Medical News

Almost half of all adults take prescription drugs

Medical News - Thu, 12/11/2014 - 13:30

“Half of women and 43% of men in England are now regularly taking prescription drugs,” BBC News reports. The figures have come to light as part of a new survey into drug prescribing patterns.

According to the survey (The Health Survey for England 2013), commonly prescribed medications included:

There was also media controversy over the number of antidepressants being prescribed – particularly for women on a low income. Nearly one in five women from economically deprived areas were taking antidepressants.

The Health Survey for England 2013 also monitored other trends in the nation’s health, including people’s weight, smoking habits, fruit and vegetable consumption, and shift work. 


Who produced the data?

The report was produced by the Health and Social Care Information Centre (HSCIC), the official provider of national health and social care statistics. The HSCIC was set up by the government in April 2013. Its role is to provide information on a range of aspects concerning health for use by commissioners, analysts and clinicians in driving patient services.

In the interests of transparency we should point out that the Behind the Headlines team, along with all NHS Choices staff, is employed by the HSCIC.

The HSCIC produces an annual Health Survey for England that monitors important aspects of the population’s health.


How was the data collected?

The data comes from interviews with a representative sample of the population, carried out by the Joint Health Surveys Unit of NatCen Social Research and the Research Department of Epidemiology and Public Health, at the University of London. The interviews consisted of core questions and groups of questions on specific issues. Measurements such as blood pressure and waist circumference, and analysis of blood and saliva samples, were taken by a nurse.

The researchers interviewed 8,795 adults and 2,185 children for the 2013 survey.


What were the key findings?

Below are the key findings from the survey on prescription medication.

  • 43% of men and 50% of women reported that they had taken at least one prescribed medicine in the last week. Almost a quarter of men (22%) and women (24%) reported that they had taken at least three prescribed medicines in the last week. This proportion increased with age, with more than half of participants aged 65-74, and more than 70% of those aged 75 and over, having taken at least three prescribed medicines.
  • On average, 18.7 prescription medicines were dispensed per head of population in 2013.
  • The most frequently reported prescribed classes of medicines were cholesterol-lowering drugs (16% of men and 12% of women), drugs to lower blood pressure (14% and 15% respectively) and for women, painkillers including NSAIDs (12%).
  • Women (11%) were also more likely than men (6%) to be taking antidepressants. Women also demonstrated a significant variation by income class. 7% of women in the highest two quintiles of income were taking antidepressants, which rose to 17% of women in the lowest quintiles.
  • The cost of medicines in 2013, including costs for use in hospitals, was more than £15 billion. More than 1 billion prescription items were dispensed in the community in England, an average of 2.7 million items every day. The Net Ingredient Cost in 2013 was £8.6 billion, an increase of £102 million from the 2012 cost.


What did the media say?

Not surprisingly, the report was widely covered in the media, with many papers focusing on the numbers of people taking prescription drugs. Much of the reporting took a negative tone.

For example, the headline in The Times was “nation hooked on prescription medicine”. This is not particularly useful language as it implies that people are addicted to their medications. Medicines such as statins and ACE inhibitors are not addictive; though people often have to take them on a long-term basis to reduce the risk of serious complications such as heart attacks or strokes.

BBC News and the Daily Mail were relatively more balanced, as they carried comments from Dr Jennifer Mindell, one of the report’s authors. Dr Mindell explained there had been big changes in the use of statins (which lower cholesterol), with millions more people eligible to take them today than a decade ago. This increase in eligibility for these drugs is likely to be the result of new evidence on cost and effectiveness, which has suggested that the benefits in terms of preventing cardiovascular disease may outweigh the risks for many people.

Depression rates were generally higher among women than men because they were more willing to seek medical help, she reportedly said. The link between poverty and depression is also not particularly surprising, and is consistent with other observations from national reports and surveys in recent years that tend to show greater prevalence of both chronic mental and physical health conditions in more deprived areas. How to address this socioeconomic health divide is another matter.

The Mail also quoted Dr Maureen Baker, of the Royal College of General Practitioners, who said: “We have an ageing population and more patients are presenting with complex and multiple conditions including mental health issues and this is reflected in today’s figures.”

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

Links To The Headlines

Nearly 50% take prescription drugs. BBC News, December 10 2014

Half of women are taking drugs on prescription... and four in ten men are doing the same. Daily Mail, December 11 2014

Almost half of all English on prescription medication. The Times, December 10 2014

HALF of women are taking prescription drugs EVERY week, new study reveals. Daily Mirror, December 10 2014

Links To Science

Health & Social Care Information Centre. Use of prescribed medicines (PDF, 647kb). December 2014

Categories: Medical News

Food additive that could reduce appetite

Medical News - Thu, 12/11/2014 - 12:54

“Appetite suppressing additive could be added to food to create 'slimming bread'," ITV News reports.

This reports on a study that showed that short-chain fatty acids (SCFAs) are released from gut bacteria as they break down dietary fibre. These SCFAs then stimulate the release of hormones that signal to the brain that we are full.

The problem is that many people don’t eat a high-fibre diet, despite the numerous benefits. Therefore, finding new ways to increase SCFAs in people’s diets would be useful.

This study looked at an SCFA called propionate. Eaten by itself, propionate is said to taste like vinegar, and is broken down by the small bowel.

In this study, researchers managed to bind propionate to a polymer, helping to mask the taste and deliver it to the large bowel intact.

60 healthy overweight adults were given either this chemical or a control daily for 24 weeks. The chemical reduced further weight gain compared to the control, and also reduced the proportion of body fat around the tummy.

This is promising proof-of-concept research. However, more research is needed to see if this supplement is effective and safe enough to become more widely available.


Where did the story come from?

The study was carried out by researchers from Imperial College London, University of Glasgow, and other research institutions in the UK and Australia, and was funded by the UK Biotechnology and Biological Sciences Research Council.

The study was published in the peer-reviewed medical journal Gut on an open-access basis, so can be read for free or downloaded as a PDF.

The UK’s media reported the study accurately, though it is a little too early to suggest that this discovery could combat the obesity crisis.


What kind of research was this?

This was a preliminary laboratory study, followed by a randomised controlled trial (RCT).

The study aimed to investigate whether giving a particular chemical to humans can satisfy appetite and reduce weight gain.

The researchers explained how the normal bacteria in the large bowel help to break down fibre in the food we eat, and in so doing produce SCFAs. These SCFAs stimulate the release of certain gut hormones, called peptide YY (PYY) and glucagon-like peptide-1 (GLP-1). These hormones signal to the appetite centres in the brain that we are full. This is why high-fibre foods – such as wholemeal bread and root vegetables such as carrots – make us feel much fuller than processed foods such as burgers.

Previous studies have found that giving these hormones to humans and animals enhances feelings of fullness and reduces food intake.

Research has shown that SCFAs stimulate the release of these hormones by stimulating a particular bowel receptor called FFAR2. Of all the SCFAs produced by the breakdown of dietary fibre, one called propionate has been shown to have the highest affinity for this receptor.

Therefore, researchers wanted to see whether giving propionate could help to regulate the appetite. Giving SCFAs by mouth is unpalatable. They are said to have an extremely bitter taste, similar to drinking very strong vinegar.

SCFAs are rapidly absorbed by the small bowel before they even get to the large bowel. Therefore, the researchers developed a novel delivery system that would release small quantities of propionate into the first part of the large bowel. The researchers expected this to stimulate the release of the PYY and GLP-1 hormones, which suppress appetite.


What did the research involve?

The researchers first carried out laboratory tests to confirm that propionate did indeed cause a release of PYY and GLP-1 hormones from large bowel cells.

They then produced a “carrier molecule”, which could deliver propionate to the large bowel intact. This involved propionate being chemically bound to a natural dietary fibre called inulin.

Their first human test involved looking at the effect of single doses of inulin-propionate upon energy intake and the release of PYY and GLP-1 hormones in 20 volunteers. They then examined the effect on stomach emptying in another 14 volunteers.

The researchers then went on to conduct an RCT to investigate whether giving inulin-propionate over 24 weeks to overweight adults would decrease weight gain. They included 60 people who were aged between 40 and 65, with a BMI of 25 to 40, and who didn’t have any significant physical or mental health illness, including diabetes. These people were randomly assigned to supplementation with either inulin-propionate or inulin-control.

The trial was double blinded, meaning participants and researchers didn’t know which had been given.

These supplements were supplied in 10g ready-to-use sachets that, once a day, could be mixed into the content of their normal diet. Participants were advised to maintain their normal diet and activity patterns.

At the start of the study and after 24 weeks, participants completed self-reported diet and physical activity records, in addition to having their weight and other body measurements taken. These measures included having blood samples taken to measure PYY and GLP-1 concentration. The main outcome they looked at was change in body weight and food intake.


What were the basic results?

In the trial, 49 of the 60 participants (82%) who completed the 24-week study were analysed. There was no difference between the two groups in compliance or completion, and ratings of nausea were also no different.

Flatulence was the only other adverse effect reported, which was experienced more than half of the time in the control group, compared to a quarter of the time in the propionate group.

Weight gain was significantly less in the intervention group: 1 out of 25 participants in the inulin-propionate group (4%) gained 3% or more of their baseline body weight, compared with 6 out of 24 in the control group (25%). None of the participants in the inulin-propionate group had substantial weight gain (defined as 5% or more gain) compared with 4 out of 24 (17%) of the control group. There was a trend towards greater weight loss in the inulin-propionate group, but this was not significant compared to the control group. The intervention group also had a significantly lower proportion of their body fat tissue distributed in the abdomen compared to the control group.

When looking at food intake, there was no significant difference between the groups in terms of food intake at the end of the trial. There was a trend towards reduced food intake in the inulin-propionate group, but this was not significant. There was no difference in blood glucose control between the two groups. Total blood cholesterol and HDL (“good”) cholesterol were found to reduce in both groups, though LDL (“bad”) cholesterol was only reduced in the intervention group.


How did the researchers interpret the results?

The researchers say that their data “demonstrate for the first time that increasing [large bowel] propionate prevents weight gain in overweight adult humans”.



This interesting study has developed from the understanding that SCFAs are released from gut bacteria as they break down dietary fibre. These SCFAs then stimulate the release of hormones that signal to the appetite centres in the brain that we are full.

Of the SCFAs, propionate demonstrated the greatest affinity for receptors in the bowel, so therefore seemed the best candidate for study. The researchers then managed to develop a novel system that would deliver propionate intact to the large bowel, without the molecule first broken down in the small bowel.

In their first 24-week trial in 60 overweight adults, they found that it reduced further weight gain compared to the control group, which was the main outcome they set out to investigate. The trial benefits from being fairly long in duration and that it was double blind, which should remove the risk of biased reporting of outcomes from either participants or investigators.

However, there are various points to consider:

  • The trial was quite small, including only 60 people; just 49 completed it. Participants were middle-aged, overweight adults with no significant health problems. Therefore, the results may not be applicable to other groups.
  • We don’t know how this supplement could be taken practically outside of this trial's context – for example, whether this would be taken in the long term or just for short periods. If taken continuously in the longer term, we don’t know whether it would continue to prevent weight gain, or lead to significant weight loss.
  • This trial studied effects alongside the continuation of previous diet and activity patterns. We don’t know how the effects may differ if other lifestyle aspects were also altered.
  • The way this drug works needs to be studied further. For example, despite the treatment reducing weight gain, there was no difference in reported food intake between the treatment and control groups. Given that the proposed method of action of this treatment was to tell our brains we are full and so suppress appetite, this doesn’t seem to correlate. 
  • The trial only briefly reported on gastrointestinal adverse effects, though increased flatulence was frequently reported. If this supplement were to be used more widely, safety needs to be studied further. This includes looking at effects on body biochemistry and other aspects of health. Possible interactions with other medical drugs would also need to be considered. 

Overall, this is promising proof-of-concept research into the use of a novel chemical to try to prevent weight gain. However, further study is needed before this supplement could ever become more widely available.

For the time being, if you want to eat foods that make you feel fuller without adding lots of calories to your diet, a high-fibre diet – such as wholemeal bread, bran, cereals, nuts and seeds, as well as fruit, such as bananas and apples – is recommended. 

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

Appetite suppressing additive could be added to food to create 'slimming bread'. ITV News, December 11 2014

Scientists discover a secret ingredient 'to make you slim' and combat UK's obesity crisis. Daily Mirror, December 10 2014

Scientists make 'feel full' chemical. BBC News, December 11 2014

Scientists find natural food ingredient makes you eat less - but it tastes 'foul'. The Independent, December 11 2014

Links To Science

Chambers ES, Viardot A, Psichas A, et al. Effects of targeted delivery of propionate to the human colon on appetite regulation, body weight maintenance and adiposity in overweight adults. Gut. Published online December 10 2014

Categories: Medical News

Gene therapy could help with inherited blindness

Medical News - Wed, 12/10/2014 - 14:25

"Procedure to restore sight in dogs gives hope for future blindness cure," The Independent reports.

Researchers have restored some modest degree of light sensitivity (though not full vision) in animals who have a similar condition to retinitis pigmentosa.

Retinitis pigmentosa is an umbrella term for a group of human inherited eye conditions, affecting around 1 in 4,000 people, in which the normal light-sensing cells contained in the retina become damaged or die.

Experiments on blind mice and dogs have found cells in the retina that are not normally light-sensing (retinal ganglion cells) can be genetically modified to respond to light.

The researchers used gene therapy to modify these cells. The cells responded to light after they were activated with an injection of a chemical called MAG, with the effects lasting up to nine days.

In some of the experiments, blind mice treated in this way were able to see light again and move around like sighted mice in a maze.

The researchers also carried out similar experiments using blind dogs to see if the method would work in a large animal.

Laboratory experiments were able to show ganglion cells in dogs could also respond to light. However, there were no experiments that showed whether the dogs could see again.

No human trials have been performed yet, but the researchers hope this will not be too far off.


Where did the story come from?

The study was carried out by researchers from the University of California, the University of Pennsylvania, and the Lawrence Berkeley National Laboratory.

It was funded by the US National Institutes for Health, the National Eye Institute, and the Foundation Fighting Blindness.

The study was published in the peer-reviewed medical journal Proceedings of the National Academy of Sciences of the United States of America.

The Independent and the Mail Online accurately reported the study, although the headline writers took the usual liberties. While both acknowledged the research involved dogs and mice, claims the animals had their sight "restored" is an overstatement.

The headlines also failed to point out this technique would only have a potential application in cases of retinitis pigmentosa and not more common causes of visual impairment, such as age-related macular degeneration.


What kind of research was this?

This animal study tested whether cells in the retina that do not respond to light could be made to respond. They used genetic modification to produce a light receptor protein and a light-sensing chemical compound. This two-step process was tested on the retinas of blind mice and dogs.

In the inherited human condition retinitis pigmentosa, there is a progressive loss of rod receptors (light-sensitive cells) and cone receptors (colour-sensitive cells). This causes tunnel vision and, eventually, blindness.

Previous research found that although there is loss of these photoreceptors on the outer level of the retina, the connecting nerves underneath still function.

Researchers were interested in whether they could get these connecting nerves (retinal ganglion cells) to act as light-sensing cells, which could restore some vision.


What did the research involve?

The researchers first used genetic engineering to insert a gene for a receptor that responds to light in the presence of a chemical called maleimide-azobenzene-glutamate (MAG).

This process uses a modified virus called adenovirus to carry the gene into cells. The genetically modified virus is injected into the retina. The scientists were able to get retinal ganglion cells to produce this receptor.

Afterwards, an injection of MAG could turn on the light receptors when they are exposed to light. However, the first set of laboratory experiments did not work well because the level of light required to activate the new light receptors was so high that it damaged the retina.

After modifications, they produced a slightly altered chemical compound called MAG460, which responded to a less damaging wavelength of light, and performed a set of experiments.

Mice genetically engineered to lose the function of rods and cones by the age of 90 days were used. The researchers injected the mice's retinas with the adenovirus containing the light receptor gene.

Afterwards, they injected the retinas with MAG460 and then measured the ability of the retinal cells to respond to light in the laboratory.

As mice naturally avoid light, they compared the behaviour of the blind mice in a box that had light and dark compartments before and after the injections into the retina of the light receptors and MAG460.

To more accurately assess the ability to see, the researchers created a maze for the mice. They compared the ability to exit the maze of wild mice and blind mice injected with either the light receptors and MAG460, or an inactive placebo injection.

Finally, the researchers injected a canine version of the adenovirus and light receptor mixture and MAG460 into the retinas of three blind dogs and one normal dog.

They euthanised at least one of the dogs so they could look at the retinas in the laboratory to see if the light receptors had joined to the retinal ganglion cells. They also took retinal biopsies from the other dogs to measure if the cells could respond to light.


What were the basic results?

The light receptors were successfully produced by most of the retinal ganglion cells. The chemical compound MAG460 they developed was able to cause the cells to react to blue or white light without causing retinal damage. The light receptor was also able to "switch off" in darkness.

The retinas of blind mice that had been injected with the light receptors and then MAG460 became responsive to blue and white light. The treated retinal cells were able to detect different levels of light.

After injecting the retina with light receptors and MAG460, the blind mice had a strong avoidance of the light compartment of a plastic box, similar to normal-sighted mice. This effect lasted about nine days.

The sighted mice and blind mice injected with light receptors and MAG460 were able to learn how to exit the maze with increasing speed over the course of eight days. The blind mice injected with placebo were not able to learn how to do the task.

Experiments using the retinas of dogs showed that after the injections, retinal ganglion cells produced the light receptor and this, with MAG460, was able to make these cells respond to light.


How did the researchers interpret the results?

The researchers concluded they have been able "to restore retinal light responses and enable innate and learned light-guided behaviour in blind mice".

They say the system is equally effective in the retinas of genetically engineered blind dogs when tested in the laboratory.

These results will pave "the way for extensive testing of high-resolution vision in a preclinical setting and for clinical development," they say.



This innovative set of experiments has shown retinal ganglion cells can be genetically modified to produce a receptor on their surface that can respond to light in the presence of a chemical compound called MAG460. This light receptor can be activated for up to nine days.

This was shown in laboratory experiments on the retinas of mice and dogs, and in sight-testing experiments using mice. The mice had been genetically engineered to lose both types of photoreceptors, rods and cones by 90 days.

This model mimics what occurs over a much longer timescale in the human condition retinitis pigmentosa.

It appears from this research that other cells that are not damaged in the retina, such as retinal ganglion cells, can be genetically reprogrammed to respond to light.

These experiments provide hope that, despite the original photoreceptors being damaged or dying, some function can be restored if other cells are undamaged.

This could help people with conditions such as retinitis pigmentosa, but would not be suitable for people with age-related macular degeneration or diabetic retinopathy, where the damage is more extensive.

The experiments so far show there is some ability to respond to light, but these behavioural tests are at an early stage. More sophisticated experiments are needed to further assess the extent of visual ability this process can restore.

No human trials have yet been performed, but the researchers hope this will not be too far off.

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

Procedure to restore sight in dogs gives hope for future blindness cure. The Independent, December 8 2014

Have scientists found a cure for blindness? Radical gene therapy that restores sight in mice and dogs could be used on humans. Mail Online, December 9 2014

Links To Science

Gaub BM, Berry MH, Holt AE, et al. Restoration of visual function by expression of a light-gated mammalian ion channel in retinal ganglion cells or ON-bipolar cells. PNAS. Published online December 8 2014

Categories: Medical News

Academic hype 'distorting' health news

Medical News - Wed, 12/10/2014 - 13:29

"Science and health news hype: where does it come from?," The Guardian asks. A new study suggests a lot of the hype comes from academics themselves, or at least their press offices, as many press releases contain exaggerations.

Researchers looked back at all health-related press releases issued by 20 major UK universities during 2011.

They found many spurious health news reports were based on misleading press releases – normally part written, or at least approved by, the scientists themselves. For example, 36% of press releases they studied made exaggerated claims about human health from research actually carried out on animals. 

But somewhat ironically, the study found press releases containing exaggerated claims were actually less likely to generate news coverage.

So the study asks who's to blame – journalists for not bothering to read the actual studies they are reporting on, or academic press releases for hyping results? Or possibly a 24/7 media culture in which the amount of content produced is seen as more important than the quality?

It would seem misrepresentations can occur at all levels. While there are many dedicated journalists and press officers who strive for transparency and accuracy, a minority are letting the side down.


Where did the story come from?

The study was carried out by researchers from Cardiff and Swansea Universities in the UK and the universities of New South Wales and Wollongong in Australia.

It was funded by the British Psychological Society, the Experimental Psychology Society, the Wales Institute of Cognitive Neuroscience, the Wellcome Trust, the Economic and Social Research Council, the Biotechnology and Biological Sciences Research Council, and Cardiff University.

The study was published in the peer-reviewed British Medical Journal on an open access basis, so it is free to read online or download as a PDF (1.5Mb).

Not surprisingly, the study was not covered widely by most of the papers, especially those whose content is often dominated by health news.

While nobody is covered in glory by this research, journalists come out of it slightly better, as the researchers found hype invented by reporters was relatively uncommon.

But some journalists would seem to be guilty of recycling press releases rather than carrying out any independent reporting (or as it is known in the trade, "Churnalism").

The Guardian did publish a blog by the scientists who conducted the study, and The Independent provided an accurate summary of the study's findings.

And the BMJ put out a press release – on the exaggerations made in press releases. 


What kind of research was this?

This was a retrospective observational study, which looked at the content of all press releases about health-related science issued in 2011 by 20 major UK universities, together with the peer-reviewed journals they originated from and the printed news stories that followed.

It aimed to identify how often news stories contain claims or advice that go beyond those in the journal articles or if they try to identify the likely source – whether press releases or the news stories themselves.

The scientists point out health-related news has the widespread potential to influence health-related behaviour, but studies they are based on are often misreported.

It is often unclear whether inaccuracies and exaggerations originate in the news stories themselves or in the press releases issued by the academic institutions producing the research.

They also point out how journalists are increasingly expected to produce more copy in less time. This means press releases have become increasingly important, and the information they provide often makes up the core of the story.

Previous research, such as a study we covered in 2012, has suggested press releases can be a source of misinformation.


What did the research involve?

Using publicly accessible information from 20 leading research universities, the researchers identified all press releases based on published studies with possible relevance to human health, which had been issued in 2011 – they found 462 press releases.

For each press release, they sourced the original study and all relevant print or online news stories from the national press (not including broadcast news) – they found 668 news stories.

They coded each journal article, press release and news story.

They focused on three different types of exaggeration:

  • advice to readers to change their behaviour because of the study
  • claims that one thing causes another, but made from observational data only – they used a seven-point scale to rate the strength of such statements
  • inferring there was a relevance to humans from findings in animals beyond (or different to) that stated in the associated peer-reviewed paper

For each category of exaggeration, both news stories and press releases were coded for the strength of their statements.

Taking the peer-reviewed study as a baseline, the researchers then asked to what extent exaggerated statements in news stories were present in each press release.

For example, if a journal article reported an association between eating biscuits and cancer risk and the news story claimed the biscuits caused cancer – a common type of exaggeration – they looked at what the press release said, too.

Or if a news story claimed a treatment for humans but the actual study was on rodents – another common problem – they examined statements in the press release.

They also searched press releases and news stories for any caveats or qualifications to the claims being made.

They analysed their results using standard statistical methods.


What were the basic results?

Below are the study's main findings:

Exaggerated advice

Forty per cent of the press releases contained more direct or explicit advice than the journal article (95% confidence interval [CI] 33% to 46%).

Exaggerated causal claims

Thirty-three per cent of the claims in press releases were more "strongly deterministic" than those present in the associated journal article (95% CI 26% to 40%).

Exaggerated claims from animal or cell research

Thirty-six per cent of press releases exhibited inflated inference to humans compared with the journal article (95% CI 28% to 46%).

They also found when press releases contained exaggerations, it was more likely that news stories would, too (58% for advice, 81% for causal claims and 86% for inference to humans).

But when press releases did not contain exaggeration, rates of exaggeration in news stories were only 17%, 18% and 10% respectively.

Exaggeration was not significantly associated with increased news coverage compared with press releases, which were more accurate. So it would seem that not only is exaggeration "bending the truth", it is also ineffective.


How did the researchers interpret the results?

The researchers say it is common to blame media outlets and their journalists for exaggerated or sensationalised news stories about health – but their main finding was most exaggeration in health news is already present in academic press releases.

The blame, they say, "lies mainly with the increasing culture of university competition and self promotion, interacting with the increasing pressures on journalists to do more with less time."

The scientific community has the ability to improve this situation, they conclude. Press releases could be a primary target to improve the accuracy of science news, with potential benefit for public health.

In an accompanying editorial, Ben Goldacre, Research Fellow at the London School of Hygiene and Tropical Medicine and author of the book Bad Science, argues academics should be made accountable for exaggerations made about their own work in press releases.



As the authors point out, this was a retrospective observational study, so it cannot prove exaggeration in press releases accompanying health studies causes exaggeration in news stories.

To find out more, they are now planning a randomised trial on how different styles of press release influence the accuracy of science news stories.

However, it does chime with anecdotal evidence on the exaggerations in press releases that are then taken up by the media. It can only be a good thing if, as a result of this and future research, scientists themselves take more responsibility for the accuracy of press releases related to their studies. 

There is always the danger of creating a "boy who cried wolf" scenario. Readers may become so mistrustful of what they perceive as hype and exaggeration in health news that they ignore valid, evidence-based advice, which could lead to real harms. 

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

Links To The Headlines

Science and health news hype: where does it come from? The Guardian, December 10 2014

Bad science reporting blamed on exaggerations in university press releases. The Independent, December 10 2014

Links To Science

Sumner P, Vivian-Griffiths S, Boivin J, et al. The association between exaggeration in health related science news and academic press releases: retrospective observational study. BMJ. Published online December 10 2014

Categories: Medical News

Around 1 in 10 maternal deaths due to flu

Medical News - Tue, 12/09/2014 - 15:25

“Nearly one in ten pregnant deaths caused by flu,” The Daily Telegraph reports. A review into maternal deaths, which thankfully remain rare, found that conditions such as the flu and sepsis account for many of the deaths. Maternal deaths are deaths in women that occur during their pregnancy or within six weeks after the end of their pregnancy.

Other headlines prompted by the review included the Mail Online’s “Half of deaths in pregnancy are 'avoidable'”, pointing out that mental health and heart problems take a “heavy toll”.

BBC News took a more positive approach, pointing out that “Maternal death rates 'are falling'”. Maternal death rates dropped from 11 per every 100,000 women giving birth during the 2006-08 period to 10 per every 100,000 women during the 2010-12 period.


What are the news stories based on?

The news stories are based on a report by researchers at the University of Oxford. It aimed to find the reasons for maternal deaths and illness (morbidity) between 2009 and 2012 in the UK and Ireland, and what lessons can be learned. They note that the focus is not on attributing blame, but on using these lessons to improve future maternity care. The UK’s maternal death rates are now among the lowest in the world.

This is part of a programme of Confidential Enquiries into Maternal Deaths, which has been running since 1952. The current programme, called the “Maternal Newborn and Infant Clinical Outcome Review Programme”, is provided by the MBRRACE-UK collaboration. MBRRACE-UK stands for Mothers and Babies: Reducing Risk through Audits and Confidential Enquiries across the UK.


What data do they look at and how do they collect it?

The current data covers the UK and, for the first time, the Republic of Ireland.

Data on maternal deaths is collected from various sources, including direct notification by individual maternity units, coroners, pathologists, midwives or members of the public, or though media reports. This is cross-checked with data from the Office for National Statistics and National Records of Scotland. The researchers also search for records of deaths in women of childbearing age, and compare these with birth records to identify any missing deaths.

The researchers send forms to the units in which the deaths occurred to find out demographic and medical details, causes of death, and provide contact details for the clinicians involved in their care. They then send questionnaires to the clinicians to ask about their views on the women’s care. All of these details and copies of the women’s medical records are provided to the MBRRACE-UK assessors for review, but only after any details that could identify the women are removed – so the records are anonymous.


What are the main findings and trends?

Their main findings were:

  • 357 women died during or within six weeks of the end of their pregnancy in 2009-12; this was equivalent to 10 in every 100,000 women giving birth.
  • This was a significant reduction from 11 deaths in every 100,000 women giving birth in 2006-08.
  • The reduction was largely due to a reduction in deaths as a direct result of a pregnancy complication such as bleeding.
  • In 2009-12, one third of mothers who died did so as a direct result of a pregnancy complication.
  • Two-thirds of the deaths were from medical or mental health problems that were not directly linked to pregnancy, but got worse during pregnancy.
  • Three-quarters of mothers who died had pre-existing medical or mental health problems when they became pregnant.
  • More than two-thirds of women who died did not receive the nationally recommended level of care during their pregnancy (antenatal care), and a quarter did not receive the recommended minimum level of care.
  • Almost a quarter of women who died had a severe infection (sepsis).
  • One in 11 of the mothers who died did so from flu, and more than half of these could have been prevented by a flu vaccination.


What recommendations do they make?

The report’s basic recommendations are that:

  • Women with pre-existing medical and mental health conditions need pre-pregnancy advice and joint care from specialists in their condition and maternity staff.
  • Women with a severe infection need early diagnosis, rapid antibiotic treatment and a review by senior doctors and midwives.
  • More women need to receive the seasonal flu vaccine in pregnancy.

The report expands on these to make more detailed recommendations for various groups of staff in the healthcare system and professional organisations.

This included, for example, keeping the possibility of sepsis in mind at all times, ensuring women with any symptoms or signs of ill health in pregnancy have a full set of basic observations – such as temperature, blood pressure and breathing rate – and ensuring that women get access to  available care. They also recommended that any maternal deaths should be reviewed locally by a multidisciplinary group.

A full version of the report is available in the further reading section below.

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

Nearly one in ten pregnant deaths caused by flu. The Daily Telegraph, December 8 2014

Maternal death rates 'are falling'. BBC News, December 9 2014

Better care urged for pregnant women with mental health problems – study. The Guardian, December 9 2014

Half of deaths in pregnancy are 'avoidable': Oxford study lays bare heavy toll of mental health and heart problems. Mail Online, December 9 2014

Categories: Medical News

Hopes for chemicals that turn 'bad' fat 'good'

Medical News - Tue, 12/09/2014 - 14:00

"Scientists discovered how to trigger a molecule which can turn 'bad' white fat cells into 'good' energy-burning brown fat cells," The Daily Telegraph reports, saying that it could "replace the treadmill". But this proof of concept lab research didn't involve any humans.

White fat is what most people think of when they are talking about fat – it stores energy, adds bulk to the body, and too much can lead to obesity.

Brown fat helps to keep body temperature stable by burning energy, and this uses up calories. Brown fat is mostly found in newborns, but researchers think if they could convert white fat cells into brown fat cells in adults, this could lead to weight loss.

In this study, researchers have identified a number of potentially promising chemicals that could be used to create a drug that can turn white fat into brown fat.

A pill that allows us to eat what we want and not gain weight might become a reality at some point in the future, but this is unlikely to be an option in the short term.

Researchers have only done tests on cells in the lab so far. They do not yet know whether the chemicals will be effective and safe in humans.

Even if an obesity-busting pill becomes a reality, it is unlikely to replace all of the benefits of keeping active and eating a healthy balanced diet – so do still ask Father Christmas for that treadmill.


Where did the story come from?

The study was carried out by researchers from the drug company Roche, Harvard University and Massachusetts General Hospital in the US.

The research was funded by F. Hoffmann-La Roche, the US Institutes of Health and Harvard University, and was published in the peer-reviewed journal, Nature Cell Biology.

Both The Daily Telegraph's and the Mail Online's reporting of the study was broadly accurate. But claims made in the headlines that the pill could replace exercise, which is reported in a quote from one researcher, are probably overly optimistic.

Even if a drug was successful in leading to weight loss without the need for exercise, exercise brings additional health benefits.

These include enhanced cardiovascular health and a reduction in the risk of some cancers, bone fractures and dementia, as well as an improvement in symptoms of mild depression.

To be fair to the Mail Online, their article does say the research team pointed this out, but not until the end of the story.


What kind of research was this?

This was laboratory research looking for chemicals that can convert fat-storing cells (white fat cells) into energy-burning cells (brown fat cells).

Mammals have two types of fat – white and brown fat. White fat stores excess energy and helps regulate feelings of fullness. Brown fat keeps body temperature stable by burning fat to produce heat.

In humans, brown fat cells are mostly found in newborn infants to help keep them warm before they are able to shiver.

As we grow, most brown fat cells are replaced by white as we have less need for them, but studies have found the more brown fat we have the less likely we are to be overweight.

Animal studies have suggested white fat cells can be prompted to change into brown fat cells by exposing them to certain conditions (such as cold) or certain molecules.

The researchers say if they could find a way to convert white fat cells to brown fat cells in humans, it could be a promising way to combat obesity.

In particular, the researchers wanted to develop a way to rapidly assess a wide range of chemicals for this fat cell-converting ability, and test any chemicals they identified as showing potential.

This is a common way to start looking for chemicals that could be developed into useful drugs. It is a very early stage of drug development, and many of the chemicals identified will never make it to the pharmacy shelf.

And those that do can take a long time to get there. If the process of creating a successful drug was similar to an X-Factor-style reality talent show, the work being done in this study would be akin to the first round of public auditions.


What did the research involve?

The researchers started with human stem cells in the lab and treated the cells with chemicals that induce them to develop into white fat cells.

Brown fat cells produce a special protein called UCP1, which white fat cells do not. The researchers used this protein as a "marker" for identifying cells that had started to behave like brown fat cells.

They tested 867 different chemicals to see if they could cause the cells to "switch" to being like brown fat cells. They also looked at whether these chemicals caused the cells to look more like brown fat cells under the microscope.

White fat cells have one or a few large drops of fat inside them, while brown fat cells contain many small droplets of fat. Brown fat cells also possess more of the energy-producing "powerhouses" of the cells called mitochondria.

The researchers also looked at whether the switched cells were producing more mitochondria and were more metabolically active, and what happened if the chemicals were removed from the cells.

They tested whether the chemicals identified could cause cells collected directly from human fatty tissue and white fat tissue from mice to turn into brown fat cells.

They also looked at whether the genes that were active in the switched cells were more like white fat cells or brown fat cells.

The researchers also carried out other experiments to look at how the chemicals they identified had their effect. This could also help them to identify other ways to get white fat cells to switch.


What were the basic results?

The researchers identified 83 chemicals that caused white fat cells to become brown fat cells, producing the brown cell-specific protein UCP1 in the laboratory. These switched cells also looked like brown fat cells under the microscope.

Three of these chemicals showed the greatest ability to get white fat cells to switch to UCP1-producing brown fat cells.

The switched cells were also producing more mitochondria and were more metabolically active, burning more fats to make heat.

Two of these chemicals inhibited proteins called JAK and SYK. One was a drug called tofacitinib, which is currently used to treat rheumatoid arthritis.

Even after these inhibitors were removed from the switched cells, they were still behaving like brown fat cells 28 days later.

The researchers carried out further tests on these compounds and found they could cause cells collected directly from human fatty tissue to turn into brown fat cells.

They could also cause white fat cells from under the skin of mice to convert into brown fat cells in the lab, but not fat cells from the abdomen.

Finally, they found although the switched cells were acting more like brown cells, they still had patterns of gene activity that were more like white fat cells. This suggested the cells had not entirely converted to brown fat cells.


How did the researchers interpret the results?

The researchers concluded they have developed a way to identify chemicals that can get fat-storing white fat cells to switch to behaving like energy-burning brown fat cells.

Using this system, they identified two inhibitors of the JAK protein, which can cause white fat cells to take on brown fat cell-like characteristics and metabolism in the lab.

They say a role for the JAK pathway in controlling fat cells was not previously known about, and this knowledge could help identify chemicals that could be used to treat obesity.



This laboratory research has identified chemicals that can make fat-storing white fat cells behave more like energy-burning brown fat cells in the lab.

They hope these or other chemicals identified using their new method could eventually help combat obesity.

A pill that allows us to eat what we want and not gain weight is a holy grail for many. While it might become a reality at some point in the future, this is unlikely to happen any time soon.

As the authors themselves note, they have only done tests on cells in the lab so far. They do not yet know whether the chemicals will have the same effect within the body or, more importantly, whether they would be safe to use.

The researchers are right in sounding a note of caution. The chemicals they have identified as working best so far inhibit a protein called JAK, which plays an important role in the immune system.

This could make using JAK inhibitors to treat obesity more difficult, as it could mean side effects for the immune system.

This research is at a very early stage, and the pill will certainly not be in the stores in time for Christmas, so you are still going have to hit the gym if you want to get rid of any excess calories you consume over the festive period.

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

Links To The Headlines

Obesity pill to 'replace treadmill' being developed by Harvard University. The Daily Telegraph, December 8 2014

The obesity pill that could replace exercise by turning 'bad' fat to 'good'. Mail Online, December 8 2014

Links To Science

Moisan A, Lee Y, Zhang JD, et al. White-to-brown metabolic conversion of human adipocytes by JAK inhibition. Nature Cell Biology. Published online December 8 2014

Categories: Medical News

Lack of sleep linked to negative thinking

Medical News - Mon, 12/08/2014 - 14:30

“Feeling anxious? Go to bed earlier: Getting more sleep really can calm the mind,” reports the Mail Online. 

However, if you’re more of a "glass half-empty" sort of person, the headline could have read “feeling anxious affects your sleep” – which is an equally valid interpretation of the same results.

A study of 100 university students has found that shorter sleep and delayed ability to get to sleep are associated with repeated negative thoughts (RNT). RNT are unwanted, unhelpful and distressing thoughts that are repeated over and over again, such as “my life is pointless”.

RNT can be a common problem in people with mental health issues such as generalised anxiety disorder and obsessive compulsive disorder (OCD).

Students filled in surveys assessing their sleep patterns, mood, anxiety levels and how often they experienced RNT. There was a clear correlation between poor sleep quality and RNT but the “direction of travel” is unclear. Does poor sleep lead to RNT or does RNT lead to poor sleep?

It’s plausible that lack of sleep might make negative thoughts or mood worse, as it does for concentration. Similarly, it’s easy to imagine that worrying about issues can stop someone sleeping well.

If you are troubled by persistent insomnia and unwelcome thoughts that you feel you cannot control, see your GP. Talking therapies such as cognitive behavioural therapy can often help with both of these issues.


Where did the story come from?

The study was carried out by researchers from Binghamton University, US. Sources of funding were not reported.

The study was published in the peer-reviewed medical journal Cognitive Therapy and Research.

The Mail Online accurately reported on the study (and somewhat unusually for the Mail, put a positive spin on the results), though it did not make it clear that the study was conducted on apparently healthy student volunteers. Similarly, it did not highlight the most important limitation of the study, the possibility of reverse causation or what is known in academic circles as “the chicken egg problem”.

The Mail also reported “a spate of studies [that] suggested getting between seven and eight hours is essential for good health”. This refers to separate research, which we have not appraised. Consequently, we cannot comment on the accuracy of these specific statements.

That said, there is a general consensus of expert opinion that persistent lack of sleep can be detrimental for both your physical and mental health.


What kind of research was this?

This was a cross-sectional study that aimed to see if the student responses to a variety of questionnaires indicated any association between repetitive negative thinking (RNT) and sleep. RNT describes when a person has distressing or worrying thoughts that are repeated over and over again and are difficult to control.

RNT occurs in a variety of mental illnesses, including generalised anxiety disorder, major depression, post-traumatic stress disorder (PTSD) and obsessive compulsive disorder (OCD). It can also occur in people who do not currently have a mental illness and generally causes increased feelings of anxiety and a lowering of mood. The researchers wanted to explore the relationship between RNT and a lack of sleep or delay in getting to sleep.

As this was a cross-sectional study, it cannot prove causation. That is, whether poor sleep causes RNT or RNT causes poor sleep. Both scenarios seem plausible.


What did the research involve?

The researchers recruited 100 US university students who had volunteered to participate in any research studies. They were on average 19 years old and 58% of them were female.

The students completed a variety of questionnaires assessing their levels of worry, thought patterns, sleep patterns and whether they were more of a morning or an evening person. This included the:

  • Worry Domain Questionnaire (WDQ)
  • Ruminative Response Scale of the Response Style Questionnaire (RRS)
  • Obsessive Compulsive Inventory (OCI)
  • Perseverative Thinking Questionnaire (PTQ)
  • Positive and Negative Affective Schedule (PANAS)
  • Negative Affect scale (PANAS-NA)
  • Pittsburgh Sleep Quality Index (PSQI)
  • Horne Ostberg Morningness-Eveningness Questionnaire (MEQ)

The researchers then performed statistical analyses to look for any associations between sleep and repetitive negative thinking from the answers to these questionnaires.


What were the basic results?

The main findings were:

  • increased RNT was associated with shorter sleep and delayed sleep
  • shorter sleep was associated with more rumination (repetitive thinking)
  • delayed time getting to sleep was associated with more obsessive-compulsive symptoms

On average, the students:

  • went to bed at 1am and got to sleep within 22 minutes
  • slept for about seven hours
  • were mostly “evening” types
  • did not score highly overall for the symptoms on any of the questionnaires


How did the researchers interpret the results?

The conclusion reached by the researchers was that repetitive negative thinking “may be uniquely related to both sleep duration and timing”.



This study has found an association between shorter sleep and increased reported RNT.

However, there are a few points to bear in mind when considering how applicable the results of this study would be to the general population, people who have a mental illness or are particularly affected by RNT:

  • due to the cross-sectional measure of sleep patterns at one point in time, we cannot tell whether lack of sleep, or delayed sleep, causes RNT or whether RNT causes sleep disturbance – both directions of effect are plausible
  • none of the participants in the study were reported to be suffering from any mental illness or other conditions that may affect the level of RNT
  • they were all young, adult students
  • it could be argued that they may have been of a certain personality type to have been willing to complete seven extensive questionnaires
  • sleep patterns of people in this particular age group who are at university are unlikely to be representative of the sleep patterns they will have at other times of their life

However, commonsense tells us that a lack of sleep is likely to make any negative thoughts or mood worse. Tips on how to get a better night’s sleep can be found here.

If you are suffering from unwanted, repetitive thoughts that are causing you distress, talk to a healthcare professional. There are a range of simple techniques that can help, in addition to more formal methods such as cognitive behavioural therapy.

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

Links To The Headlines

Feeling anxious? Go to bed earlier: Getting more sleep really can calm the mind. Mail Online, December 5 2014

Links To Science

Nota JA, Coles ME. Duration and Timing of Sleep are Associated with Repetitive Negative Thinking. Cognitive Therapy and Research. Published online January 4 2014

Categories: Medical News

Text alerts 'help prompt people to take their pills'

Medical News - Mon, 12/08/2014 - 12:55

"A text messaging service could help people remember to take the medicines they have been prescribed," BBC News reports, after a small trial scheme in London helped increase drug adherence in people with cardiovascular disease.

Lack of adherence – not sticking to a recommended treatment plan – is a known problem in some people with chronic diseases, such as heart disease.

The BBC reports up to half a billion pounds a year is wasted as a result of people not taking medication and resulting complications that could have been avoided.

The study recruited 303 adults who were taking blood pressure tablets such as Perindopril, or pills to lower their cholesterol (statins).

Half the participants received text messages over a six-month study period and the other half did not – more people in the text group took their medication as prescribed compared with the "no text" group (91% versus 75%).

The main difference between the groups appeared to be related to people being telephoned by a healthcare professional if they did not respond to the text, or if they replied they had stopped taking their medication.

This telephone call resolved medication issues in almost all cases. In contrast, it does not appear any such measures were in place for the other group.

Text messages could be a cost-effective method of improving adherence and could potentially be used for other chronic conditions, such as HIV.


Where did the story come from?

The study was carried out by researchers from Queen Mary University London and was funded by AstraZeneca, Barts Hospital Special Trustees and Queen Mary Innovation.

The authors stated that: "The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript."

It was published in the peer-reviewed medical journal PLOS One. This is an open-access journal, so the study is free to read online.

The BBC reported the news accurately and included an informative video interview with the lead researcher, though they did not discuss any of the study's limitations.


What kind of research was this?

This was a randomised controlled trial (RCT) that aimed to see if the use of text messaging improved adherence to taking medication.

Non-adherence is a relatively widespread problem, especially in people with chronic diseases, who are often required to take a range of different drugs.

An RCT is considered the "gold standard" in assessing how effective an intervention or treatment is. But this RCT wasn't double blinded, which does increase the risk of (often unconscious) bias. 


What did the research involve?

The researchers recruited people from seven GP practices in London. To be eligible, they had to have a mobile phone number on the GP records and be taking blood pressure or lipid-lowering medication.

A text was sent to 6,884 suitable people to see if they were interested in the trial. In the end, 303 people agreed to participate.

Half the participants were randomly assigned to receive text messages and the other half were not. The groups were similar in terms of gender, smoking status, the reason for taking the medication, and the types of medication used.

There was no description of concealing the allocation of the treatment groups (blinding) to medical staff assessing adherence or those carrying out data analysis of the two groups. This may be a source of bias.

It wasn't possible to blind the participants to their treatment allocation – obviously, people are going to know if they are getting text messages or not.

Those in the text group had:

  • daily texts at the specified pill-taking time for the first two weeks
  • texts on alternate days for the next two weeks
  • weekly texts for 22 weeks

The participants in the text group were asked to respond to say if:

  • they had taken their medication
  • the text had reminded them as they had forgotten
  • they had not taken their medication

These responses were automatically received. A computer programme then alerted a healthcare worker to call the participant if they had not taken their medication or had not responded to the text.

During the call, the reason why the person wasn't taking their medication was discussed with a view to resolving any issues or concerns.

Medication use at six months was assessed at clinic visits in most cases, although a small group was assessed by looking at prescription records.

At the end of the trial, people who were using blood pressure-lowering medications had their blood pressure recorded, and those using lipid-lowering medication had their cholesterol measured.


What were the basic results?

By six months, more people in the text group were taking medication than in the "no text" group (91% adherence versus 75% adherence). In the text group, 65% had been reminded to take their medication on at least one occasion.

At some point during the six-month window, 15% did not take their medication on at least one occasion. The reasons for this were either:

  • uncertainty over the need for treatment
  • concern over side effects
  • another medical illness meant the medication was discontinued

This prompted a telephone discussion, after which almost all (20 out of 23) started taking their medication again. In comparison, 11% (16) of the "no text" group stopped medication.

Counterintuitively, despite the differences in adherence to the medicines, there was no difference between the groups in terms of average blood pressure or cholesterol level at the end of the trial.


How did the researchers interpret the results?

The researchers concluded that: "In patients taking blood pressure or lipid-lowering treatment for the prevention of cardiovascular disease, text messaging improved medication adherence compared with no text messaging."

They further say it may be a result of the "bidirectional texting", as this then prompted a discussion so the reasons for not taking medication "could be determined and advice provided".



This randomised study found a text messaging reminder service led to more people taking medication as prescribed.

It appears this was because not taking the medication or not responding to the text led to a discussion with a healthcare professional, which influenced people to continue taking their medicines.

The study was clearly reported and was of adequate size to find a difference between the two groups, if there was one. But, as with all studies, there are some limitations to consider.

  • The results of the study may not be applicable to everyone. The recruitment process meant the participants were already interested in receiving text prompts to remember to take their medication. There could be many reasons for this, but perhaps the most obvious one is they already recognised they sometimes forgot to take their pills and were keen on a reminder.
  • There was no clinical difference between the two groups in terms of blood pressure or cholesterol. But these measurements were only taken on one occasion at the end of the trial. As there was no baseline level, we do not know if there was any improvement in the levels because of their use of medication during the trial period.
  • The study did not blind the treatment allocation to either the clinical assessors of medicine adherence or the researchers analysing the data. Although unlikely, the medical assessors could have introduced bias into the results, especially if they had preconceived ideas about whether text messaging would help their patients. It is unlikely the data analysis was biased, as almost all the data was analysed. Only two people of the 303 starting the trial were not included in the final analysis.
  • Although plausible, these results do not automatically mean text messaging reminder services would work for all medicine regimes, such as those used to treat tuberculosis or HIV. Different regimes are likely to present different challenges and reasons for non-adherence. These may or may not be able to be addressed via a text or phone call, as was the case in this trial.

In conclusion, text message prompts similar to those used in this trial may help some people take their medicines as prescribed.

The trial also indicates it is useful to talk to your GP if you decide not to take your medication as prescribed so you can discuss the reason for this.

If the results of this trial are anything to go by, your GP may be able to reassure you, and you might be able to continue taking your medicines. Or there may be more suitable alternative medicines available, which can also be discussed.

Conditions such as high blood pressure and high cholesterol often cause no symptoms, but that does not mean they can be safely ignored. Poorly controlled cholesterol and blood pressure can trigger serious and potentially life-threatening complications, such as heart attack or stroke.

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

Links To The Headlines

Text messaging service 'helps people take their pills'. BBC News, December 6 2014

Medication text alert service 'could save millions' (video). BBC News, December 6 2014

Links To Science

Wald DS, Bestwick JP, Raiman L, et al. Randomised Trial of Text Messaging on Adherence to Cardiovascular Preventive Treatment (INTERACT Trial). PLOS One. Published online December 5 2014

Categories: Medical News

Obesity could 'rob you' of 20 years of health

Medical News - Fri, 12/05/2014 - 14:30

"Obesity knocks 20 years of good health off your life and can accelerate death by eight years," the Mail Online reports.

A study has estimated very obese men aged 20 to 39, with a body mass index (BMI) of 35 or above, have a reduced life expectancy of eight years.

This is as a result of their higher risk of cardiovascular disease and type 2 diabetes. For women of this age, the life expectancy is six years less.

What is also worrying is the much larger number of healthy years of life lost because of the chronic illness caused by these two conditions, which are obesity related.

Obesity in this age group is estimated to cause 11 to 19 fewer years of healthy life, which could have a considerable negative impact on a person's quality of life.

This is likely to be an underestimate, however, as it did not take into account other illnesses associated with increased weight, such as certain cancers, liver and kidney diseases. 

A truism is that a model is only as good as the data you put into it. Reassuringly, the researchers used a well-regarded data set.

The researchers hope these results can help healthcare professionals give people a greater understanding of how much obesity is putting people at risk of long-term chronic ill health.


Where did the story come from?

The study was carried out by researchers from the University Health Centre in Montreal, McGill University, the University of British Columbia and the University of Calgary.

It was funded by the Canadian Institutes of Health Research.

The study was published in the peer-reviewed medical journal The Lancet: Diabetes & Endocrinology.

The UK media's reporting was generally accurate, although some of the details were fudged. The Mail Online went with, "obesity knocks 20 years of good health off your life", which referred to the 18.8 and 19.1 years of life lost in very obese men and women respectively aged 20-39.

Other headlines tended to use an "eight years of life lost" figure. This referred to very obese men aged 20-39. The equivalent estimate was less for women (six years), older age groups, and for those who were overweight or obese.


What kind of research was this?

This was a modelling study to estimate how obesity affects life expectancy and the number of years of poor health that result from cardiovascular disease and type 2 diabetes.

Modelling studies are able to estimate events occurring over time in large samples of the population, which would otherwise take too many years and resources to collect. They are based on risk estimates and population data.


What did the research involve?

The researchers designed a computer model for predicting life outcomes from type 2 diabetes and cardiovascular disease, according to body mass index (BMI) and waist circumference.

A previous health model was used to predict the likelihood and outcomes of cardiovascular disease. The researchers combined this model with a new model for type 2 diabetes.

The researchers used data collected from the National Health and Nutrition Examination Survey (NHANES) to feed into the computer model. This is an ongoing cohort study, though the researchers used data from 2003-10.

They used information about adults from the US aged 20 to 79 years old. The information included BMI, gender, smoking status, blood pressure, fasting glucose and HDL cholesterol (so-called "good cholesterol").

The computer model then calculated the probability of each participant developing type 2 diabetes or cardiovascular disease each year.

The model took into account that similar risk factors increase the risk of both conditions (such as smoking) and each condition increases the risk of the other.

Once entered into the system, each year their health status could either:

  • stay the same
  • a new diagnosis could be made
  • existing disorders could cause complications or progress
  • the individual could die from type 2 diabetes, cardiovascular disease or another cause

The model went through many cycles and individuals remained in the system until death or they reached 102 years old.

The researchers then calculated the average life expectancy and healthy life expectancy free from diabetes or cardiovascular disease. They validated their results by comparing them with other models.


What were the basic results?

Healthy life years lost were two to four times higher than the total years of life lost for all age groups and body weight categories.

Very obese people consistently had the largest number of years lost and healthy years lost.

The largest life lost was in very obese women aged 20-39 years, at 19.1 years. Very obese men in the same category were the highest for healthy years lost, at 18.8 years.

The figures were consistently lower for those in the obese and overweight categories than the severely obese category.

Similarly, the years of life and years of healthy life lost estimates were generally much higher in the younger groups (20-39 years) than the older groups. This was not particularly surprising, as the risk is cumulative over a person's lifetime.

Healthy years lost compared with ideal body weight

The healthy years of life lost for obese men (BMI 30kg/m2 to less than 35kg/m2):

  • aged 20 to 39 was 11.8 years (95% confidence interval [CI] 9.9 to 13.7)
  • aged 60 to 70 was 3.9 years (95% CI 2.8 to 5.0)

The healthy years of life lost for very obese men (BMI 30kg/m2 to less than 35kg/m2):

  • aged 20 to 39 was 18.8 years (95% CI 16.8 to 20.8)
  • aged 60 to 70 was 3.9 years (95% CI 2.8 to 5.0)

The years of life lost for obese women (BMI 30kg/m2 to less than 35kg/m2):

  • aged 20 to 39 was 14.6 years (95% CI 12.0 to 17.2)
  • aged 60 to 79 was 6.3 years (95% CI 5.2 to 7.4)

The years of life lost for very obese women (BMI over 35 kg/m2):

  • aged 20 to 39 was 19.1 years (95% CI 16.7 to 21.5)
  • aged 60 to 79 was 7.3 (95% CI 6.1 to 8.5)
Life years lost compared with ideal body weight

The years of life lost for obese men (BMI 30kg/m2 to less than 35kg/m2):

  • aged 20 to 39 was 5.9 years (95% CI 4.4 to 7.4)
  • aged 60 to 79 was 0.8 years (95% CI 0.2 to 1.4)

The years of life lost for very obese men (BMI over 35 kg/m2):

  •  aged 20 to 39 was 8.4 (95% CI 7.0 to 9.8)
  •  aged 60 to 79 was 0.9 (95% CI 0 to 1.8)

The years of life lost for obese women (BMI 30kg/m2 to less than 35kg/m2):

  • aged 20 to 39 was 5.6 years (95% CI 4.1 to 7.1)
  • aged 60 to 79 was 1.6 years (95% CI 0.8 to 2.4)

The years of life lost for very obese women (BMI over 35 kg/m2):

  • aged 20 to 39 was 6.1 years (95% CI 4.6 to 7.6)
  • aged 60 to 79 was 0.9 (95% CI 0.1 to 1.7)


How did the researchers interpret the results?

The researchers concluded that, "When the effect of living with a chronic illness such as type 2 diabetes or cardiovascular disease is considered, healthy life years lost were two to four times greater than total years of life lost and, in some instances, as much as eight times greater."



This modelling study has shown estimates of the number of years of poor health associated with type 2 diabetes and cardiovascular disease is much higher than the number of years lost because of the conditions.

The researchers hope these results can help healthcare professionals give people a better understanding of how much obesity is putting people at risk of long-term chronic ill health.

The results of this model show the risks are greatest for younger people and increase with higher levels of obesity.

But there are some limitations to take into account when considering this study:

  • The participants were all of white ethnicity, so the results may not be applicable to people of different ethnic backgrounds, especially as diabetes prevalence can vary by ethnicity.
  • The model did not take into account other illnesses associated with increased weight, such as certain cancers, liver and kidney diseases, so may underestimate the number of life years and healthy years lost.
  • The results are estimates at a population level, and they should not be used to predict an individual's likely health or life outcomes.

This study highlights the pressing need for obesity to be tackled to reduce the years of likely chronic illness and premature death rates from type 2 diabetes and cardiovascular disease. There is no quick fix for obesity, but the first steps to weight loss can be found here.

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

Obesity knocks 20 years of good health off your life and can accelerate death by eight years. Mail Online, December 5 2014

Obesity will take eight years off your life, study says. The Independent, December 5 2014

Obesity reduces life expectancy by eight years, scientists claim. Daily Express, December 5 2014

Links To Science

Grover SA, Kaouache M, Rempel P, et al. Years of life lost and healthy life-years lost from diabetes and cardiovascular disease in overweight and obese people: a modelling study. The Lancet Diabetes & Endocrinology. Published online December 5 2014

Categories: Medical News

More breastfeeding 'would save NHS millions'

Medical News - Fri, 12/05/2014 - 13:30

"Increase in breastfeeding could save NHS £40m a year," The Independent reports after a recent economic modelling study projected a reduction in childhood diseases and breast cancer rates would lead to considerable savings for the health service.

Proven key benefits – and potential savings – associated with breastfeeding a baby include a reduced risk of bowel infection (gastroenteritis), lower respiratory tract infection (bronchiolitis), middle ear infection (otitis media) and an uncommon, but serious, condition called necrotising enterocolitis (bowel tissue death).

Breastfeeding also brings benefits to the mother, such as a reduced risk of breast cancer.

Increasing breastfeeding rates in neonatal units from 35% to 75% could save £6 million per year by reducing the incidence of necrotising enterocolitis, according to the study.

In the general population, if the percentage of women who breastfed for at least four months increased from 7% to 45%, the NHS would save £11 million per year from a reduction in the types of common infant conditions described above.

Similarly, the same increase could result in NHS savings of around £21 million related to breast cancer alone over the course of a first-time mothers' lifetime.

While the figures presented in the study are only estimates, it would certainly seem breastfeeding is not only good for mother and baby: it is also good for the NHS.


Where did the story come from?

The study was carried out by researchers from Brunel University, London and was funded by Unicef UK.

It was published in the peer-reviewed medical journal Archives of Disease in Childhood on an open access basis, so it is free to read online or download.

The UK media has reported the findings of the analysis accurately, though the difference between annual savings and savings over the course of a lifetime was not made as clear as it should have.


What kind of research was this?

This research used economic modelling to estimate the potential cost savings that could be made if more women breastfed.

The researchers tell us the number of women starting to breastfeed has increased over the last 20 years to around 81% in 2010, up from 62% in 1990.

But this figure hides the fact rates of breastfeeding exclusively by six weeks are low (23% in 2010), and that most women who start have to stop before they want to as a result of problems.

Using breast milk substitutes is associated with an increased risk of breast cancer in the mother and four illnesses in infants:

  • bowel infection (gastrointestinal infection)
  • lower respiratory tract infection (bronchiolitis)
  • middle ear infection (acute otitis media)
  • bowel tissue death in preterm infants (necrotising enterocolitis) – the other three conditions are common, but this is rarer, developing in around 0.3-2.4 cases per 1,000 live births

The researchers aimed to show how many cases are likely to be a result of not breastfeeding, using the relative risk for each illness and how much this is costing the NHS. They then aimed to show what effect raising the rate of breastfeeding by varying amounts would have.


What did the research involve?

The researchers identified the five illnesses increased by using breast milk substitutes by looking at systematic reviews.

They used NHS figures from 2009-10 to calculate the cost of treatment for each condition. They then calculated the likely numbers that were related to using breast milk substitutes.

UK breastfeeding rates were taken from the 2005 Infant Feeding Survey. The researchers then calculated how many fewer cases of the five illnesses would occur if the rate of breastfeeding increased.

They used a mixed bag of definitions of breastfeeding, including "exclusive breastfeeding at four months" and "any breastfeeding at six months". From these figures, they calculated how much the NHS might save per year.


What were the basic results?

Overall, if the proportion of women exclusively breastfeeding for at least four months increased from 7% to 45%, the NHS would save £11 million per year for the three reduced infant infections.

Increasing the breastfeeding in neonatal units from 35% to 75% could save £6.12 million per year by reducing the incidence of necrotising enterocolitis.

To save £21 million from breast cancer, breastfeeding rates for women would have to halve the number who have never breastfed (from 32% to 16%) and double the number of women who breastfeed for 7 to 18 months (from 16% to 32%).

If the health gains for women using National Institute for Health and Care Excellence (NICE) figures for Quality of Life Years is added, the widely reported saving of £31 million is estimated.


How did the researchers interpret the results?

The researchers concluded that, "Increasing the current breastfeeding rates is likely to generate substantial cost savings to the NHS in the UK; the actual amounts saved will depend on the extent of the increase and the effectiveness of interventions."

They say that, "While the cost of these interventions must be considered, the potential savings indicate that substantial further investment has a strong economic case."



This economic model estimates that increasing the number of women who start and continue to breastfeed would save the NHS tens of millions of pounds.

These savings would come through reduced incidence of three infectious diseases that occur in infancy, reducing the number of newborns who have necrotising enterocolitis, and reducing the incidence of maternal breast cancer, all of which are beneficial to the health of mother and baby.

But these savings, as with all economic models, have been calculated using a number of assumptions, including the estimated rate of breastfeeding in the UK, which was taken from 2005 figures. 

As the Infant Feeding Survey is conducted every five years, it is unclear why the more recent figures from the 2010 survey were not used.

The 2010 survey indicated the UK rate of breastfeeding for four months has already increased from 7% to 12%. Using this updated figure would clearly reduce the estimated cost savings.

Although it is encouraging that breastfeeding rates appear to be on the increase in the UK, we are still very far behind other developed countries, such as Australia, where the rate of exclusive breastfeeding at three months was 39% in 2010.

If you are able to breastfeed, the benefits to you and your baby are numerous:

  • breast milk is the only natural food designed for your baby
  • breastfeeding protects your baby from infections and diseases
  • breast milk provides health benefits for your baby
  • breastfeeding provides health benefits for mum
  • it's free
  • it's available whenever and wherever your baby needs a feed
  • it's the right temperature
  • it can build a strong physical and emotional bond between mother and baby
  • it can give you a great sense of achievement

This economic analysis indicates that not only would increasing the rate of breastfeeding be beneficial for the health of mothers and babies, it could save the NHS tens of millions of pounds.

If you are having problems breastfeeding or you are expecting a baby and want to learn more about breastfeeding, the breastfeeding section of our pregnancy and baby guide may help.

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

Links To The Headlines

Increase in breastfeeding could save NHS £40m a year, claim health economists. The Independent, December 5 2014

More breastfeeding 'could save NHS millions'. BBC News, December 5 2014

More mothers should breastfeed for 18 months to save NHS money, say researchers. The Daily Telegraph, December 4 2014

Breastfeed Longer To Save NHS Cash, Study Says. Sky News, December 5 2014

Mothers who breastfeed for longer could save the NHS £50m a year by preventing childhood illness and breast cancer, claim academics. Mail Online, December 4 2014

Breastfeed for longer and save the NHS £40m. The Times, December 5 2014

Links To Science

Pokhrel S, Quigley MA, Fox-Rushby J, et al. Potential economic impacts from improving breastfeeding rates in the UK. Archives of Disease in Childhood. Published online December 4 2014

Categories: Medical News

Drug found to help repair spinal cord injuries

Medical News - Thu, 12/04/2014 - 15:00

“Renewed hope for patients paralysed by spine injuries,” The Independent reports.

This hope is due to the possibility of developing a new drug based on a molecule called intracellular sigma peptide. The drug helped restore varying degrees of nerve functions in rats that had spinal cord injuries.

The spinal cord is a cable of nerve cells that transmits signals from the brain to the rest of the body. Damage to the spinal cord can result in paralysis; the higher up the injury occurs, the greater the degree of paralysis.

In this study, researchers identified some of the processes that create a barrier to nerves being able to sprout out through the nerve scar tissue. This sprouting could potentially repair the injury. They then developed a drug that could cause a disruption to this barrier.

Rats with a spinal cord injury were given a daily injection of the drug for seven weeks, 11 weeks after the injury, 21 out of 26 rats had regained some function in their bladder and/or hind legs.

Further tests will be conducted to see if the drug can be made more effective. Longer-term tests will be required to look for any side effects before any human studies can be performed.


Where did the story come from?

The study was carried out by researchers from Case Western Reserve University in Ohio, Ohio State University, the University of Manitoba in Canada and other US institutes. It was funded by the National Institute of Neurological Disorders and Stroke, the Case Western Reserve University Council to Advance Human Health, Unite to Fight Paralysis, the Brumagin Memorial Fund, Spinal Cord Injury Sucks, United Paralysis Foundation and the Kaneko Family Fund.

The study was published in the peer-reviewed journal Nature.

The research was accurately reported by the UK media. However, some of the headlines were a little premature, as the novel drug needs to undergo a significant amount of animal testing before it could progress to any human trials.


What kind of research was this?

This was an animal study, which aimed to test a new approach to nerve regrowth after a spinal injury.

Normally, part of the scar tissue that is formed around the nerves creates a barrier, preventing nerve regrowth. Recent research identified a protein that can inhibit too much of this scar tissue from forming.


What did the research involve?

The research involved several laboratory experiments, using nerves from rats and mice to determine the function of several proteins involved in nerve regeneration. This increased the researchers’ understanding of which proteins were stimulating unhelpful growth of certain nerve cells that were stopping normal growth.

The researchers then developed a molecule called intracellular sigma peptide (ISP) that could bind to a receptor to stop the unwanted growth. A second molecule called LAR wedge-domain peptide (ILP) was also identified, which naturally bound to the receptor, but less strongly.

Using the results of these tests, the researchers moved on to an animal experiment. Rats had a spinal cord injury inflicted on them (a “dorsal column crush”), which caused damage between the nerves of the bladder and the brainstem. This prevented them from being able to urinate very often, causing an increased volume of urine to collect in the bladder.

The injury also prevented them from moving their hind legs. 

The day after the spinal cord injury was inflicted, rats were given a daily subcutaneous injection (just under the skin of the back, just above the level of the injury) for seven weeks, of either:

  • ISP
  • ILP
  • placebo (a dummy treatment)

The researchers compared the three groups of rats 12 weeks after injury to determine nerve regrowth in terms of:

  • the frequency of urination and amount of fluid in the bladder
  • the ability to move their hind legs


What were the basic results?

Some form of functional recovery was seen in 21 out of the 26 rats treated with ISP.

Rats given ISP were able to urinate twice as frequently as rats given the placebo. They also had significantly less urine accumulating in the bladder.

Of the rats treated with ISP, 10 out of 15 had developed some bladder muscle co-ordination compared to none of the rats treated with ILP or placebo. This indicated a degree of normal nerve regrowth and connections.

30% of the ISP-treated rats were able to walk with “coordinated stepping” using their hind legs by week 11. There was also some recovery of coordination and balance. The rats given ILP or placebo were only able to do occasional weight bearing by this time.

The researchers report that the ISP-treated rats did not experience neuropathic pain (pain from the damaged nerves).


How did the researchers interpret the results?

The researchers concluded that “Systemic modulation of PTPσ [the receptor] opens a new therapeutic avenue in non-invasive treatments for enhancing functional recovery after a variety of injuries or diseases in which proteoglycans inhibit the attempt of axons [nerve cell fibres] to regenerate or sprout.”

In other words, the injection of ISP can improve normal regrowth of the nerves at the site of injury in rats.



This exciting piece of research has found that the immediate treatment of spinal cord injuries using a newly-developed molecule can improve nerve regeneration, leading to some functional recovery in rats. The drug appears to work by disrupting the unhealthy pattern of scar tissue that develops and usually stops nerves from growing and lengthening, instead forming tight knots.

The tests performed on rats appear to show that injections of the drug following a spinal cord injury led to improved bladder function, walking ability and balance.

The researchers report that the rats did not develop neuropathic pain, which often happens when damaged nerves do not grow back normally. They also did not report any side effects with the treatment, aside from some inflammation at the injection site. When the research gets to the point of human trials, the accuracy of these observations will be much easier to determine, but this is a long way off.

Further tests will now be conducted to see why the drug did not work for five of the rats and to determine the optimal dose. Longer-term tests will also be required to look for any side effects that may occur with this treatment before any human studies can be performed. 

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

Drug can repair spinal cord injuries, study shows. BBC News, December 4 2014

Renewed hope for patients paralysed by spine injuries. The Independent, December 3 2014

Major breakthrough for paralysed people after drug that restores movement shows 'extraordinary promise'. Mail Online, December 3 2014

New drug could help millions with spine damage walk again. Daily Express, December 3 2014

Links To Science

Lang BT, Cregg JM, DePaul MA, et al. Modulation of the proteoglycan receptor PTPσ promotes recovery after spinal cord injury. Nature. Published online December 3 2014

Categories: Medical News

Nitrate-rich leafy greens 'good for the heart'

Medical News - Thu, 12/04/2014 - 14:30

“Leafy vegetables contain chemical nitrate that improves heart health,” the Mail Online reports. In a recent study, researchers looked at the effects of a nitrate-rich diet on rats.

Nitrate is a chemical that can react to a number of different substances in a range of ways. For example, it can be used as a fertiliser or as the active ingredient in a bomb. Some nitrates are used as medication for angina, as they dilate the blood vessels.

This study found that rats given nitrate had lower levels of red blood cells (which carry oxygen) compared to a control group. This was associated with a reduction in the hormone erythropoietin (EPO), which regulates red blood cells.

Excessive amounts of red blood cells (polycythaemia) can sometimes trigger blood clots.

Blood clots can sometimes lead to serious complications, such as a stroke.

This study found that increasing nitrate in your diet stops low oxygen levels causing the over-production of EPO. The increased nitrate optimises the production of EPO from the liver and kidneys, which in turn reduces the blood’s thickness, but without compromising oxygen supply.

While the study involved rats not people, it’s always a good idea to eat up your greens. They contain a number of nutrients thought to help prevent cancer and heart disease.


Where did the story come from?

The study was carried out by researchers from the Universities of Cambridge and Southampton. It was funded by the British Heart Foundation, the Research Councils UK, the WYNG Foundation of Hong Kong, the European Union Framework 7 Inheritance project, the Wellcome Trust and the University of Southampton.

The study was published in the peer-reviewed Journal of the Federation of American Societies for Experimental Biology.

The reporting in the Mail Online and the Daily Express appears to be based on a press release that combined the findings of three related studies on nitrates:

  • The study we are analysing today (we chose this, as it is the most recent research).
  • study on the effects that nitrates have on how efficient the heart is in pumping blood around the body.
  • study into whether nitrates could have a protective effect against obesity and type 2 diabetes.

The reports in both the Express and the Mail overstate the results of all the studies, including the one we are discussing today. Neither paper mentioned that these were laboratory studies carried out in rats. Perhaps this is not surprising, given that the accompanying press release – and the authors quoted by it – did not mention it either.


What kind of research was this?

This was a laboratory study, which looked at the effect of nitrate supplementation on the red blood cells of rats.

EPO is responsible for regulating red blood cells in mammals, to meet the need for oxygen. In conditions of severe oxygen shortage, such as during critical illness and at high altitude, EPO increases, stimulating the production of more oxygen-carrying red blood cells.

While red blood cells are needed to supply enough oxygen, they can also lead to an increase in the blood’s “viscosity” or thickness, which may impair blood flow, as happens in chronic obstructive pulmonary disease, preventing it from flowing through small blood vessels in the lungs.

There is also the risk of a blood clot developing, which can lead to serious complications, such as a heart attack, stroke or pulmonary embolism.

A balance therefore needs to be met to get the optimum number of red blood cells and oxygen around the body.

Nitrate has already been shown to have beneficial effects on the heart and circulation. Here, the researchers wanted to test the theory that dietary nitrate might limit rises in the red blood cells needed for oxygen delivery by improving the efficiency of the body’s use of oxygen.


What did the research involve?

Two rat studies were performed to assess the effect of dietary supplementation with nitrates.

The first involved 40 rats. Half of them had nitrate added to their drinking water, while the other half acted as a control group with no supplementation. After four days, both groups were put in a chamber of low oxygen (12% rather than normal air, which is 21%). They continued to have either nitrate supplement or no supplement for 14 days.

The researchers compared their food and water intake, any change in body weight and plasma nitrate and haemoglobin (oxygen carrying component of red blood cells) levels in normal air and in low oxygen.

The second study aimed to see how fast and at what concentration the nitrate made changes to the haemoglobin levels. 24 rats were kept in normal oxygen conditions. After 12 days, half the group had their water supplemented with 0.7mm of nitrate. They measured the haemoglobin level in the blood after 0, 2, 4, 6, 9 and 12 days.


What were the basic results?

The researchers report that in both experiments rats given nitrate had lower concentrations of red blood cells in normal and low oxygen conditions compared with control groups.

They found that these rats also had lower levels of EPO. They say this suggests that the effects of nitrate were mediated via changes in EPO production.

The researchers found that nitrates reduced the amount of EPO released by the liver, but increased the amount released by the kidneys. They report that this balance meant that the nitrates were able to help the body produce the optimum minimum amount of haemoglobin that they required.

Nitrate supplementation did not alter the amount of food or water intake of the rats, or on their weight or growth.


How did the researchers interpret the results?

They conclude that nitrate acts to suppress the production of EPO by the liver, thereby lowering circulating red blood cells. Nitrate prevented an expected rise in circulating red blood cells in rats deprived of oxygen and also decreased red blood cells in rats with a normal oxygen supply.

They point out that nitrate levels used are readily achievable in humans via the diet, through eating green leafy vegetables.

In an accompanying press release, co-author Professor Martin Feelisch, from the University of Southampton, said: "These findings suggest simple dietary changes may offer treatments for people suffering from heart and blood vessel diseases that cause too many red blood cells to be produced. It is also exciting as it may have broader implications in sport science, and could aid recovery of patients in intensive care by helping us understand how oxygen can be delivered to our cells more efficiently."



It’s always a good idea to eat up your greens. This research suggests that one possible benefit is through the mechanism of nitrate “thinning” the blood and protecting against heart disease.  While the research is interesting, it’s a pity that no one thought to mention that this was a laboratory study on rats. It is important to remember that high levels of nitrates can be toxic, which is why there are safety limits for the level of nitrates in drinking water. High nitrate levels are especially harmful for infants.

A healthy diet – including plenty of vegetables – and regular exercise are important for a healthy heart and weight.

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

Links To The Headlines

Now there's no excuse not to eat your greens: Leafy vegetables contain chemical nitrate that improves heart health and combats diabetes. Mail Online, November 4 2014

Eat up your greens and slash the risk of diabetes and obesity. Daily Express, November 4 2014

Links To Science

Ashmore T, Fernandez BO, Evans CE, et al. Suppression of erythropoiesis by dietary nitrate. The FASEB Journal. Published online November 24 2014

Categories: Medical News

Do time-restricted eating habits reduce obesity?

Medical News - Thu, 12/04/2014 - 12:00

“Want to lose weight? Eat all your food in an eight-hour time frame – and never snack at night,” reports the Mail Online. However, these tips are based on a mouse study – no humans were involved.

Nearly 400 mice were studied in a series of experiments for up to 26 weeks. Sets of mice were given unrestricted 24-hour access to high-fat food, high-fat and high-sugar food or low-fat, high-fruit sugar foods. Their weight gain was compared to mice given the same types of food, but restricted to 9, 12, or 15 hours per day.

Mice ate the same number of calories per day irrespective of the number of hours they had access. All mice on high-fat or high-fat and high-sugar diets gained a large amount of weight regardless of access timescales. However, those with time-restricted access gained less weight.

The current stage of this research has limited application for people. We already know that high-fat and high-sugar diets cause weight gain, as was found here. It may be that future randomised controlled trials in humans will show that the amount of weight gain is more if the calories are consumed at times which do not make the most of our natural metabolic rhythm. However, despite the continued quest to “have your cake and eat it”, at present the best advice to combat obesity is to eat a balanced diet and to take regular exercise.


Where did the story come from?

The study was carried out by researchers from the Salk Institute for Biological Studies in La Jolla and the University of California. It was funded by the US National Institutes for Health, grants from the American Federation for Aging Research, Leona M and Harry B Helmsley Charitable Trust, the Glenn Center for Aging, the American Diabetes Association, the Philippe Foundation and the American Association for the Study of Liver Diseases.

The study was published in the peer-reviewed medical journal Cell Metabolism.

BBC News reported the story accurately; however, the Mail Online’s report was misleading. Its headline implies this study was conducted on humans, when it was only on mice. It also says that people should stop “eating after 4pm”. The restricted feeding times used in this study were for mice with nocturnal eating habits. There is no evidence from this study that weight gain would be avoided in people if we stopped eating at 4pm.


What kind of research was this?

This was a piece of animal research that aimed to look at whether restricting the timing of feeding could prevent weight gain or cause weight reduction in obese mice.

Obesity rates are increasing at an alarming rate and traditional methods of weight control – such as calorie restriction, change in diet and increase in exercise – are hard for many people to adhere to.

A person’s metabolic rhythm changes over the course of the day. Previous research has shown that this rhythm is heavily dependent on eating at the same time each day. Therefore, the researchers wanted to see if sticking to the optimal time of eating within this rhythm would prevent weight gain. They called this time-restricted feeding (TRF). As this study was conducted on mice, the optimal nine-hour feeding time was chosen to be during the night.

Research such as this is a good starting point for understanding the biological processes within an animal’s body, and seeing what can influence this, but we don’t know that the results will be directly applicable to people.

As the researchers conclude, a randomised controlled trial in people would be required.


What did the research involve?

The researchers used 392 male wild-type mice aged 12 weeks for a series of experiments lasting up to 26 weeks.

The mice were given free access to food 24 hours a day or TRF for either 9, 12 or 15 hours overnight. Some mice were switched from one type of access to the other.

The mice were given one of the following types of diets:

  • high-fat (32%), high-sucrose (25% table sugar) diet
  • high-fat (62%) diet
  • low-fat (13%) and fructose (60% fruit sugar) diet
  • normal chow diet

The weights of the mice on each regime and diet were compared. Further studies looked at the effect of obese mice switching to TRF regimes.


What were the basic results?

Mice fed a high-fat, high-sucrose diet for 12 weeks gained at least a fifth of their body weight. Weight gain doubled if they could eat at any time, despite eating the same number of calories:

  • 9 hours of access caused 21% weight gain
  • 24-hour access caused 42% weight gain

Mice fed a high-fat diet had higher weight gain with longer periods of food accessibility, despite consuming the same number of calories:

  • 9-hour access caused 26% weight gain
  • 15-hour access caused 43% weight gain
  • 24-hour access caused 65% weight gain

To measure whether a “lapse” in TRF had any effect, mice were fed a high-fat diet for five days using TRF and two days of unrestricted feeding (to mimic the two-day weekend). They gained 29% body weight over 12 weeks, similar to the weight gain without the lapse.

Mice fed a low-fat, high-fructose diet had a 6% weight gain in both feeding situations over 12 weeks, which was similar to control mice fed a normal chow diet.

Mice fed a high-fat diet for 13 weeks using TRF and then given 24-hour access for 12 weeks, rapidly gained weight after switching so that they gained the same amount of weight as mice with unrestricted access for the whole 15 weeks (111% to 112% body weight). A control set who had TRF for the 25 weeks gained 51% body weight.

In mice with pre-existing dietary-induced obesity from having 24-hour access to a high-fat diet, switching to TRF caused them to consume the same number of calories within a few days. However, they lost weight:

  • switching from 13 weeks of unrestricted access to 12 weeks TRF caused a drop in weight from 40g to 38g (5% body weight loss)
  • switching from 26 weeks of unrestricted access to 12 weeks TRF caused a drop in weight from 53.7g to 47.5g (12% body weight loss)

MRI images showed that the difference in body weight for all of these experiments was due to fat mass rather than lean body mass. There were also inflammatory markers in the fatty tissue of mice with round the clock access compared to no inflammatory markers in TRF mice.


How did the researchers interpret the results?

The researchers concluded that these “results highlight the great potential for TRF (time-restricted feeding) in counteracting human obesity and its associated metabolic disorders”. They believe “it is worth investigating whether the physiological observations found in mice apply to humans” and say that “a large-scale randomised control trial investigating the role of TRF would show whether it is applicable to humans”.



Time-restricted feeding caused less weight gain than all-hour access for mice eating a high-fat, high-sugar diet over 12 to 26 weeks. It also led to weight loss of up to 12% when applied to mice that were already obese. TRF does not appear to have an influence on weight gain for mice eating a healthy or normal diet.

The current stage of this research means it has limited application for humans. We already know that high-fat and high-sugar diets cause weight gain, as was found here. It may be that future randomised controlled trials in humans will show that the amount of weight gain is more if the calories are consumed at times that do not make the most of our natural metabolic rhythm.

Even if the timing of eating patterns do have an effect on weight gain, we suspect that any beneficial effects would be modest. If you regularly consume high-fat and high-sugar foods, and do not exercise, you will put on weight regardless of any time-restricted eating habits. Sadly, there is no quick fix to weight loss.

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

Links To The Headlines

Why late night dining may encourage weight gain. BBC News, December 2 2014

Eat within 12-hour window to lose weight, say scientists. The Daily Telegraph, December 2 2014

Want to lose weight? Eat all your food in an eight-hour time frame - and NEVER snack at night. Mail Online, December 3 2014

Links To Science

Chaix A, Zarrinpar A, Mu P, et al. Time-Restricted Feeding Is a Preventative and Therapeutic Intervention against Diverse Nutritional Challenges. Cell Metabolism. Published online December 2 2014

Categories: Medical News

NICE recommends home births for some mums

Medical News - Wed, 12/03/2014 - 14:00

Home births have dominated the UK media today, following the publication of guidance by the National Institute for Health and Care Excellence (NICE) on the care of healthy women and their babies during childbirth. The main talking point was the recommendation that women thought to have a low risk of pregnancy complications would be better served by giving birth at home or at a midwife-led unit, rather than at hospital.

NICE has reviewed the evidence for the vast majority of pregnant women in England and Wales who have healthy, uncomplicated pregnancies. The rate of interventions, such as the use of forceps or a caesarean section, in these low-risk women are generally slightly lower in the home or midwife-led units, compared with hospital-based maternity wards.

For women having their second or subsequent baby, a birth in either the home or a midwife-led unit are equally safe options. However, for low-risk first-time mothers, the midwife-led unit may be the best choice.

No woman will be “forced” to give birth at home or a midwife-led unit. NICE advises that all low-risk women should be free to choose their birth setting, and be supported in this choice.  


Who does the new guidance cover?

This new guidance focuses on the care of healthy women with uncomplicated pregnancies and low risk of complications. This represents the majority of pregnant women and childbirth in this country.

According to NICE, about 700,000 women give birth in England and Wales each year, around 40% of whom are having their first baby. The majority of these women will have a straightforward pregnancy and birth – around 90% giving birth at full term (over 37 weeks of pregnancy) to a single baby who is presenting head first. Around two-thirds of women will also go into labour spontaneously (without needing to be induced).


What was the media reaction to the guidelines?

Media reaction to the guidelines has been mixed. Some news organisations, such as The Guardian, have been broadly supportive, emphasising the benefits of home or midwife-led unit births, such as a lower risk of interventions, which include caesarean sections. Others, such as the Daily Mirror, have taken a more negative tone, implying that the guidelines have been influenced by concerns that some hospitals are under-resourced or are unsafe to handle cases of labour.

Claims by the Mail Online that “new rules” have been introduced are also misleading. As mentioned, all women will have the choice of where they want to give birth.


What do NICE say about the safety of home compared to hospital births?

NICE has compared the outcomes for “low-risk” women giving birth in four different settings: the standard hospital maternity (obstetric) unit, alongside midwifery units (separate midwife-led units alongside an obstetric unit), a freestanding midwifery unit and birth at home.

When looking at rates per 1,000 women, they found that most outcomes were generally similar or slightly better in the home, compared to the hospital setting. Results included the following:

  • Rates of spontaneous (not induced) vaginal birth were broadly the same in all settings, though slightly higher at home and in freestanding units. For multiparous mothers (i.e. women who have already had at least one baby) rates were 984 per 1,000 at home, 980 at a freestanding midwifery unit (FMU), 967 at an alongside midwifery unit (AMU) and 927 in a hospital obstetric unit. For first-time mothers, rates were 794 at home, 813 FMU, 765 AMU and 688 at hospital.
  • Use of epidural or spinal anaesthesia for pain relief was lower at home compared to other settings: for multiparous mothers, 28 per 1,000 at home, 40 at FMU, 60 at AMU and 121 in hospital. For first-time mothers, 218 at home, 200 FMU, 240 AMU and 349 at hospital.
  • Instrumental delivery rates (i.e. use of forceps or ventouse): for multiparous mothers, 9 per 1,000 at home, compared with 12 in FMU, 23 in AMU and 38 in hospital. For first-time mothers, 126 at home, 118 FMU, 159 AMU and 191 at hospital.
  • Rates of caesarean: for multiparous mothers, 7 per 1000 with planned home birth, 8 for FMU, 10 for AMU and 35 for planned hospital births. For first-time mothers, 80 for planned home birth, 69 at FMU, 76 at AMU and 121 for planned hospital births. 

When looking at outcomes for the baby, there was no difference in rates of complications between birth settings for babies born to multiparous women:

  • Babies born without serious medical problems: 997 per 1,000 babies of planned home birth, 997 for FMU, 998 for AMU and 997 for planned hospital births.
  • Babies born with serious medical problems (e.g. breathing in meconium, or brain problems): 3 per 1,000 babies of planned home birth, 3 for FMU, 2 for AMU and 3 for planned hospital births.

For babies born to first-time mothers, there were four extra babies born with serious medical problems:

  • Babies born without serious medical problems: 991 per 1,000 babies of planned home birth, 995 per 1,000 babies for all other settings.
  • Babies born with serious medical problems: nine per 1,000 babies of planned home birth, five per 1,000 babies for all other settings.

Therefore, birth in a hospital obstetric unit is generally associated with slightly higher rates of interventions and lower rates of spontaneous vaginal birth, compared to the other settings. While a number of possible reasons for the slightly higher rate of interventions in hospital have been discussed (such as women finding the hospital setting more stressful), none have been proven. Further research is therefore required.

For multiparous women, either at home or a in midwife-led unit are equally safe. However, for low-risk first-time mothers, the finding that four extra babies per 1,000 are born with serious medical problems with home births compared to other settings suggests that the midwife-led unit may be the best option for them.


What does NICE recommend?

A summary of the main guideline recommendations in terms of patient care, on place of birth, are as follows:

  • Explain to both multiparous and first-time mothers that they may choose any birth setting (home, FMU, AMU or hospital obstetric unit), and support them in their choice of setting wherever they choose to give birth.
  • Advise low-risk multiparous women that planning to give birth at home or in a midwifery-led unit is particularly suitable for them, because the rate of interventions is lower and the outcome for the baby is no different compared with an obstetric unit.
  • Advise low-risk first-time mothers that planning to give birth in a midwifery-led unit is particularly suitable for them, because the rate of interventions is lower and the outcome for the baby is no different compared with an obstetric unit.
  • Explain that if they plan their birth at home, there is a small increase in the risk of an adverse outcome for the baby.



NICE concludes that for low-risk women, whether having their first or subsequent baby, birth is generally very safe for both mother and baby, and they should be free to choose any of the four birth settings and be supported in their choice.

As their findings suggest, it is important that the woman is able to make a fully informed decision, by being given all the relevant information about birth in the different settings – including, as Professor Mark Baker of NICE states: “Where and how a woman gives birth to her baby can be hugely important to her. Although women with complicated pregnancies will still need a doctor, there is no reason why women at low risk of complications during labour should not have their baby in an environment in which they feel most comfortable.” He suggests that the new guidance “will encourage greater choice in these decisions and ensure the best outcomes for both mother and baby”.

As Susan Bewley, Professor of Complex Obstetrics at King’s College London, importantly highlights, women should not feel pressured into giving birth outside of a hospital if this is not their preference: “If a woman would prefer to have her baby in a hospital because it makes her feel ‘safer’, that is also her right. Giving birth is a highly personal experience and there is no ‘one size fits all’ model that suits all women.

“What’s important is that women and their families are given the most up-to-date information based on the best available evidence, so that they can make an informed decision about where the mother gives birth to her child.”

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

Home births are 'best for many mothers'. BBC News, December 3 2014

New NHS guidance could mean thousands more home births. The Independent, December 3 2014

Doctors are not needed at births, says NHS. The Daily Telegraph, December 3 2014

Home safer than hospital for birth, mothers told. The Times, December 3 2014

More mothers 'should be having their baby at home': New rules say half of women who give birth are at such low risk of problems they don't need to visit labour ward. Daily Mail, December 3 2014

Low-risk pregnant women urged to avoid hospital births. The Guardian, December 3 2014

Mums-to-be warned 'have your baby at home - it's SAFER' by health chiefs. Daily Mirror, December 3 2014

Women should give birth at home or in midwife-led centres advises NHS. Daily Express, December 3 2014

Categories: Medical News

Weight loss surgery 'not a quick fix' for good health

Medical News - Tue, 12/02/2014 - 18:43

"Weight loss surgery isn't just a quick fix to becoming healthy – you have to exercise too," the Mail Online reports.

Weight loss surgery, such as fitting a gastric band, usually results in significant weight loss.

But this weight loss doesn't automatically lead to improvements in important markers for metabolic health, such as insulin sensitivity. A low level of insulin sensitivity is a major risk factor for type 2 diabetes.

In a new study, 128 adults were randomised into two groups. One group received a six-month moderate exercise programme, while the other received a six-month health education programme.

After six months, those that followed the exercise programme had better insulin sensitivity than those following the educational programme.

But the picture was not completely clear. Quite a few people dropped out of the study or did not adhere to the six-month exercise programme fully.

This could mean the programme as a whole would not yield any significantly better improvements at a population level. This balance of cost and benefit influences whether a supervised exercise plan would (or should) be funded on the NHS.


Where did the story come from?

The study was carried out by researchers from the University of Pittsburgh, East Carolina University and Florida Hospital in the US.

It was funded by the US National Institutes of Health.

The study was published in The Journal of Clinical Investigation, a peer-reviewed medical journal, on an open access basis, so it is free to read online or download as a PDF.

The Mail Online's coverage of the science was generally accurate, although they did not discuss the issues around compliance to the exercise programme. 


What kind of research was this?

This was a single-blinded, prospective, randomised clinical trial (RCT) to find out whether, after weight loss surgery, an exercise programme improved insulin sensitivity, compared with a health education programme.

A single-blinded RCT means the researchers analysing the data at the end of the trial did not know what programme each individual was assigned to.

The study reports weight loss surgery can result in dramatic weight loss and helps partially cure type 2 diabetes in a large percentage of obese patients.

However, it seems their insulin sensitivity does not return to healthy levels, despite significant weight loss.

Insulin helps lower blood glucose levels. How sensitive the body is to insulin (insulin sensitivity) varies from person to person.

People with type 2 diabetes are not very sensitive to insulin (insulin resistant), meaning they need more insulin to lower their blood sugar levels than someone who is more insulin sensitive.

Insulin sensitivity is often used as an indicator of how well the body is regulating blood glucose levels and can be a sign of diabetes.

The researchers thought exercise might help insulin sensitivity in patients after weight loss surgery, so they designed the trial to test this theory.


What did the research involve?

The researchers randomised 128 mainly female adult volunteers who had recently undergone weight loss surgery into two groups.

One group was assigned a six-month semi-supervised moderate exercise programme (66 people), while the other group was assigned a health education programme over a similar period to act as a control group (62 people).

After six months, the researchers compared the two groups for insulin sensitivity, fitness and body composition.

All participants had a Roux-en-Y gastric bypass within one to three months of the study's start date. This procedure involves creating a small pouch at the top of the stomach.

This pouch is then connected directly to a section of the small intestine, bypassing the rest of the stomach and bowel, so it takes less food for a person to feel full.

The Roux-en-Y gastric bypass was described in the research as the most commonly performed weight loss surgery in the US.

Participants had to be aged between 21 and 60 to be included in the study. They were excluded if they had a diagnosis of diabetes, hypertension, anaemia, hypothyroidism, elevated liver enzymes, current malignancy or a history of cancer within the past five years.

They were also excluded if they had had a stent placement within the past three years, or if they had a history of myocardial infarction, angioplasty, angina, liver disease or neuromuscular disease.

The exercise intervention was three to five exercise sessions per week, with at least one directly supervised session a week to ensure that target exercise intensity and duration was achieved.

Participants used a heart rate monitor and recorded detailed logs of their exercise sessions, including the type of exercise, duration and average heart rate.

Exercise was built up gradually, but they were aiming to achieve a minimum of 120 minutes of exercise a week for the last three months of the intervention.

The health education control group was asked to attend six health education sessions. The sessions were held once a month, and involved lectures, discussions and demonstrations providing up-to-date information on topics such as medication use, nutrition and upper body stretching.

The participants in the exercise group also received the same health education sessions, including advice on nutrition (six sessions, one every month).

As well as insulin sensitivity, the team measured glucose effectiveness, which was worked out from an intravenous glucose tolerance test.

Data was analysed to assess whether the exercise programme worked better than the education programme for:

  • all participants using intention-to-treat (ITT) calculations
  • participants who completed the exercise and education interventions using a per protocol (PP) approach


What were the basic results?

A total of 128 participants were randomised at the start of the trial, and 100 completed the six-month interventions as planned, giving an overall completion rate of 78%.

This breaks down into 67% completing the exercise intervention and 90% completing the educational intervention.

There was a similar and significant decrease in body weight, waist circumference and fat mass for both groups following surgery and the interventions. Insulin sensitivity also significantly improved in both groups post-surgery.

The main finding was that exercise intervention led to a greater improvement in insulin sensitivity than the education intervention.

But this was only true (statistically significant) using the per protocol data. This means the people who completed the exercise intervention from start to finish benefited more than the education group.

However, not everyone assigned to the exercise intervention completed it. When these "non-completers" were included in the analysis (ITT analysis), the improvement for each group was the same.

The fact that a relatively large minority dropped out of the exercise programme has wider implications when considering whether such a programme would be effective and efficient if it was rolled out to larger populations. 

Additional ITT analysis showed exercise improved cardiorespiratory fitness compared with the education group.


How did the researchers interpret the results?

The authors interpreted their results as meaning that, "Moderate exercise following RYGB [Roux-en-Y gastric bypass] surgery provides additional improvements in SI, SG, [insulin sensitivity and blood glucose control] and cardiorespiratory fitness compared with a sedentary [non-active] lifestyle during similar weight loss."



This study provides some tentative evidence that adding a six-month exercise programme shortly after people have weight loss surgery might lead to more improvements in insulin sensitivity compared with a six-month-long educational programme.

However, the picture is muddied by the fact quite a few people dropped out or did not adhere to the exercise programme fully. It seemed that if people were able to stick to the exercise programme, it was more beneficial than no exercise.

This might seem obvious, but if this programme was introduced more widely, you might expect a similar proportion of people not to complete it. This could mean the programme as a whole would not yield any significant improvements at a population level.

Indeed, when all participants in each group were included in the analyses, there was little difference between the groups.

The authors reported high completion rates for both exercise and educational interventions – both over 90%. However, our calculations put this at a significantly lower 67% and 90% respectively.

Irrespective of the exact figures, those that did not complete the intervention did influence the results. This suggests the exercise intervention may be more effective than an education-only programme, but there is an important group who failed to adhere to it.

If the reasons for this non-compliance are not explored, they have the potential to widen health inequalities.

The study also mostly recruited adult women who were free from many additional diseases, such as cancer. This group might not be representative of the wider UK population undergoing weight loss surgery. Further trials involving more representative groups would give more generally applicable results.

In sum, for those who completed the trial as planned, exercise improved their insulin sensitivity, but there were adherence issues that call into question whether it would be effective at a population level.

If you want to gain the maximum benefit from weight loss surgery, it is important to adhere to any post-surgical advice, such as recommendations on diet and exercise.

Failure to do so could lead to a worsening of your health and possibly regaining some of the weight you previously lost.

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

Links To The Headlines

Weight loss surgery isn't just a quick fix to becoming healthy - you have to exercise too, doctors warn. Mail Online, December 1 2014

Links To Science

Coen PM, Tanner CJ, Helbling NL, et al. Clinical trial demonstrates exercise following bariatric surgery improves insulin sensitivity. The Journal of Clinical Investigation. Published online December 1 2014

Categories: Medical News

HIV evolving into less deadly form

Medical News - Tue, 12/02/2014 - 13:29

“HIV is evolving to become less deadly and less infectious,” BBC News reports.

A new study showed that HIV adapts to a person’s immune system, and that some of these adaptations may reduce the virulence of the virus.

The research team looked specifically at HIV in Botswana and South Africa. It found that over time, human immune system proteins, in addition to the use of HIV drugs, may have forced the virus to change into less virulent forms.

This is consistent with the theory that viruses get less virulent over time. The optimal evolutionary strategy for a virus is to be infectious (so it creates more copies of itself) but non-lethal (so its host population doesn’t die out). The "poster boy" for successful long-living viruses is, arguably, the family of viruses that cause the common cold, which has existed for thousands of years.

The authors warn that HIV, even at the reduced virulence, can still trigger the onset of AIDS.

Similarly, this study does not show that HIV virulence in the UK is decreasing, and that the virus remains life-threatening.

The simplest way to protect yourself against HIV infection in the UK is to use a condom during sex and never share needles if you are an injecting drug user.

Where did the story come from?

The study was led by researchers from Oxford and several institutes in Canada, the US, South Africa, Botswana and Japan. It was funded by grants from the National Institutes of Health (US), the Wellcome Trust (UK), the Medical Research Council UK and the Canadian Institutes of Health.

The study was published in the Proceedings of the National Academy of Sciences of the United States of America (PNAS), a peer-reviewed science journal. It is an open-access study, meaning that anyone can read it online or download it for free.

The UK media reported the story accurately. It was important that they included a warning that, despite a small decrease in the virus’ potency in some areas of Africa, HIV still causes AIDS. This can significantly shorten life, due to impairment of the immune system if the correct treatment is not followed and made available soon after infection.


What kind of research was this?

This was a laboratory study investigating whether HIV virulence has changed over time, and what might be influencing it.

The term virulence means the ability of the virus to cause disease. This is generally described in terms of:

  • how likely the virus is to be passed on to a different person (transmissibility)
  • how much of the virus the person carries in their bloodstream (viral load)
  • how quickly the virus replicates itself (viral replicative capacity)

Individuals can have slightly different immune responses to HIV infection. This (and other factors) can affect how virulent HIV is in the person’s body and how long it takes HIV infection to cause AIDS. Understanding this variation is important in the effort to minimise the suffering and deaths from the disease.

After HIV infection, some people develop AIDS quicker than others. This natural variation is partly caused by changes in human leukocyte antigen (HLA) genes, a group of genes that encode HLA proteins involved in the immune response. This study wanted to find out how HIV evolution has been shaped by specific HLA proteins that are known to protect against disease progression. They also wanted to know whether HIV drugs (antiretroviral therapy) had influenced the evolution of the virus.


What did the research involve?

This study looked at the genetics and virulence of HIV from epidemic regions in Botswana and South Africa, two countries severely affected by HIV infection. They compared many measures of virulence in the two areas and looked at whether HIV genetics had adapted to HLA proteins known to be protective against disease progression.

In characterising virulence they looked at:

  • prevalence of the virus in adults in the two countries
  • how much virus people carried in their bloodstream (viral load)
  • how quickly the virus replicated itself (viral replicative capacity)
  • CD4 count (CD4 cells are key to a person’s immune system, but HIV infects and destroys them; once CD4 cell level falls below a certain point, the person has AIDS)

The study also contained data from Japan, where HIV prevalence has remained low, and never exceeded 0.1% of the adult population.


What were the basic results?

The epidemic in Botswana started earlier than in South Africa. As such, the adult prevalence of HIV infection in Botswana was consistently and significantly higher than South Africa over the last 20 years. So too was the use of antiretroviral therapy to prevent disease progress to AIDS.

Despite the higher prevalence, viral load and viral replicative capacity of HIV in Botswana was significantly lower than HIV in South Africa. This meant that the virus was slightly less virulent. This appeared to be due to both an adaptation to different HLA proteins that forced the virus into a less virulent form and the use of antiretroviral therapy.


How did the researchers interpret the results?

The research team concluded that “HIV evolution is progressing rapidly” and that “The contrasts between Botswana and South Africa, in the degree of adaptation of HIV to prevailing HLA molecules in the populations and in the protective impact of protective alleles such as HLA-B*57 and HLA-B*58:01, coincide with the substantial differences in duration and magnitude of the epidemic in these two localities”.



This study shows that HIV adapts to a person’s immune system, and that some of these adaptations may reduce the virulence of the virus. It appears that over time, the virulence of HIV in Botswana has decreased compared with HIV in South Africa, because of such adaptations and the use of HIV drugs. Specific HLA proteins present in adults in Botswana have, over time, forced the virus to change into less virulent forms, allowing it to survive, replicate and spread.

This is consistent with a broader theory that epidemic viruses get less virulent over time, due to natural selection. The most severe viruses kill their hosts too early to be passed on. Hence, eventually, the very severe strains die out or mutate into milder forms.

This study furthers our understanding of the evolution of HIV in Botswana and South Africa. However, we cannot be complacent. HIV, even at the reduced virulence in Botswana, does cause pain, suffering and death. While HIV can be managed over the long term to push back the development of AIDS, this is dependent on quick and appropriate access to HIV drugs. This may not be the case for everyone.

Similarly, this study does not show that HIV virulence in the UK has decreased or is decreasing, so it is important not to be complacent or to diminish the serious and life-threatening risk of HIV infection.

The simplest way to protect yourself against HIV infection is to use a condom during sex; 95% of cases in the UK in 2011 were as a result of unprotected sexual contact. You should also never share needles if you are an injecting drug user. Some NHS trusts and local authorities run needle exchange programmes – this link can provide information about drug support services in your local area.

Read more about HIV prevention.

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

HIV evolving 'into milder form'. BBC News, December 1 2014

HIV is evolving to become less deadly. Metro, December 2 2014

HIV evolves into less deadly form. New Scientist, December 1 2014

Links To Science

Payne R, Muenchoff M, Mann J, et al. Impact of HLA-driven HIV adaptation on virulence in populations of high HIV seroprevalence. PNAS. Published online December 1 2014

Categories: Medical News

Can a pill cure binge drinking and dementia?

Medical News - Mon, 12/01/2014 - 15:00

"'Wonder' drug could cure binge drinking, Alzheimer's and dementia," the Mail Online reports. But before you raise a glass or two, these are premature claims based on research in rats that has not yet been proven, or even tested, in people.

Researchers gave rats alcohol to mimic the habits of human binge drinking. After three weeks of binging, the rats had signs of damage to their brain and performed worse at tasks that involved running through mazes.

When the scientists gave some of the mice a compound called ethane-β-sultam, it significantly reduced the alcohol-associated brain damage and inflammation, and resulted in improved performance in the maze tests.

This research suggests there may be a way to reduce the effects of excessive alcohol consumption on brain cells. But this is not a "cure" for binge drinking. Researchers only looked at short-term effects in rats, so the effects in humans remain unknown.

Also, the study only focused on the potential protective effects of the drug on the brain. Excessive alcohol consumption can also damage the liver. But the drug was not designed to work in this way and this was not looked at as part of the study.

Claims the compound could also be used to treat dementia are also pure speculation at the moment, as this was not tested.


Where did the story come from?

The study was carried out by researchers from universities in Italy, Belgium and the UK, and was funded by the European Foundation for Alcohol Research and the European Cooperation in Science and Technology (COST).

It was published in the peer-reviewed journal Alcoholism and Drug Dependence on an open access basis, so it is free to read online.

The science was covered by the Mail Online, which exaggerated the findings by implying the rat results also applied to humans and binge drinking, as well as Alzheimer's and other "brain diseases".

This may be the case, but it is too early to say with any confidence or assurance. The study did not test the effects of the drug, even in animal models of Alzheimer's or non-alcohol-related brain diseases.

Describing the drug as "curing" binge drinking is also misleading. While the drug showed some protective effect on brain cells and function, there was no assessment on damage to the liver, which is a significant cause of alcohol-related disease and death.

However, the Mail's coverage may have been influenced by a rather overexcited press release issued by the University of Huddersfield, which claimed that, "Huddersfield scientists develop breakthrough compound, reducing harmful side effects of 'binge drinking', and offering potential new ways to treat Alzheimer's and other neurological diseases that damage the brain".


What kind of research was this?

This was an animal study using rats to study the potential protective effects of the chemical ethane-β-sultam on the brain against the effects of binge drinking.

Intermittent excessive alcohol consumption – euphemistically termed "binge drinking" – is defined as drinking more than the maximum daily recommended units in a single session. This is often followed by a period of abstinence.

The research team says binge drinking harms brain cells, causes inflammation in the brain, and worsens learning and memory.

This research sought to use rats to better understand the underlying biology of the effects of binge drinking on the brain, and investigate whether a drug could be used to protect against some of the harms.

Researchers often use mice or rats for research purposes because, as mammals, they share similar biology to humans. This means research in rats can tell us what might happen in humans without directly experimenting on people in ways that would not be feasible or ethical.

However, there is no guarantee results in rats will be replicated in humans because, while we are similar, our biology is far from identical and these differences can be crucial. Often, direct study on humans is the only way to get the right results.


What did the research involve?

The research took a group of rats and gave them alcohol to mimic various scenarios of human binge drinking. Some of the mice were also given a drug called ethane-β-sultam to see if it was protective against harm from alcohol.

After different binge drinking simulations, the rats underwent tests assessing the levels of cellular degeneration and inflammation in their brains, as well as a test of their spatial memory involving escape from a maze.

Ultimately, the researchers were looking for differences between mice given ethane-β-sultam and those that were not.

The team tested two binge drinking levels: 1g/kg and 2g/kg. The human equivalent for a person of average weight would be eight units of alcohol for the first level (around two-and-a-half pints of strong lager) and 16 units for the second level (around one-and-a-half bottles of wine).

The rats had at least two different binge drinking sessions followed by a period of no drinking. 

Ethanol (alcohol) doses (20%) were administered three times per day with three-hour intervals on two consecutive days, followed by five days of abstinence. This was repeated for a total of three weeks.

Those allocated to receive ethane-β-sultam were given it every day of the three-week experiment and one week prior to starting the binge drinking simulation.

The rats underwent brain surgery at day five and after three weeks to see how alcohol was affecting their brains.


What were the basic results?

The main results showed the rats on the binge drinking regime had brain cell loss in a specific area of their brains called the hippocampus, and this was also associated with inflammation in those areas.

Daily supplementation of ethane-β-sultam suppressed much of the inflammation and reduced the loss of brain cells, particularly in rats given the lower of the two alcohol doses (1g/kg).

Binge-drinking rats administered 1g/kg ethanol took longer to solve a spatial navigation test compared with rats not consuming alcohol.

However, test results were almost normal for the group of rats receiving the same 1g/kg binge drinking regimen but also supplemented with daily ethane-β-sultam.


How did the researchers interpret the results?

The team said that, "Such results confirm that the administration of ethane-β-sultam to binge drinking rats reduces neuroinflammation in both the periphery and the brain, suppresses neuronal loss, and improved working memory of rats in a water maze study."



This research shows there may be a way to reduce the harmful effects of excessive alcohol consumption on brain cells, and potentially protect against associated deterioration in brain function.

However, none of this was conclusively proven in rats or humans, so the headlines suggesting a "cure for binge drinking" in people are premature.

While the results are promising, they represent a very early step on the road towards treatment in people. For example, the study looked at the effects of the drug in rats. While biologically similar to humans, they are not identical, and sometimes the differences are crucial.

As a result, the effects in humans could be different in many important ways. At this stage, there have been no experiments using people.

This is the first test of its kind, so ideally it will be repeated in other groups of rats to ensure the results are reliable and repeatable. If these do well, tests in humans may well begin.

It is likely to be unethical to force people to binge drink for the purposes of research, so it may be tricky to replicate these studies in humans.

Researchers will also need to know whether the drug has any effect if given after binge drinking, rather than at the same time as the alcohol. The drug will not be able to reverse brain cell loss that has already happened.

This study only focused on the potential protective effects of the drug on the brain. But some of the most serious consequences of excessive alcohol consumption affect the liver, and can ultimately lead to liver scarring and potentially death. The drug was not designed to stop any of these liver-related harms, and may not do so.

Some of the news coverage mentioned the potential for this drug to be used in other diseases associated with inflammation and deterioration in the brain, such as Alzheimer's disease.

Inflammation of the brain is also a problem in these conditions, so it is biologically plausible theoretically, but this was not tested in this study.

The issues around developing a drug to treat what some people perceive as a lifestyle choice and others an addiction may also attract some ethical debate.

On this point, lead author Professor Page was quoted in the Mail Online as saying: "If you accept that alcohol abuse is going to continue, then it might be sensible for society to try and treat it in some way."

Ethical considerations aside, if this drug works in people, it may be a pragmatic way of minimising some of the brain-related harms associated with binge drinking, and potentially other types of harmful drinking.

As we have said, though, it will do nothing to combat harms to other body organs, such as the liver, which are serious. 

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

Links To The Headlines

'Wonder' drug could cure binge drinking, Alzheimer's AND dementia, scientists claim. Mail Online, November 28 2014

New Drug Created To Reduce Harmful Effects Of Binge-Drinking. Huffington Post, November 28 2014

Links To Science

Stefanini C, Colivicchi MA, Della Corte L, et al. Ethane-β-Sultam Modifies the Activation of the Innate Immune System Induced by Intermittent Ethanol Administration in Female Adolescent Rats. Journal of Alcoholism and Drug Dependence. Published online February 20 2014

Categories: Medical News

HIV drug may slow the spread of prostate cancer

Medical News - Mon, 12/01/2014 - 14:40

“A drug used to treat HIV infection can slow the spread of prostate cancer, research has shown,” The Independent reports.

The news centres on the drug maraviroc (Celsentri), which researchers have found may slow the spread of prostate cancer into the bone and brain in early tests in mice.

Each man’s prostate cancer can progress in different ways. Many cases grow slowly, and the cancer remains within the prostate. A minority of cases are highly aggressive and can spread into other areas of the body, such as bones and the brain – a process known as metastasis.

In this research, scientists found a way to prompt mouse prostate cells to take on the characteristics of metastatic cancer cells, and then studied what proteins played a role in this change.

A protein called CCR5 was found to be implicated. Luckily maraviroc, a drug licensed for treating people with HIV, is already known to inhibit this protein. Giving maraviroc to mice that had been injected with the prostate cancer-like cells reduced the spread of the cancer to brain and bone by more than 60%.

This is still very early-stage research, and we will need to see the results of human trials before we know whether this drug is effective for preventing or treating prostate cancer metastases in humans.


Where did the story come from?

The study was carried out by researchers from Thomas Jefferson University in the US and other universities in the US, Italy and Mexico. It was funded by the US National Institutes of Health, the Dr. Ralph and Marian C. Falk Medical Research Trust, the Margaret Q. Landenberger Research Foundation, the Pennsylvania Department of Health, The National Autonomous University of Mexico and Thomas Jefferson University.

One of the authors is the founder of a company called ProstaGene, LLC and AAA Phoenix, Inc., and owns patents relating to prostate cancer cell lines and uses for these.

The study was published in the peer-reviewed medical journal Cancer Research on an open access basis, so it's free to read online.

The Independent covered this study accurately, if briefly, stating that the research was at an early stage and carried out on mice. The Daily Express also provides an accurate summary of the study, along with some useful background information about prostate cancer.


What kind of research was this?

This was animal research looking at how prostate cancer cells spread (metastasise) to bone, and how this might be stopped.

When prostate cancer spreads in the body, it often spreads to bone. Researchers would like to know why this is and how to stop it. None of the existing mouse models of prostate cancer reliably develop bone metastases, and this makes it difficult to study. The researchers wanted to develop a mouse model of prostate cancer, which would develop bone metastases, and use it to study this condition.

Animal studies are often used to get a better understanding of the biology of human disease and how it might be treated. The biology of animals such as mice has a lot of similarities to humans, but there are also differences. This means that results seen in mice won’t always be seen in humans, so human studies are needed to confirm initial findings in mice.


What did the research involve?

The researchers obtained cells from mouse prostate tissue and used genetic engineering to get them to produce an abnormally active form of a protein called Src, which encourages cells to become cancerous. They then looked at whether the cells divided and moved more in the lab, allowing them to “invade” a gel substance that resembles body tissue. These characteristics indicate whether the cells are behaving more like cancer cells spreading in the body. They also looked at what happened if they injected these cells under the skin or into the bloodstream of mice.

The researchers then compared which genes were active in normal mouse prostate cells, in the genetically engineered prostate cancer-like cells grown in the lab and those injected into the mice. Genes that are more active in the cancer-like cells could be contributing to their growth and spread. After this, the researchers looked at whether any of these genes were also more active in human prostate cancer tissue, using a bank of existing data on gene activity in human tissues.

Once they identified a gene that could be playing a role in prostate cancer, they carried out a range of experiments to further look at its effects. These included tests looking at whether stopping the protein produced by this gene from working may stop the spread of the genetically engineered prostate cancer tumours in the mice.


What were the basic results?

Prostate cells producing the abnormally active Src protein divided and moved more, and were more invasive in the lab. They grew into tumours if injected under the skin of mice, and if injected into the bloodstream, they spread to various organs, including the bone and brain. The tumours in the bone still had the appearance of prostate cancer tissue.

Genes playing a part in a particular pathway called the CCR5 signalling pathway were more active in these prostate cancer-like cells than in normal mouse prostate cells. The CCR5 gene was also found to be more active in human prostate cancer, particularly metastatic cancers. This and previous research suggests this gene could be contributing to the spread of the prostate cancer cells.

An HIV drug called maraviroc stops the protein produced by the CCR5 gene from working as effectively, so the researchers tested whether it could prevent the cells from spreading. They found maraviroc stopped the mouse prostate cancer-like cells from being invasive in the lab.

The researchers also found that giving maraviroc to mice injected with mouse prostate cancer-like cells also reduced metastases by more than 60%.


How did the researchers interpret the results?

The researchers concluded that they had developed a new mouse model of human prostate cancer, which may be a useful addition to the existing models of this disease. The protein CCR5 appears to be more active in metastatic prostate cancer cells. The spread of these cells in mice is reduced by the oral CCR5 inhibiting drug maraviroc, which is already approved as a treatment for HIV. The results suggest that clinical trials might be warranted for maraviroc or similar CCR5 inhibiting drugs in men with prostate cancers found to have high levels of CCR5 activity.



This animal research has identified the protein CCR5 as potentially playing a role in how prostate cancer cells spread (metastasise) through the body. The study has also shown that a drug already on the market for treating HIV, called maraviroc (brand name "Celsentri") can reduce prostate cancer-like metastases in mice.

As the drug maraviroc has already obtained a license for HIV use, there is already evidence suggesting that it is safe enough for use in humans. This could mean that clinical trials of this drug for prostate cancer could take less time to happen than if this was a new chemical compound whose safety had not been previously tested in humans.

However, it’s worth bearing in mind that this is still very early-stage research. Researchers are likely to want to carry out more studies on human prostate cancer tissue and cells in the lab, and in animals, to confirm that CCR5 is playing a role in the spread of prostate cancer. We will need to see what the results of human trials are before we know whether this drug is effective for preventing or treating prostate cancer metastases in humans.

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

HIV drug maraviroc may slow prostate cancer. The Independent, November 30 2014

HIV drug 'dramatically SLOWS' spread of prostate cancer. Daily Express, December 1 2014

Links To Science

Sicoli D, Jiao X, Ju X, et al. CCR5 Receptor Antagonists Block Metastasis to Bone of v-Src Oncogene–Transformed Metastatic Prostate Cancer Cell Lines. Cancer Research. Published online December 1 2014

Categories: Medical News

Majority of supermarket chickens carry food bug

Medical News - Fri, 11/28/2014 - 15:00

“More than 70% of fresh chickens being sold in the UK are contaminated,” BBC News reports.

A Food Standards Agency (FSA) investigation found worryingly high levels of contamination with the campylobacter bug, which can cause food poisoning, on chickens being sold across the country. The Guardian reported a food scientist, Professor Tim Lang, calling for a “boycott of supermarket chicken because of 'scandalous' levels of contamination”.

Campylobacter is a type of bacteria thought to be the leading cause of food poisoning in the UK. Eating food contaminated with campylobacter can trigger symptoms such as nausea, vomiting, diarrhoea and stomach cramps.

Who produced the report?

The FSA released the latest figures from its testing of raw chickens in the first half of 2014. The agency has a key role in preventing foodborne illnesses. Reducing campylobacter in chickens is one of its main priorities because more than 280,000 people are infected with it each year in the UK.

The European Food Standard Authority (EFSA) has reported that up to 80% of campylobacter cases are due to raw poultry. It has estimated that the number of cases could be cut by between 50% and 90% if the levels of campylobacter in poultry across Europe was reduced to a tenth of the current levels.


What did the survey involve?

The FSA tested 1,995 fresh whole raw chickens and their outer packaging for the presence of campylobacter from February 2014 to August 2014. The chickens came from a wide range of UK supermarkets, small independent stores and butchers. The chickens were UK-produced standard, free range or organic, and not frozen, stuffed or marinated.

The FSA recorded the level of campylobacter on the chicken skin and outer packaging, and also reported whether the level on the skin was greater than the level at which the bug is thought to be most likely to infect humans (1,000 colony forming units per gram (cfu/g)).


What are the findings of the report?

Overall, 70% of raw chickens contained campylobacter on the skin:

  • 18% were over the threshold where human infection is most likely (1,000cfu/g)
  • 31% had moderate levels (between 100 and 1000cfu/g)
  • 21% had low levels (between 10 and 99cfu/g)

Outer packaging was contaminated in 6% of chickens:

  • One chicken’s outer packaging had levels over the 1,000cfu/g threshold
  • 1% had moderate levels (100 to 1000cfu/g)
  • 5% had low levels (10 to 99cfu/g)

The rates of campylobacter in chickens from different supermarkets or shops varied between 64% and 69%.

Some supermarkets had slightly better results than others, but all needed to improve.

The results grouped of all of the independent retailers and butchers together, so were unable to provide figures for these different types of chicken sellers. The assessment was not specifically designed to give a robust comparison between different supermarkets or shops. The FSA was unable to analyse the data to determine if there was a difference between the types of chicken tested – housed, organic or free range.


What are the potential health risks associated with chicken containing campylobacter?

Eating food contaminated with campylobacter – such as raw poultry, undercooked chicken liver pate and unpasteurised milk – can cause food poisoning. The symptoms usually start within two to five days, but can take up to 10 days to begin.

Campylobacter is the most common cause of diarrhoea in the world. Other symptoms can include abdominal pain, fever, headache, nausea and vomiting. It is usually a mild infection, lasting from three to six days, but can be fatal for very young children, the elderly and people whose immune system is not working well.

Cooking chicken will kill off campylobacter. The concern is that someone may handle raw contaminated chicken and then touch their mouth, which could lead to infection. Also, incorrect storage of chicken (see below) could lead to the cross-contamination of other foods.

Seeking medical advice for treating campylobacter-related food poisoning is usually not necessary, as it should clear up by itself, but it is essential to drink lots of water to replace the extra fluid lost by the diarrhoea, to prevent dehydration. Some more severe cases may require giving salts and other substances to maintain the balance of these in the body, and the use of antibiotics.


What advice has been given to protect against food

The FSA want campylobacter levels to be as low as possible when chicken reaches consumers, but even if it is present, chicken is safe to eat if you stick to the following measures.

Cover and chill raw chicken:
  • Cover raw chicken and store at the bottom of the fridge so juices cannot drip on to other foods and contaminate them with bacteria that can cause food poisoning such as campylobacter.
Don’t wash raw chicken:
  • Do not wash raw chicken before cooking as this can spread germs by splashing onto other surfaces. There is no need to wash the chicken as cooking will kill any bacteria present.
Wash used utensils:
  • Thoroughly wash and clean all utensils, chopping boards and surfaces used to prepare raw chicken. Wash hands thoroughly with soap and warm water after handling raw chicken. This helps to stop the spread of campylobacter between different surfaces by your hands.
Cook chicken thoroughly:
  • Cooking will kill any bacteria present, including campylobacter. Make sure chicken is steaming hot all the way through before serving. Cut in to the thickest part of the meat and check that it is steaming hot with no pink meat and that the juices run clear.


What happens next?

The FSA is continuing to check chickens for campylobacter to complete a year’s worth of data. It intends to have sampled 4,000 chickens by February 2015. It says this will serve as a “baseline” for assessing if there are improvements over time.

Its goal, in partnership with the chicken industry, is to reduce the number of chickens with the highest levels of campylobacter (1,000cfu/g) to less than 10% by the end of 2015. Some schemes to address the problem are already underway, and their impact may well be seen when the next batch of results is released.

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

Links To The Headlines

Supermarket chickens: 70% affected by food bug. BBC News, November 27 2014

Dirty chicken scandal: food expert calls for boycott of chicken. The Guardian, November 27 2014

Supermarkets Named And Shamed On Chicken Bug. Sky News, November 27 2014

Asda disappointed with findings from study on campylobacter in chickens. The Guardian, November 27 2014

The chicken bug, what has caused it and how it affects you. The Daily Telegraph, November 27 2014

Chicken bug: 70 per cent of British supermarket chickens test positive for food poisoning bacteria. The Independent, November 27 2014

Named and shamed: The supermarkets where up to 78% of fresh chickens are contaminated with potentially lethal food poisoning bacteria. Mail Online, November 27 2014

Categories: Medical News

Could depression be the result of a brain infection?

Medical News - Fri, 11/28/2014 - 14:40

"Depression should be re-defined as an infectious disease … argues one scientist," the Mail Online reports.

The news comes from an intriguing opinion piece by an American academic, which argues the symptoms of depression may be caused by infection.

But, as the author of the paper says, his hypothesis is purely "speculative". 

It's fair to say feelings of depression can follow some illnesses such as flu, but this is not the same as saying it is caused by infection. And, as this is an opinion piece, the author may have cherry-picked certain articles in support of his hypothesis.

That said, the author does provide some interesting examples of how an infection can lead to a change in mood and emotion.

Infection with the T. gondii strain of bacteria can cause rats to become fearless around cats, a natural predator for these animals.

And a study we looked at in 2012 suggested people who owned cats had a higher risk of suicide, as their pets could make them vulnerable to a Toxoplasma gondii (T. gondii) infection.

Despite the lack of any hard evidence, it is an interesting hypothesis that arguably deserves further investigation, especially given the considerable burden depression places on many people.


Who wrote this piece?

The article was written by Dr Turhan Canli of the department of Psychology at Stony Brook University, New York.

It was published in the peer-reviewed journal Biology of Mood and Anxiety Disorders. 

The piece has been published on an open access basis, so it is free to read online.

There is no information about external funding, though the author declared no conflicts of interest.


What are the main arguments?

Dr Canli argues that despite decades of research, major depressive disorder (MDD) remains among the most common mental health conditions.

He argues the illness often recurs, regardless of treatment with antidepressants, and states it is time for "an entirely different approach".

Instead of seeing MDD as an emotional disorder, it should be reconceptualised as a form of infectious disease, he says.

Canli says future research should conduct a "concerted search" for parasites, bacteria or viruses that may play a role in causing depression to develop.

The paper presents a series of arguments in favour of this theory.

Inflammatory markers
  • patients with MDD exhibit "sickness behaviour" – they experience loss of energy, have difficulty getting out of bed, and lose interest in the world around them
  • studies of inflammatory biomarkers in major depression "strongly suggest an illness-related origin" – inflammatory biomarkers are chemicals in the blood that may indicate inflammation in the body
  • these inflammatory markers may represent activation of the immune system in response to some kind of pathogen, which could be a parasite, bacterium or virus
  • the author admits there is no direct evidence that major depression is caused by such organisms, but says such a process is conceivable
Examples from nature

There are existing examples of how parasites, bacteria or viruses can affect human behaviour:

  • for example, T. gondii, which lives in cats' intestines, lays eggs that are dispersed into the environment on excretion
  • when a rat is infected with these eggs, it becomes attracted to the scent of cat urine
  • the rat's loss of fear may be caused by parasitic cysts in the rodent's brain affecting levels of various chemicals
  • one-third of the world's population are believed to be infected with T. gondii, and infection is associated with inflammatory markers similar to those found in depressed patients
  • research has identified a link between T. gondii and national suicide rates, major depression and bipolar disorder

The paper argues bacteria could be another cause of depression, with rodent studies showing a link between various bacteria and levels of emotional stress.

In humans, there is data to suggest bacteria in the gut may contribute to major depression – a controversial suggestion known as "leaky gut theory".

Viruses are the third possible cause of MDD, the author states. One meta-analysis of 28 studies, which examined the link between infectious agents and depression, found viruses that had significant links included herpes simplex, varicella zoster (which causes chickenpox and shingles), Epstein-Barr and Borna disease virus.


The author says reconceptualising major depression as being causally linked to parasites, bacteria or viruses is useful when thinking about the genetics of the illness.

Perhaps the reason the search for specific genes related to depression has "come up empty" is because scientists have been looking for the wrong organism.

Researchers have been looking for internal changes in human genes that might explain depression, but 8% of the human genome is based on external changes from retroviruses.

Dr Canli goes on to portray the human body as an ecosystem that acts as host to "numerous micro-organisms" that may be passed across generations and could be linked to the risk of depression.

He concludes by suggesting unknown pathogens play a causal role in depression by altering the immune response. He speculates there may even be a class of pathogens that share common modes of action targeting the nervous system.

Such pathogens may work together with other factors, Canli argues. For example, some people may have a latent infection, but depressive symptoms may only emerge after the pathogen is activated by a stressful life event.

Large-scale studies of depressed patients and healthy controls are needed to look at the potential role of pathogens in the development of depression. Such efforts might represent the first step towards developing a vaccination for major depression.


What is the evidence?

The author quotes a variety of sources to support his hypothesis. Many are rodent studies, and others are laboratory studies looking at levels of certain inflammatory biomarkers in depressed and healthy patients, for example.

But this is not a systematic review of the evidence. The author has not carefully searched all the literature on the topic, assessed its quality, and come to a conclusion. He may have cherry-picked studies that might support his hypothesis while ignoring studies that don't.


How accurate is the reporting?

The Mail Online gave the paper's arguments considerable prominence in an article that was accurate but uncritical. Independent expert opinion was not included to balance the argument.

The New York Times took a more discursive approach based on an interview with the author. The item was part of a longer discussion with various experts.



The paper's hypothesis is interesting, but it remains just that – a hypothesis. While it is true that some pathogens, such as the Borna disease virus mentioned in the article, have been linked with neuropsychiatric disorders, there is no proof as yet that bacteria, viruses or parasites could cause major depression.

Still, as the old truism goes: "Absence of evidence is not the same as evidence of absence". The lack of evidence could be because nobody has bothered to look for it before.

The author concludes that, "It would be worthwhile to conduct large-scale studies of carefully characterised depressed patients and healthy controls using gold-standard clinical and infectious disease-related study protocols." This seems to be a reasonable and sensible suggestion.

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

Links To The Headlines

Could depression be an INFECTIOUS DISEASE? Condition is caused by parasites, bacteria or virus and could be prevented with a jab, expert claims. Mail Online, November 27 2014

What If We're Wrong About Depression? New York Times, November 26 2014

Links To Science

Canli T. Reconceptualizing major depressive disorder as an infectious disease. Biology of Mood and Anxiety Disorders. Published online October 21 2014

Categories: Medical News