCT), to see whether diluted apple juice followed by the child's normal preferred drinks (such as milk, water or juice) worked as well to prevent dehydration as rehydration solutions.
RCTs are a good way to see which of two treatments works best. But in this case, the study was designed to see whether apple juice worked as well as rehydration solutions, not to say for certain which works best.What did the research involve?
Researchers from a specialist children's hospital recruited 647 children aged from six months to five years who'd been brought into the emergency department with an upset stomach. Children were randomly divided into two groups and assigned to the different treatments.
The children were given their allocated fluids, designed to look the same, as soon as they'd been seen by the nurse. Their parents were told to start giving them sips of the fluid straight away. They were then seen by a doctor, who could change the treatment if necessary.
When they went home, parents were told to either keep on using the rehydration salts to replace fluid lost by diarrhoea or vomiting, or to use the diluted apple juice followed by the child's normal preferred drink. A research nurse phoned daily to check how they got on.
At the end of the study, researchers compared how many children had either needed additional treatment (such as fluids given through an IV drip) or to switch to the other treatment, or had long-lasting illness, dehydration or weight loss, or needed to go back to hospital or see the doctor with the same episode of upset tummy, within seven days.
A combination of any of these factors was called a "treatment failure".
They analysed the results to see if apple juice worked as well as rehydration salts, and to look for patterns that might explain it, such as the child's age.What were the basic results?
Children who had apple juice followed by their preferred drinks did at least as well as those who had rehydration drinks:
- 16.7% of children who'd had apple juice had treatment failure, and 2.5% needed fluids given through a drip
- 25% of children who'd had rehydration drinks had treatment failure, and 9% needed fluids given through a drip
There were no significant differences between the two treatments in terms of frequency of diarrhoea and vomiting, weight loss and admission to hospital.How did the researchers interpret the results?
The researchers say that diluted apple juice "may be an appropriate alternative" to rehydration drinks for children with mild tummy upsets in high income countries such as Canada, where few children get serious infections and there's easy access to healthcare.
They warn the results may not be relevant to low and middle income countries where children are more likely to get serious infections and to become dangerously dehydrated.
They point out that parents have been discouraged from giving children with stomach upsets sugary drinks like fruit juice, because it could make diarrhoea worse. However, they say their results provide evidence that "in children with minimal dehydration, promoting fluid consumption is more important" than how much sugar is in the fluid.
They say that children over two years of age seemed to get most benefit from apple juice, perhaps because they were more used to drinking sweetened drinks and were fussier about taste.Conclusion
This study shows that diluted apple juice may work as well as rehydration salts for children with mild stomach upsets in preventing dehydration. But it might not work for all children, especially those with more serious stomach upsets, babies under six months, or children who are already more severely dehydrated.
It's important to remember that the children in this study were seen by a doctor before being allowed to continue with the diluted apple juice. They were all over six months old, didn't have other conditions that might have made the stomach upset more serious (such as diabetes) and had been checked for dehydration or other signs of serious illness.
There is also some missing information from the study that could have affected the results. We don't know whether parents continued to use apple juice or rehydration drinks as directed when they got home, or whether the child was receiving any treatment other than the hydration or anti-sickness tablets.
Most of the study results came from databases recording treatments given and visits to doctors or hospitals, or from phone calls by research nurses to the families after they'd left hospital. Not many parents returned the diary they'd been given to record their child's symptoms and whether the parents were happy with the treatment, so we don't know for sure if the parents were happy with the advice and their child's recovery.
If other studies also show that diluted apple juice works well for children with mild stomach upsets, doctors might decide to start recommending it instead of rehydration drinks.
For now, NICE advice is to encourage your child to drink fluids when they have a tummy bug, but to avoid giving your child fruit juice. See a doctor if you're worried your child is losing too much fluid.
Links To The Headlines
Scientists have revealed which fruit can stop toddlers crying due to stomach pains. Daily Mirror, May 3 2016.
Diluted apple juice 'ideal for treating tummy bug in children'. Daily Express, May 3 2016.
Links To Science
Freedman SB, Willan AR, Boutis K, et al. Effect of Dilute Apple Juice and Preferred Fluids vs Electrolyte Maintenance Solution on Treatment Failure Among Children With Mild Gastroenteritis: A Randomized Clinical Trial. JAMA. Published online April 30 2016.
"Breast cancer treatment breakthrough after 'milestone' genetic discovery," says The Independent, about widely reported research investigating genetic mutations in people with breast cancer.
The researchers took samples of cancer cells from 560 people with breast cancer (556 women and four men). They compared the DNA from the cancerous cells with DNA from normal cells.
They found 93 genes that had mutated in the cancer cells and concluded that they could have caused normal tissue to become cancerous. They also found 12 genetic patterns linked with breast cancer.
These findings have been called "groundbreaking" in the media. While they are certainly interesting, it's important to remember that, even if the gene is present, it doesn't mean the person will get cancer, just that their risk is increased.
It's hoped that the study will lead to more personalised treatments for breast cancer, similar to drugs used for other DNA mutations that are already known.
If there is a history of breast cancer in your family, you may be worried about your own risk. It's best to visit your GP, who can assess you and refer you to a genetic clinic if necessary.
The study was carried out by researchers from a number of institutions, including the Wellcome Trust Sanger Institute, East Anglian Medical Genetics Service, and the Cambridge University Hospitals NHS Foundation Trust.
Funding for the study was provided by multiple organisations, including the European Community's Seventh Framework Programme, the Wellcome Trust and the Institut National du Cancer (INCa) in France. The ICGC Asian Breast Cancer Project was funded through a grant from the Korean Health Technology R&D Project, Ministry of Health and Welfare, Republic of Korea.
The study was published in the peer-reviewed scientific journal Nature.
These findings have been reported accurately in the media. It's good to see explanations stating that, while this may be an important discovery, it may still be decades before targeted treatments become available. One of the researchers told the media: "Overall, I'm optimistic, but it's a tempered optimism".
Links To The Headlines
Breast cancer treatment breakthrough after 'milestone' gene discovery. Independent, May 3 2016
Breast cancer: Scientists hail 'milestone' genetic find. BBC News, May 3 2016
Study points towards personalised treatment for breast cancer. The Guardian, May 3 2016
Links To Science
Nik-Zainal S, Davies H, Staaf J, et al. Landscape of somatic mutations in 560 breast cancer whole-genome sequences. Nature. Published online May 2 2016
"'Secret' of youthful looks in ginger gene," BBC News reports. Dutch researchers have found evidence that a gene associated with red hair – the MC1R gene – may also have an impact on how young or old a person looks for their age.
This study examined the facial appearance and genetics of thousands of Dutch elderly adults. The researchers found four DNA sequence variants in the MC1R gene were linked to perceived facial age. These variants were already known to be associated with red hair, pale skin and sun spots.
People who carried two copies of these variants looked almost two years older than people who didn't carry any. Those who carried a single copy looked about one year older.
The researchers hope their findings may spark new leads into understanding the biological basis of youthful looks, and maybe even lead to new anti-ageing treatments.
However, this is some way off. There are likely to be various other genetic factors associated with ageing.
Of course, our genetics don't provide the whole answer to youth and vitality. Our lifestyle and environment – such as whether we drink or smoke and how much UV exposure we get – have a massive influence.
All of these factors can cause premature ageing of the skin. Conversely, a good diet and regular exercise can help boost the appearance of your skin.
We can't change our genetics, but we can change our lifestyle to give us the best chance of a healthy and happy life.
Read more about how to look after your skin.Where did the story come from?
The study was carried out by researchers from the Beijing Institute of Genomics in China, Erasmus MC University Medical Center and Leiden University Medical Center in the Netherlands, and the University of Leeds.
Funding was provided by the Erasmus University Medical Center Rotterdam, Unilever, and the Netherlands Genomics Initiative and the Netherlands Organization of Scientific Research.
Three of the authors work for Unilever. The study says: "Although no products were tested, this work could potentially promote the use of anti-ageing products and lead to financial gain for Unilever."
Some sections of the media got themselves into a right muddle regarding the implications of the research, as several headlines imply that redheads look two years younger. This isn't the finding of this research.
The study examined four variants in the MC1R gene that are known to be associated with red hair, pale skin and sun spots.
It found people who carried two copies of any of these four variants looked two years older. So, if anything, this seems to imply that the "ginger" variants were associated with looking older, not younger.
But it's not as simple as this. The variants were lumped together, so you can't assess the effect of any particular variant combination, therefore muddying any specific links.
The researchers also don't make any explicit links with hair colour or skin colour – and argue age perception was independent of these variables.
Why the MC1R gene can have an influence on skin appearance therefore remains a mystery.What kind of research was this?
This genome-wide association study involved a large cohort of Dutch people of European descent. It aimed to identify genes linked to perceptions of facial ageing and wrinkles.
As the researchers say, the desire to look young for your age is a long-standing one, which is likely to be due to its associations with health and fertility.
However, the biological basis of why people look older or younger for their age isn't understood. Understanding this could potentially be a step towards the development of new anti-ageing therapies.What did the research involve?
The first part of the study involved participants of the Rotterdam study – an ongoing follow-up cohort set up in 1990 that has included 2,693 elderly Dutch Europeans.
Researchers of all ages, mainly British, looked at front and side photos of their faces and guessed their age to fit within five-year age bands.
Facial features such as wrinkles and pigment marks were measured objectively using image analysis software.
The researchers then analysed participants' entire DNA, looking at more than 8 million single letter variants – single nucleotide polymorphisms, or SNPs – in the DNA sequence to identify those that had the strongest link with perceived facial age.
The researchers then verified their findings in two other cohorts: the Leiden Longevity Study, including 599 Dutch Europeans, and the TwinsUK Study, including 1,173 female Europeans.What were the basic results?
In the Rotterdam cohort, the researchers identified several DNA variants on the MC1R gene that were significantly associated with perceived age, after adjustment for age, sex and wrinkles.
Four of these MC1R DNA variants were highlighted as markers for further study, given that they have been previously associated with red hair, pale skin and age spots.
Compared with people who did not carry any of these four variants, people who carried a single copy of one of them looked about one year older, while people who carried two copies of any of the ageing variants looked about two years older. The effect of these variants seemed to be greater in men than women.
In the Leiden and Twin studies, they confirmed the association with these four MC1R DNA variants.
The link seemed to be consistent regardless of sun exposure and skin colour, but was weaker for darker skin tones.How did the researchers interpret the results?
The researchers concluded that, "A role for MC1R in youthful looks independent of its known melanin [pigment] synthesis function is suggested.
"Our study uncovers the first genetic evidence explaining why some people look older for their age and provides new leads for further investigating the biological basis of how old or young people look."Conclusion
As the researchers rightly say, the quest for prolonged youth and vitality is a longstanding one. This study uncovers another possible genetic reason why some people of the same age may look slightly older or younger than each other.
The researchers hope their findings may spark new leads into understanding the biological basis of youthful looks, and maybe even one day lead to new anti-ageing treatments.
The findings will undoubtedly provide a valuable contribution to the science of ageing, but we shouldn't assume that DNA sequence variants in the MC1R gene give the whole answer.
There are likely to be many other unexplored genetic variants that have a link with ageing, maybe with greater or less of an effect than the variants studied here.
Of course, our genetics don't give the whole answer to youth and vitality. Our lifestyle and environment – such as our diet, the amount of exercise we take, whether we drink or smoke, and how much UV exposure we give our skin – have a massive influence.
Another factor to consider is that this study was only looking at perceived ageing on account of how the person's face looked. Looking more youthful may not necessarily correlate with good physical health and fertility.
If new anti-ageing treatments are developed, they will be some way down the line, and one thing we can't change is our genetics.
What we can change, though, is our lifestyle to give us the best chance of a healthy and happy life.
Find out how becoming more active can boost both your mental and physical wellbeing – so even if you don't look younger, you could end up feeling younger.
Links To The Headlines
'Secret' of youthful looks in ginger gene. BBC News, April 29 2016
Gene linked to youthful looks has been discovered, scientists claim. The Guardian, April 28 2016
Ginger gene helps you to look two years younger. The Daily Telegraph, April 29 2016
Secret to 'eternal youth' found in GINGER gene that makes you look two years younger. Daily Mirror, April 28 2016
Links To Science
Liu Fm Hamer MA, Deelen, J, et al. The MC1R Gene and Youthful Looks. Current Biology. Published online April 28 2016