NHS Choices

Leaving babies to cry 'will improve their sleep', study says

NHS Choices - Behind the Headlines - Fri, 27/05/2016 - 15:40

"Babies do sleep better if you leave them to cry," the Daily Mail reports.

A small study suggests that "graduated extinction" – better known as controlled crying in this country – increased sleep length and reduced the number of times babies woke up during the night.

Controlled crying involves waiting a set number of minutes while your baby is crying, without picking them up, to see if they drop off again.

The study compared this approach with a standard sleep education approach based on the principle of setting a standard bedtime routine, as well as a different approach known as bedtime fading.

This involves pushing back your baby's bedtime by 30 minutes if they took a while to settle the previous night.

The results suggest these two approaches work better than a sleep education only control group approach.

This didn't lead to any increases in stress to the infant or affect parental-child bonds a year later.

A problem with the study is its size – there were only 14 to 15 infants in each of the three test conditions at the start of the study.

There were even less after three months, when most of the results were analysed – only seven in each group. This isn't enough to make reliable statements about which sleep method works best.

There may not be a one-size-fits-all "trick" to getting your baby to sleep. Some babies may respond to controlled crying, others may prefer bedtime fading or a set bedtime routine.

Where did the story come from?

The study was led by researchers from Flinders University, Australia, and was funded by the Australian Rotary Health Fund, Channel 7 Children's Research Fund, and the Faculty of Social and Behavioral Sciences.

It was published in the peer-reviewed journal, Pediatrics.

The Mail's reporting was accurate, but took the findings at face value, not discussing any of the study's limitations, such as its small size, and how these could affect the findings.

What kind of research was this?

This randomised control trial (RCT) looked at two approaches to improving an infant's disturbed sleep, compared with a standard control intervention.

Many parents experience trouble getting their infant to have a good night's sleep. Struggles can include settling your infant before bed, helping them fall asleep, or frequent waking in the night.

There are a lot of approaches people suggest to help. The researchers wanted to find which one worked the best:

  • Should you comfort your child each time they cry, or show "tough love" and leave them to cry and sooth themselves?
  • Should you pick up your infant to comfort them, or is it best to only show your face but leave them where they are?
  • Is setting a standard bedtime better, or does it make more sense to be flexible, depending on how tired your baby seems to be?

These questions can leave parents confused, and sometimes feeling guilty about what's best – and they aren't the only ones.

Researchers couldn't find any clear answers from past studies they'd seen, either. They designed this trial to test two behavioural approaches against an educational-only approach to improve infants' disturbed sleep, hoping there would be a clear winner.

What did the research involve?

All families in the study answered yes to the question "Do you think your child has a sleep problem?", so they were a special group of disturbed sleepers.

Infants with mothers with significant postnatal depression scores were excluded. Most parents were graduates and middle- to high-income earners.

A total of 43 infants aged 6 to 16 months – mostly (63%) girls – were randomised to one of three sleep test groups:

  • graduated extinction (14 infants) – gradually delaying parents' responses to their infant's cry each night and each time they wake in the night. Parents were told to put their infant to bed awake, and leave within one minute. When re-entering the room, they were allowed to comfort their child, but couldn't pick them up or turn on the lights.
  • bedtime fading (15 infants) – delaying the infant's bedtime by 30 minutes each time they took more than 15 minutes to fall asleep.
  • sleep education (14 infants) – this was the control group. Parents were given information on reasons for night wakings, settling tips, and sleep cycles in infants. The graduated extinction and bedtime fading groups also received this information.

Parents filled in sleep diaries to document their infant's sleep habits, wore ankle tags to track their night-time movements, and filled in ratings scales assessing the mother's level of depression, mood and stress.

Infants' stress levels were also monitored in the morning and afternoon, testing their saliva for the stress hormone cortisol.

Parental-reported changes in sleep patterns were obtained before the test and one week, one month, three months and one year into the test to monitor change.

A year after the tests, mothers rated their children for emotional or behavioural problems, and a series of separation and reunion tests assessed parent-child attachment.

All mothers and infants who started the test finished it through to a year, but there was data missing for approximately half (seven) of the families by the third month.

The main analysis compared the two active tests – graduated extinction and bedtime fading – with the control group, sleep education given to all, and for changes over time.

The focus was on any changes in the time it took for the infant to fall asleep (sleep latency), how often they woke in the night, and whether they woke up after falling asleep.

What were the basic results?

Three months into the intervention, a lot of sleep measures had improved across all three groups.

However, it wasn't clear whether they were statistically different across the three test conditions, or before and after the study, as they were presented as graphs.

After three months:

  • The time it took infants to go to sleep had fallen from around 18 minutes to less than 10 minutes in both graduated extinction (-12.7 minutes) and bedtime fading groups (-10 minutes). Stayed more or less the same in the control at around 20 minutes (+2 minutes).
  • Average number of times the infant woke in the night appeared to decline in all groups, but it wasn't clear if these were statistically significant compared with the education only group, or over time.
  • The time spent awake after first falling asleep fell across all groups. For graduated extinction, it fell from just under an hour at the start of the study to around 15 minutes (44.4 minutes). The control group and bedtime fading improved a little less, by 31.7 minutes and 24.6 minutes respectively.
  • Total time asleep improved for those trying graduated extinction  (+19.2 minutes) and the control group (+21.6 minutes) but there was little change for bedtime fading (+5.4 minutes).

Over the first month, maternal stress in the control group was largely unchanged, but reduced in both sleep test conditions. Maternal mood improved in all groups, most of all for bedtime fading.

At one year no effects on parent-child bonding or emotional or behavioural problems were found.

How did the researchers interpret the results?

The researchers concluded that their study showed "meaningful effects for both graduated extinction and bedtime fading".

They went on to say that, "Compared with the control group, large reductions in nocturnal wakefulness resulted from each treatment.

"Despite assertions that extinction-based methods may result in elevated cortisol, emotional and behavioural problems, and insecure parent-infant attachment; our data did not support this hypothesis."


This randomised control trial suggests two behavioural approaches to remedy disturbed sleep in infants may work better than a sleep education only control group approach.

This may be true, but may also be a chance finding or affected by bias. For example, the statistical significance of some of the results was hard to interpret, as many were presented as graphs only. This means we can't be sure that some, or even many, of the differences are down to chance.

The study was also very small, with only 14 to 15 people in each of the three test conditions at the start of the study.

There were even less after three months – only seven in each group. This isn't enough to make accurate, reliable or generalisable statements about which method works best.

Small studies like this are also more likely to throw out unusual and unrepresentative results. For these reasons, we can't say anything too solid based on it.

You may wish to experiment with different techniques to see if a specific approach suits your baby better.

If you have persistent problems getting your baby to sleep and it is beginning to have a significant impact on your quality of life and ability to function during the day, speak to your health visitor or GP.

Read more advice about helping your baby (and you) get a good night's sleep.

Links To The Headlines

Babies DO sleep better if you leave them to cry: Letting them nod off alone could help the parents, too. Daily Mail, May 27 2016

Links To Science

Gradisar M, Jackson K, Spurrier NJ, et al. Behavioral Interventions for Infant Sleep Problems: A Randomized Controlled Trial. Pediatrics. Published online May 24 2016

Categories: NHS Choices

Could cannabis damage DNA that is then passed down generations?

NHS Choices - Behind the Headlines - Thu, 26/05/2016 - 14:40

"Smoking cannabis can alter a person's DNA, causing mutations that expose a user to serious illnesses," the Mail Online reports.

A new review has looked at the role cannabis may play in what is known as chromothripsis.

A relatively recent discovery, chromothripsis is when the DNA of a cell suffers large-scale damage, but not enough to kill the cell. It has been linked to some types of cancer and birth defects.

In this review, researchers considered the evidence about whether one of the active ingredients in cannabis – tetrahydrocannabinol (THC) – could trigger chromothripsis, which could potentially cause cancer and other illnesses.

The researchers also raised the possibility that the DNA damage could be passed down to later generations.

There is a great deal of uncertainty about how the included studies were chosen, so there is a possibility not all relevant research was considered.

This type of study serves to stimulate debate and further research. It is not reliable enough to form the foundation of policy change on its own.

Arguably, a longer-term study would be needed to see if cannabis use could have an intergenerational effect.

We do know that cannabis, a class B illegal drug, is known to contain cancer-causing chemicals (carcinogens) and has previously been linked with lung cancer, psychosis, schizophrenia and fertility problems.

Find out more facts about cannabis.

Where did the story come from?

The review was carried out by two researchers from the University of Western Australia. There was no external source of funding.

It was published in the peer reviewed journal, Mutation Research: Fundamental and Molecular Mechanisms of Mutagenesis.

The Mail Online's headline, "Smoking cannabis can alter a person's DNA, causing mutations that expose a user to serious illnesses", made it sound like the researchers' hypothesis was proven by newly uncovered evidence, which is not the case.

The headline and article did largely reflect the researchers' findings, but failed to add any notes of caution, balance or discussion about the limitations of the research, instead taking it at face value.

What kind of research was this?

This was an evidence-informed narrative review of research exploring the hypothesis that cannabis use causes errors in human DNA, potentially leading to cancer and affecting brain development in unborn babies.

Non-systematic reviews like this are useful for summarising scientific research in a particular area, but can miss relevant research and counter-arguments.

Without a clear and systematic review of the published and unpublished science, there is a risk the authors cherry-picked the evidence, consciously or unconsciously, to fit their views. 

Such a one sided-argument has its place in stimulating debate, but should not be viewed on a par with a systematic review, one of the highest levels of evidence.

A systematic review of well-designed long-term cohort studies would be one of the best ways to assess the causal links between cannabis and DNA damage and disease.

What did the research involve?

The research is a narrative review of evidence that presents the idea that cannabis can disrupt a person's DNA, potentially raising their risk of cancer and causing genetic toxicity that could be passed from one generation to the next.

The review assembled data from 189 research articles. However, it had no reported methods. As such, we cannot assume the researchers employed systematic review methodology.

As the authors didn't mention how they found the articles, the study risks being biased to fit a coherent story, or may have missed other relevant research.

Some limitations in the evidence were presented, although quite briefly. The relative strength and balance of evidence for and against their hypothesis is not clear.

What were the basic results?

The review starts by providing scientific background on key moments in cell division – a complex and crucial process of normal cell growth and tissue maintenance.

It then outlines evidence that cannabis disrupts this process at specific points, leading to potentially cancer-causing DNA mutations.

This is a relatively recent discovery known as chromothripsis, which in a literal Greek translation means "chromosomes shattering into pieces".

Some of the main points revolve around the effects of cannabis on cancer and foetal abnormalities.

It also touches on the possibility that genetic mutations may be passed down through generations – meaning a child who has never touched cannabis could be negatively affected because of their parents' past use.

Cannabis and cancer

The review describes several observational studies linking cannabis to cancer, including brain, prostate and lung. Many also showed the higher the cannabis use the higher the cancer risk, a tentative sign of causation.

The authors acknowledge that other studies showed no link, but suggest this might be because the participants were quite low cannabis users, making a link easier to detect, or that the link only exists after a certain threshold is passed.

For example, one study reported "heavy cannabis use" as more than 0.89 joints in one day, which may not have been enough to cause DNA damage.

Cannabis and foetal abnormalities

The review discusses several studies showing a positive link between cannabis use and foetal abnormalities such as spina bifida or low birth weight as a result of disruptions in cell growth.

As before, the authors pointed out that harms were generally found when cannabis use was high (around 50-300mg/kg) – although the definition of this was variable. 

Other addictive substances

The review says that the effects of other addictive substances – alcohol, opioids, tobacco and benzodiazepines – on the development of tumours and foetal abnormalities are similar to cannabis. In other words, they all disrupt the cell cycle in a similar way.

The harmful link between alcohol consumption and tobacco use during pregnancy has long been known.

Cannabis use and future generations

Transmission of cannabis-related genetic damage from parent to child has been shown in rat and human studies, as well as for damage caused by alcohol, cocaine and opioids.

As this type of research has only just scratched the surface, the review authors said it was "an exciting time" for continuing research in this area.

How did the researchers interpret the results?

The researchers concluded that cannabis use was likely associated with cancers and other serious illnesses because it causes DNA damage in a person's cell during and around cell division.

The authors highlighted that this was an important finding as the use of cannabis is increasing globally, as is the strength of cannabis, while many countries are starting to legalise its use.


This review presents a useful summary of evidence backing the idea that cannabis can disrupt cell division, causing genetic damage, potentially leading to the development of cancer and foetal abnormalities.

The review was transparent in exploring the evidence behind one theory. And while this is a valuable body of research, a systematic review would have been more reliable, providing a more balanced view of the evidence.

Because of the uncertainty about how the included studies were chosen, there is a possibility that not all the relevant research was considered.

The strength of the included evidence was also not discussed. So we don't know whether it was generally strong or weak, or how it stacks up against counter-evidence. Results are only as good as the studies included, and this can vary depending on study design and assessment.

This type of study serves to stimulate debate and further research. It is not systematic or reliable enough to form the foundation of policy change on its own.

Read more about the potential harms of cannabis use.

Links To The Headlines

Smoking cannabis ALTERS your DNA 'causing mutations that can trigger serious illness, including cancer'. Mail Online, May 24 2016

Links To Science

Reece AS, Hulse GK. Chromothripsis and epigenomics complete causality criteria for cannabis- and addiction-connected carcinogenicity, congenital toxicity and heritable genotoxicity. Mutation Research: Fundamental and Molecular Mechanisms of Mutagenesis. Published online May 4 2016

Categories: NHS Choices

Exam stress linked to teen suicide

NHS Choices - Behind the Headlines - Thu, 26/05/2016 - 13:15

"First detailed study into 130 [teen] suicide cases in England finds range of common anxieties," The Guardian reports, citing factors including exam stress, bullying and bereavement.

The study into teenage suicide also found there was a history of self-harming in half of suicide cases in young people.

Researchers identified multiple factors that might have contributed to the deaths.

These include having experienced bereavement, relationship problems or breakdown; having long-term physical health problems, including asthma and acne, family problems, self-harm, bullying, and alcohol or drug use.

It's unclear if any single factor was a cause of death. It could be possible that in many cases multiple risk factors triggered suicidal thinking and behaviour.

However, we cannot be sure that these factors contributed to the deaths of the children and young people involved in all cases. This is partly because they are very common.

For example, the study showed that 27% of those who died had experienced exam stress or other academic pressures, but we don't know what proportion of under-20s in the general population also experience exam stress.

One striking fact is that in 54% of cases there was a previous history of self-harm. And one in four had talked about suicide in the week before they died.

It's important to get help quickly if you are thinking about self-harming and suicide, or think a friend or relative may be affected by similar thinking and behaviour. Seek advice from your GP. 

Where did the story come from?

The study was carried out by researchers from the National Confidential Inquiry into Suicide and Homicide by People with Mental Illness, based at the University of Manchester, and was funded by the Healthcare Quality Improvement Partnership. 

It was published in the peer-reviewed journal The Lancet Psychiatry on an open-access basis, so it's free to read online.

Coverage in the UK media was widespread. Different organisations chose to highlight different factors from the report, perhaps reflecting their own interests.

For example, The Sun reported that, "The Internet played a role in a quarter of recent teen suicides in England", while the Daily Mail stated that, "Drugs linked to one in three teen suicides". The Times, The Guardian and The Daily Telegraph highlighted exam stress.

Not all news stories were clear that these factors cannot be seen as direct causes of suicide.

For example, most teenagers have exam stress and develop acne, and many dabble in drugs and alcohol. But, thankfully, most teenagers don't kill themselves.

The Guardian did the best job of explaining the study findings and putting them in context. 

What kind of research was this?

This was a consecutive case series where researchers tried to collect relevant documents and information about every death by suicide in a person under 20 that occurred in a 16-month period.

They wanted to see how many deaths had been preceded by one of a number of recognised "antecedents", or factors linked to suicide, and whether the child or young person had been in touch with health or social care services or the criminal justice system.

Case studies can help to identify factors associated with an outcome, but they cannot tell us whether those factors actually contribute to it.

In this case, they can tell us how many people had records of specific factors in their history, but not whether those factors contributed to their death.

What did the research involve?

The researchers contacted coroners' offices in England, as well as other bodies that may investigate child deaths, to ask to be notified of any deaths by suicide or possible suicide that happened between January 1 2014 and April 30 2015.

They checked the reports for factors previously identified as being linked to suicide and calculated how many deaths were linked to each factor.

The researchers had information from the Office for National Statistics that 145 children or young people died by suicide or possible suicide during the study period.

However, the coroners did not provide copies of the inquest recording or documents in all cases, so these could not be included in the study.

Other information sources included reports from Local Child Safeguarding Children Boards, NHS Trusts, the Prison and Probation Ombudsman, and the Independent Police Complaints Commission.

The researchers collected data about a number of pre-set factors linked to suicide in general, or in young people in particular.

They presented their figures as proportions, and looked for differences between male and female children and young people, and under and over-18s.

What were the basic results?

Of the 130 people who died by suicide or possible suicide in the study period, 70% were male.

Deaths were more common among over-18s than younger people (79 deaths in people aged 18 or 19, and 66 in people younger than 18). Most (57%) had some contact with health, social care or justice agencies.

The researchers identified many different factors that have been linked to suicide. These are some of the more commonly reported factors:

  • recent relationship problems or relationship break-up (58% total)
  • expressing suicidal ideas (57%)
  • previous self-harm (54%)
  • any diagnosis of mental illness (39%)
  • physical health condition (36%)
  • bereavement (28%)
  • academic pressures (27%)
  • excessive alcohol use (26%)
  • illegal drug use (29%)
  • bullying (22%)

We do not know if these factors caused people to take their own lives or contributed to their decision to do so.

However, they may help families, schools and doctors to be alert to children or young people who are struggling with life, especially if several of these factors are involved.

How did the researchers interpret the results?

The researchers say they found "a complex pattern of stresses and adverse events" before the suicides took place.

Of the factors that affect young people specifically, they singled out academic pressures, which they said were often unrecognised at the time, and bullying, which was more often face to face rather than online.

They also point to "suicide-related internet use", by which they mean searching online for suicide methods or posting suicidal thoughts online, in 25% of people.

Regarding the perhaps surprising finding that physical health conditions were common, they say that acne and asthma, which were most commonly reported, could both lead to social isolation or withdrawing from social activities.

They point out that, "Many of these factors are common in young people in general and on their own cannot be used to predict suicide risk."

They suggest some "long-term" stresses, such as child abuse, substance misuse or mental illness in the family, could be worsened by later experiences such as bereavement or bullying, before a "final straw" pressure such as exam stress or a relationship break-up finally leads to suicide.

They go on to say that this pattern "could offer opportunities to intervene" if society as a whole has a better understanding of the pressures that can lead to a young person taking his or her life.


Any death in a child or teenager is devastating for friends and family, but suicide is perhaps especially hard to bear. Thankfully, it is uncommon – young people are less likely to take their lives than older people.

There are about 4.4 deaths for every 100,000 people among 15 to 19-year-olds, compared with 15.1 for every 100,000 people aged 40 to 44.

However, because young people are also less likely to die of other causes, suicide among young people is a leading cause of death in this age group. Better understanding of the stresses that can lead to suicide are crucial for helping avert these deaths.

It is striking that more than half of young people in this study had previously harmed themselves or expressed suicidal ideas. This suggests that many troubled youngsters are showing signs that suicide is a possible risk before their deaths.

There are some drawbacks with this study, which are acknowledged by the researchers. The sources for the information – for most cases, coroner inquests – are not designed to be used for research. Inquests don't look systematically at all the possible factors that might contribute to a death.

People giving evidence may be looking for a reason for the death, so may mention factors such as academic pressure, which were not necessarily a contributing cause. Other factors, such as sexual abuse, may be kept secret and not come to light.

Because this is a case series study, we don't know how common any of these factors are in a comparable group of young people who did not take their own lives. This means we can't say that these factors are more common among young people who die by suicide.

For example, most young people experience relationship problems or break-ups in their teenage years. For the vast majority, this does not lead to suicide.

Although the newspapers focus on particular factors, such as exam stress or internet use, any one of an array of factors can contribute to someone feeling unable to cope with life.

The key message is that everyone needs to be alert for children and young people who are under pressure, especially if they have self-harmed or talked about suicide.

Read more advice about spotting possible warning signs of suicidal thinking and behaviour.

You can contact Samaritans in the UK online or by phoning 116 123.

Links To The Headlines

Acne and exam stress among factors leading young people to suicide, study finds. The Guardian, May 25 2016

Drugs link to one in three teen suicides: New research adds to growing evidence suggesting a connection between cannabis and mental illness. Mail Online, May 26 2016

Exam stress among causes of teen suicide. The Daily Telegraph, May 26 2016

Exam stress and relationship breakdowns often 'final straws' in teenage suicides. ITV News, May 26 2016

Exam pressure and relationship breakdowns linked to suicide among young people. The Independent, May 26 2016

A quarter of teen suicides now 'linked to the web' thanks to online bullying, research and cries for help. The Sun, May 26 2016

Exam pressure behind quarter of teenage suicides. The Times, May 26 2016 (subscription required)

Links To Science

Rodway C, Tham S, Ibrahim S, et al. Suicide in children and young people in England: a consecutive case series. The Lancet Psychiatry. Published online May 25 2016

Categories: NHS Choices

Link between stillbirth and air pollution 'inconclusive'

NHS Choices - Behind the Headlines - Wed, 25/05/2016 - 13:30

"Air pollution may raise risk of stillbirth and pregnant women should consider leaving cities, say scientists," The Daily Telegraph reports.

This is somewhat radical advice given the study that prompted the headline produced no significant or conclusive results.

Stillbirth is when a baby dies before birth, but after 24 weeks of pregnancy. There are about 3,600 stillbirths every year in the UK. It is a rare but devastating outcome, and it can be difficult to know why it's happened.

Possible risk factors include infection during pregnancy, maternal smoking, maternal alcohol consumption, or having twins or multiple pregnancies. Often there is no obvious reason why a stillbirth happened.

Scientists don't know whether air pollution is linked to stillbirth. This study was carried out to summarise all the research on the subject so far. But the results are still unclear.

The pooled risks from the different studies showed a small increase in the chances of stillbirth if a woman lived in an area with raised pollution levels. But the increases in risk were so small that they could be down to chance.

While air pollution is clearly not good news for anyone's health, and governments should do all they can to reduce it, this study does not prove that it causes stillbirth. Impractical and unrealistic advice that pregnant women should move out of cities does not help anyone.

Where did the story come from?

The study was carried out by researchers from the University of Oulu, Finland, and the University of Cape Coast, Ghana, and was funded by the University of Oulu. 

It was published in the peer-reviewed journal Occupational Environmental Medicine on an open-access basis, so you can read it for free online.

The Telegraph and the Daily Mail both led on comments from one of the researchers that it would be "wise advice" to tell a pregnant woman to move to a greener area, without discussing how realistic or practical such advice actually is for most mums-to-be.

The news stories also fail to explain that the findings of this study were not statistically significant, meaning they could have been the result of pure chance.

The Independent and the Daily Mirror give more cautious views of the research and include comments from other experts, which balance their reporting.

What kind of research was this?

This was a systematic review and meta-analysis of observational studies, including cohort studies and case control studies aiming to gather evidence to see whether there may be a link between air pollution and stillbirth.

Systematic reviews are good ways of summarising the state of evidence on a topic, but they are only as good as the studies they include.

There is always a possibility with observational studies that other confounding factors – such as the health and lifestyle of the individual woman – could bias the results.

What did the research involve?

Researchers searched for studies that looked at air pollution, including a wide range of air pollutants, and stillbirths.

They included observational studies that gave information about mothers' estimated exposure to pollution (based on where they lived) and pregnancy outcomes.

They then pooled the data for different types of pollutants to see whether any of them were linked to a raised risk of stillbirth.

Most of the studies used data from air pollution monitoring stations and death certificates. Most balanced the results for confounding factors, such as the women's age and health.

Some adjusted their results to take account of the effects of other types of pollution, although most did not. Some adjusted for factors like the time of year and weather, which can affect pollution concentrations.

The researchers carried out a meta-analysis of the effect of each of six types of pollutant on the risk of stillbirth. The studies covered 11 types of pollutant, but there was not enough comparable information to do a meta-analysis on all types.

What were the basic results?

None of the six pollutants studied showed a clear risk of stillbirth. The pollutants included were:

  • sulphur dioxide
  • nitrogen dioxide
  • carbon monoxide
  • course particulate matter (PM10)
  • fine particulate matter (PM 2.5)
  • ozone

All the pollutants were linked to an increased risk when levels were higher than average, but this raised risk was too small to be sure it was not down to chance – in other words, it was not statistically significant.

In each case, the results' "95% confidence intervals" included the possibility that the raised pollution levels had no effect on risk of stillbirth.

This was true for each of the pollutants studied at every stage of pregnancy. The results showed the effect of stage of pregnancy differed from one pollutant to another, so in some the possible risk was higher in the first trimester and in others it was higher in the third trimester.

How did the researchers interpret the results?

The researchers say they found "suggestive evidence" that air pollution is a risk factor for stillbirth.

They say pregnant women "should be aware" of this risk, but that the main action required is by governments to reduce pollution levels.

They do not state in the paper itself that pregnant women should move to the countryside.


Pregnancy can be an anxious time for women – well-meant but alarming advice about possible risks to your unborn baby is not always helpful.

It's difficult to know what to make of a paper with inconclusive findings, like this one. As one expert says: "A reasonable headline for a press release on this work could have been 'Air pollution and stillbirth – we still don't know whether they are linked'."

The quote comes from Professor Kevin Conway, professor of applied statistics at the Open University, who concludes: "I don't think these new findings should be a serious cause for concern for individual pregnant women – if there is an increased risk of stillbirth, this review indicates that the increase is pretty small."

To put the risk into context, several of the pollutants studied were associated with a non-significant risk increase of around 2%. The non-significance means there's no evidence for a link, but even if there is one, it seems the risk increase from air pollution is likely to be very small.

Compare to this the findings of a previous systematic review, which found that secondhand smoke exposure increased stillbirth risk by 23% – and this time it was a significant link.     

However, Professor Conway and other experts agree that pollution and the potential risk of stillbirth are important topics to investigate, and future studies should be carried out to look at this area.

While the study doesn't show that pollution definitely causes stillbirth, it doesn't rule out the possibility.

One issue that needs to be addressed in future research is an accurate assessment of how much pollution individual women breathe in.

The studies assessed women's pollution exposure based on where they lived in relation to the nearest air quality monitoring station.

For some women, that was up to 25km away, so the levels monitored at the station may not reflect the quality of the air women were breathing.

Other studies have shown that just moving one street back from a busy road can make a big difference to your exposure to pollution.

We also don't know enough about the women's lives – where they worked, whether they travelled away from their homes, or what the air quality was like in their houses or workplaces.

Another major problem with the study is that even if scientists did show a strong link to pollution, we don't know whether this might have been caused by other confounding factors.

For example, people living in more polluted areas might have poorer health for other reasons, such as taking less exercise or having less money to spend on healthy food.

Finding out whether air pollution might be a cause of stillbirth is not easy. It's good that scientists are doing this research and making an effort to find out about the effects of air pollution. So far, however, we don't have enough reliable information to know its effects for sure.

The researchers' suggestion that pregnant women should consider moving to the countryside, as reported by the media, cannot be supported based on the evidence seen here. Aside from the impracticalities, moving house while pregnant could add unneeded stress during a pregnancy.

The most effective steps you can take to reduce your risk of having a stillbirth are to avoid smoking and drinking and be cautious of sources of infections known to be harmful.  

Links To The Headlines

Air pollution may raise risk of stillbirth and pregnant women should consider leaving cities, say scientists. The Daily Telegraph, May 25 2016

Pregnant women 'should consider moving to the countryside' because air pollution may raise the risk of stillbirth, doctors warn. Daily Mail, May 25 2016

Air pollution could increase risk of stillbirth, research suggests. The Independent, May 25 2016

Stillbirth risk increased by exposure to air pollution caused by car and industrial emissions, warn experts. Daily Mirror, May 24 2016

Links To Science

Siddika N, Balogun HA, Amegah A, et al. Prenatal ambient air pollution exposure and the risk of stillbirth: systematic review and meta-analysis of the empirical evidence. Occupational and Environmental Medicine. Published online May 24 2016

Categories: NHS Choices

Proof opiates are useful for chronic back pain 'lacking'

NHS Choices - Behind the Headlines - Tue, 24/05/2016 - 14:30

"Powerful painkillers doled out in their millions are ineffective against back pain," the Daily Mail reports.

An Australian review found evidence for the effectiveness of opiate-based painkillers, such as tramadol and oxycodone, for chronic back pain was "lacking".

The review pooled the findings of 20 trials investigating the safety and effects of opioid painkillers for non-specific or mechanical chronic lower back pain.

This is back pain with no identified cause, such as a "slipped" disc or injury. This is a common, yet poorly understood, type of back pain that is often challenging to treat.

The trials found opioids had a minimal effect on pain compared with an inactive placebo – about half the level that would be needed for a clinically meaningful effect.

The rate of intolerance was also very high, with often half or more people experiencing side effects like nausea and constipation, and withdrawing from treatment as a result.

The findings lend support to national guidelines for the management of non-specific lower back pain, which suggest it is inadvisable for a person to rely solely on painkillers.

Self-management techniques, such as education, exercise programmes, manual therapy and sometimes psychological interventions, may deliver greater lasting benefits.

If pain relief is needed, weaker painkillers, such as paracetamol, and anti-inflammatory drugs, such as ibuprofen, are advised initially, with strong opioids only used for a short period of time for severe pain.  

If you are having trouble coping with chronic pain, contact your GP, who may be able to recommend additional treatments and services.

Where did the story come from?

The study was carried out by researchers from the George Institute for Global Health at the University of Sydney, and other institutions in Australia.

Funding was provided by the Australian National Health and Medical Research Council.

The review was published in the peer-reviewed journal JAMA Internal Medicine on an open-access basis, so it is free for you to read online.

The Mail's reporting of the study was generally accurate, but the headline in the print version of its story – "Back pain drugs 'do more harm than good'" – is unsupported.

The study only considered short-term side effects such as nausea and constipation, and not the longer-term problems addressed in the paper's reporting, like addiction and overdose.

What kind of research was this?

This systematic review and meta-analysis pooled the results of randomised controlled trials, aiming to see whether opioid painkillers such as codeine, tramadol and morphine are safe and effective for managing lower back pain.

Although people with chronic lower back pain may often resort to the use of opioids because lesser painkillers are ineffective, the researchers say there has been no systematic study examining their effects and tolerability at different doses.

A systematic review is the best way of gathering the available evidence to look at safety and effectiveness, but the strength of a review's findings are only as good as the studies it includes.

What did the research involve?

The researchers searched several literature databases to identify randomised controlled trials of opioid use in people with non-specific lower back pain.

Sometimes called mechanical lower back pain, this is back pain where no specific cause can be identified, such as a herniated, or "slipped", disc, inflammatory conditions, infection, or cancer, for example.

Trials were eligible if they compared an opioid with inactive placebo, or compared two different drugs or doses, and reported outcomes of pain, disability or adverse effects.

There were no restrictions on the duration of back pain, painkiller use, use of other medications, or the presence of other illnesses. Two researchers reviewed and quality assessed studies, and extracted data.

The trials included rated pain on visual or numerical scales (for example, rating pain from 0 to 100) and disability scores on questionnaires such as the Roland Morris Disability Questionnaire and Oswestry Disability Index.

The researchers reported the mean difference in scores between the opioid and control groups. A difference of 10 points on a 100-point scale was a minimal difference required for any effect on pain, but a 20-point difference was considered a clinically meaningful effect.

The researchers were mainly interested in short-term effects on pain relief. They also looked at the number of people who withdrew from the trial or were lost to follow-up as a result of adverse effects or lack of effect.    

Twenty trials involving 7,295 people were identified, 17 of which compared opioids with placebo, while two compared opioids with each other.

All the trials examined effects in the short term only – the maximum treatment and follow-up period was three months. The trials were generally high quality. 

What were the basic results?

The pooled results of 13 studies (3,419 people) found opioids had a minimal effect on pain – there was a mean 10.1 score difference between opioids and placebo (95% confidence interval [CI] 7.4 to 12.8 reduction).

The difference when using single-ingredient opioids was 8.1, and 11.9 when using an opioid combined with another simple painkiller, like paracetamol.    

There was limited data available for disability. Two studies found the combination of tramadol and paracetamol had no effect on disability compared with placebo, while another found no effect for morphine. However, the quality of evidence for these outcomes was said to be very low.

The researchers looked at studies with a run-in period separately. This is where only those who responded favourably during the trial phase were actually randomised. Such trials therefore preferentially only include good responders.

These results found increasing opioid dose was associated with better pain relief, but clinically meaningful effects on pain were still not seen at any of the doses evaluated.

When looking at the two head-to-head trials directly comparing two opioids/doses, both trials found around a five-point score difference.

The proportion of participants who withdrew was high in all trials – up to around 50% or greater withdrew.

The main cause for withdrawal was lack of effect or adverse effects. More than half the people taking opioids experienced side effects such as nausea, constipation and headaches. 

How did the researchers interpret the results?

The researchers concluded: "For people with chronic low back pain who tolerate the medicine, opioid analgesics provide modest short-term pain relief, but the effect is not likely to be clinically important within guideline recommended doses." 


This systematic review found no evidence that opioids provide a meaningful effect on chronic non-specific lower back pain.

Opioids are often used as a last resort for people who have not responded to other painkillers. But these results found opioids gave only half the size of the effect that would be needed to make a real difference – about a 10-point score difference, rather than 20.

On the whole, the body of evidence was high quality. A large number of trials where identified, and most were multi-centre trials with good sample sizes carried out in the US, Canada, Australia and Europe. This means the findings should be representative of people with this condition in the UK.

Most of the evidence compared the effect of opioids with placebo only, rather than any other active intervention.

And 17 of the studies were funded by the pharmaceutical industry, giving uncertain potential for publication bias.

However, in these cases, if anything, you would expect to see an overly favourable effect of opioids, which is not the case.  

The extremely high dropout rate also cannot go unnoticed – 50% or greater in many studies.

This may have contributed to the lack of effect seen, but also demonstrates the difficulty there is tolerating these strong painkillers. Many people experience debilitating side effects when taking them, such as nausea, vomiting and constipation.  

Chronic non-specific lower back pain is an extremely common cause of disability in the UK. Perhaps overreliance on pain killers and anti-inflammatory drugs isn't the best answer.

As the guideline body the National Institute for Health and Care Excellence (NICE) says, a key focus should be on helping people manage their condition themselves through education and information, exercise programmes, or manual therapy.

Chronic non-specific pain can sometimes also have a psychological element, and interventions such as cognitive behavioural therapy can be helpful.

NICE recommends regular paracetamol as the first-choice option for pain relief. If this is insufficient, they suggest moving to non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, or weak opioids, such as codeine, but being aware of the potential side effects of both.

Stronger opioids, such as fentanyl or oxycodone, are only advised for short-term use for severe pain.     

These recommendations, and the findings of this review, do not apply to people with identified causes of their back pain, such as inflammatory conditions, infections, cancer, or trauma. 

If you have been taking opiate-based painkillers for some time and feel you no longer need or want to take them, you should talk to your GP. Stopping suddenly is not a good idea as this could trigger withdrawal symptoms.

For more information, visit the NHS Choices guide to back pain.

Links To The Headlines

Powerful painkillers for back pain like morphine and tramadol are 'NOT effective and can be dangerous'. Daily Mail, May 23 2016

Links To Science

Shaheed CA, Maher CG, Williams KA, et al. Efficacy, Tolerability, and Dose-Dependent Effects of Opioid Analgesics for Low Back Pain. JAMA Internal Medicine. Published online May 23 2016

Categories: NHS Choices

Report attacks official guidance on low-fat diets

NHS Choices - Behind the Headlines - Mon, 23/05/2016 - 15:40

"Low-fat diet bad for your health and cutting back on meat, dairy and eggs a disastrous mistake," the Daily Mirror reports.

That is the main message of a controversial report attacking official UK guidelines on diet and weight loss.

The report suggests it doesn't matter how much saturated fat we eat, and doesn't recommend counting calories.

Critics have pointed out there were no agreed criteria about what evidence would be considered in the report, leaving it open to accusations of cherry-picking.

This means the report's authors may have promoted evidence supporting their argument while ignoring evidence they saw as unhelpful.

Dr Mike Knapton, associate medical director at the British Heart Foundation (BHF), said: "This report is full of ideas and opinion.

"However, it does not offer the robust and comprehensive review of evidence that would be required for the BHF, as the UK's largest heart research charity, to take it seriously."


Who produced the report?

The report was published by the Public Health Collaboration, a not-for-profit organisation described as being dedicated to informing the public and implementing healthy decisions.

The report is said to follow decades of work and experience that founding and advisory board members have gathered through working with thousands of patients to improve their health.

The listed advisory board members are named health professionals, including dietitians, GPs, a cardiologist, a diabetes specialist and a psychiatrist. They also list a number of patrons.

It is unclear where Public Health Collaboration's funding comes from. Nor is it clear who wrote the report.

No author or authors are named, and it does not appear to have been peer-reviewed by independent experts.

The aim of the report is said to be to raise concerns about the government's current recommendations about healthy eating and weight loss, and also provide new evidence-based solutions to help people obtain healthy lifestyles and improve public health.   


What does the report say?

The report states the current prevalence of obesity in the UK is 25%, costing the economy £47 billion a year. 

It summarises the recommendations of the current Eatwell Guide for healthy eating, saying it has three main concerns with this guidance:

  • the avoidance of foods because of their saturated fat content
  • the dietary reference value of no more than 35% total fat
  • the quality and quantity of carbohydrates
Saturated fat

The researchers say current recommendations given on NHS Choices are to opt for low-fat dairy options, as high saturated fat can increase the risk of heart disease.

They highlight a large US cohort study from 2010 that concluded saturated fat intake was not associated with risk of cardiovascular disease.

They quote several other observational studies that supported the notion that high-fat dairy was not linked to obesity or cardiovascular and diabetes risk.

The researchers say: "In retrospect, there was never any strong evidence to recommend reducing total and saturated fat consumption, and in the 30 years since, the deteriorating health of the UK population suggests such advice may have been a dire mistake, however well intentioned."

They consider that if people had been opting for foods in the natural form, rather than manufactured low-fat foods, we wouldn't have the obesity problem we do today.

The Public Health Collaboration concludes the UK should stop recommending the avoidance of high saturated fat foods and focus on consuming food in its natural form – however much saturated fat it contains.

No more than 35% total fat

The authors question recommendations that too much fat in your diet raises the risk of heart disease and makes you overweight, saying this is not backed by scientific evidence.

They reference a trial published this year, which found people on low-carb diets experienced more weight loss than people on low-fat diets, and say how recent US dietary guidelines have removed their previous 30% total fat limit and no longer place any restriction on fat.

They conclude the UK should remove the recommendation to eat no more than 35% total calorie intake from fat and instead focus on the health benefits of eating food in its natural form – regardless of fat content.

Quality and quantity of carbohydrates

As the authors say, good blood glucose control is important to maintain health and reduce the risk of developing diabetes or pre-diabetes conditions.

However, they say eating lots of foods that raise blood glucose and promote the release of insulin are factors likely to increase this risk – and high carbohydrates do just that.

They discuss the glycaemic index (GI) of different foods, and say the UK's Eatwell Guide "illogically" recommends high-GI foods, advising people to "base meals on potatoes, bread, rice, pasta or other starchy carbohydrates".

They suggest that such recommendations are behind the increase in rates of type 2 diabetes and obesity.

The Public Health Collaboration concludes people should avoid foods that have a high carbohydrate density, and instead focus on food and drink that has a carb density of less than 25%. Such foods are usually in their natural form.

"Real food" lifestyle

The Collaboration sets out a new form of the Eatwell Guide called "The Real Food Lifestyle", which has a 50:50 split of fats and proteins against carbohydrates, but all food and drinks on the wheel are in their natural form.

They emphasise carbs with a density less than 25% and a minimum of 1g protein per 1kg bodyweight per day.

They also emphasise eating "real" foods that will fill you and avoiding processed "fake foods", which won't.

For example, they recommend natural oils and butter, including coconut oil, ghee, lard and cold-pressed olive oil – the "fake" ones are rapeseed, sunflower and corn oil – and no juices or processed sugar products.

If you were being critical you could argue that the division between “real food” and “fake food” is scientifically meaningless.

What evidence is this based on?

The report is presented in the form of a narrative, where individual pieces of evidence are cited as coming from particular studies. A list of references is then provided at the end.

However, the report does not provide any information about how the authors identified and selected the research reviewed.

As such, it is not possible to say this was a systematic review, and we cannot know for sure this is a balanced report that has reviewed all evidence relevant to diet and nutrition.

The standard warnings about cherry-picking – evidence that is inconvenient may be ignored – apply.

Also, without reviewing the individual studies referenced, it is not possible to appraise the quality and strength of this evidence. However, many are observational.

There is potential for various sources of confounding and bias to influence associations between self-reported diet and health outcomes, such as inaccurate recall on food questionnaires or the potential influence of other unmeasured health and lifestyle factors.

It can be difficult to know to what extent a particular outcome can be directly attributed to a particular food – or the absence of it.

The report further says it "clearly and concisely provides an insight into the decades of work and experience that our founding members and advisory board have accumulated from working with thousands of patients".

But it's not known what sort of experience or data from patients has contributed to informing this.  

We also don't know, for example, whether the recommendations on fat and carbohydrate intake would be applicable to all stages in life, or whether there might be different advice for children.

The report makes much of the fact that in spite of UK dietary guidelines, the number of people with obesity and type 2 diabetes has grown in recent decades. However, this does not prove that the guidelines are to blame. 

What response has there been to the report?

The report has attracted quite considerable criticism.

Some professionals, such as the professor of diet and population health at the University of Oxford, note the lack of systematic review methods and accuse the report of potentially cherry-picking studies to support its viewpoint.

Other studies presenting contradictory findings do not seem to have been included, they say.

As a scientist from the University of Reading says: "As with any public health measure, it is important that any recommendations are based on solid evidence and take the wider implications of implementation into account. That doesn't seem to be the case in this instance."

Professor Tom Sanders, emeritus professor of nutrition and dietetics at King's College London, says statements such as "fat doesn't make you fat", "saturated fat doesn't cause heart disease", and "avoid 'low fat' " are potentially harmful and could mislead the public.

Other opinion is more mixed, with one professor saying the report has "good, bad and ugly elements in it". There are views that snacking and added sugar are to be avoided, but ideas that we should eat limitless fat and cut out sugar altogether are criticised.

BBC news quotes Dr Alison Tedstone, Public Health England's chief nutritionist, who says: "In the face of all the evidence, calling for people to eat more fat, cut out carbs and ignore calories is irresponsible."

She says thousands of scientific studies have been considered when making current UK health and nutrition recommendations.

"It's a risk to the nation's health when potentially influential voices suggest people should eat a high-fat diet, especially saturated fat," she says.

"Too much saturated fat in the diet increases the risk of raised cholesterol, a route to heart disease and possible death." 

Links To The Headlines

Low fat diet bad for your health and cutting back on meat, dairy and eggs a disastrous mistake. Daily Mirror, May 23 2016

Public Health England: Advice to eat more fat 'irresponsible'. BBC News, May 23 2016

Official advice on low-fat diet and cholesterol is wrong, says health charity. The Guardian, May 23 2016

Now experts say low fat diets are BAD for you: Obesity charity claims you should stop counting calories and eat more healthy fats. Daily Mail, May 23 2016

'Eat fat to get thin': Official diet advice is 'disastrous' for obesity fight, new report warns. The Daily Telegraph, May 23 2016

Eating full fat foods 'can lower chance of obesity'. The Independent, May 23 2016

Get fat to get fit: A diet rich in full fat dairy and meat can lower the chance of obesity, health charity claims. The Sun, May 23 2016

Row over 'eat more fat' dietary advice. ITV News, May 22 2016

Categories: NHS Choices

Healthier lifestyles 'could cut cancer death rates'

NHS Choices - Behind the Headlines - Fri, 20/05/2016 - 17:10

"Half of all cancer deaths could be avoided if people simply adopted a healthier lifestyle," the Daily Mail reports.

A new study adds to the weight of evidence that says combining simple lifestyle changes can dramatically cut cancer death rates.

More than 100,000 health professionals from the US were asked to complete questionnaires about their lifestyle and cancer status every two years, and diet every four years.

The researchers compared cancer rates between people with low- and high-risk lifestyle factors, and also compared rates in the low-risk group with the general white population in the US.

They found a large number of cancer cases and deaths could be attributed to a high-risk lifestyle, such as an individual being overweight, smoking, drinking heavily, or being physically inactive.

The researchers estimated between a quarter and a third of all cancer cases in this population group could be attributed to poor lifestyle factors.

These findings are in agreement with past research and the understanding that a healthier lifestyle may reduce the risk of various types of cancer.

But this study has limitations, including the population group, which only involved white American health professionals, and the possibility that the estimates are inaccurate. 

The study would appear to confirm that any small lifestyle changes you can make, such as quitting smoking, could considerably reduce your risk of developing cancer. And the more of these small changes you can combine, the greater the effect.

Read more about how lifestyle changes can help prevent cancer.

Where did the story come from?

The study was carried out by researchers from Harvard Medical School and was funded by the US National Institutes of Health.

It was published in the peer-reviewed journal, JAMA Oncology.

The Daily Mail reported on the study fairly accurately, but did not present any of its limitations.

It's nice to see that the article included clear recommendations from the research team about how a person can reduce their risk of cancer.

However, the headline figure of "half of all cancer deaths" seems a bit of a fudge, as the study presented a range of different results for specific cancer types.

What kind of research was this?

This prospective cohort study followed a large population group over time, and assessed the incidence of cancer and related deaths.

The researchers looked at how these cancer outcomes were related to various lifestyle factors, and then estimated the proportion of cancers that could be attributed to these factors.

The observational nature of this type of study means it is not able to prove causation, but it can find links and potential risk factors.

This type of study has strengths in terms of being able to follow a large number of participants over a long period of time, but the number of people who become non-responsive to follow-up assessments may increase over the years.

What did the research involve?

The researchers recruited participants from two cohort studies:

  • The Nurses' Health Study – which started in 1976 and enrolled female nurses aged 30 to 55
  • The Health Professionals Follow-up Study – which started in 1986 and enrolled male health professionals aged 40 to 75

Participants completed questionnaires about their medical history and lifestyle at the beginning of the study and every two years thereafter. Dietary information was collected every four years using a validated food frequency questionnaire.

The researchers split the participants into two groups according to the level of health risk associated with their lifestyle.

To be considered low risk, a participant had to meet the following requirements:

  • have never smoked or be a past smoker more than five years ago
  • drink no or a moderate amount of alcohol – no more than one drink a day for women and two for men
  • have a body mass index (BMI) of at least 18.5 and lower than 27.5
  • do at least 75 minutes of vigorous-intensity or 150 minutes of moderate-intensity aerobic physical activity a week

If all of these requirements were not met, the participant would be considered high risk.

The outcomes of interest were the incidence of total and major individual cancers and associated deaths. Cancer was self-reported in the questionnaires. Where a participant failed to respond, the National Death Index was used to identify deaths.

The researchers compared the cancer rates between the low- and high-risk groups. They then compared cancer rates in the low-risk group with cancer rates in the general population using national surveillance data.

They used this information to help them calculate population-attributable risk (PAR).

This is an estimate of the proportion of all cancer cases that can be attributed to poor lifestyle factors, or the number of cancers that would not occur in a population if the risk factor – in this case, a high-risk lifestyle – was eliminated.

For example, a PAR could be used to estimate how many people in a given population would not die of lung cancer if nobody in that population smoked.

What were the basic results?

A total of 135,910 people were included in the study (89,571 women and 46,339 men). The low-risk group contained 21% of all participants (12% women and 9% men) with the remaining 79% classed as high risk (54% women and 25% men).

The incidence of cancer per 100,000 people was 463 for women and 283 for men in the low-risk groups, compared with 618 for women and 425 for men in the high-risk groups.

From this, the researchers estimated that 25% of cancers in women and 33% of cancers in men could be attributed to high-risk lifestyle factors. For cancer-related deaths, 48% of cancer deaths in women and 44% of cancer deaths in men could be attributed to a high-risk lifestyle.

For individual cancers, the proportion of cancers estimated to be caused by high-risk lifestyle factors were:

  • lung – 82% for women, 78% for men
  • bowel – 29% for women, 20% for men
  • pancreas – 30% for women, 29% for men
  • bladder – 36% for women, 44% for men

Estimates were similar for cancer death, though there were additional associations for some other sites, including breast (12%), womb (49%), kidney (48% in men), and oral and throat (75% in women and 57% in men) cancers.

The general US populations were at higher risk than the whole study population, meaning that the PARs for these cancers resulting from a poor lifestyle were even higher than the researchers' estimates – for example, the PAR for bowel cancer jumped to 50%. 

How did the researchers interpret the results?

The researchers concluded that, "In this cohort study of a portion of the US white population, about 20-40% of cancer cases and about half of cancer deaths can be potentially prevented through lifestyle modification.

"These figures increased to 40-70% when assessed with regard to the population of US whites, and the observations are potentially applicable to broader segments of the US population." 


This prospective cohort study assessed the number of cancer cases and related deaths associated with poor lifestyle factors in a sample of US health professionals.

As the findings demonstrate, a large number of cancer cases and deaths in both men and women can be attributed to a high-risk lifestyle, such as being overweight, smoking, drinking heavily, or being physically inactive.

Worryingly, a poor lifestyle was estimated to account for an even greater number of cancers in the general population.

These findings are in agreement with much research, which has found that a healthier lifestyle may reduce the risk of various cancers.

The study has both strengths and limitations to consider. It contained a large number of participants and excluded types of cancer where incidence may be related to environmental factors rather than lifestyle, both adding strength to the findings.

It did have limitations, however:

  • The use of questionnaires for collecting information is prone to bias, either by people reporting what they think they should be doing rather than what they are doing, or because of difficulty recalling information over a period of time.
  • Only medical professionals were included in the study. This group are potentially more health conscious, so may not be a good reflection of the whole population. This is supported by the fact that even the high-risk study group were healthier than the US population overall, and PAR estimates for cancer from poor lifestyle factors were higher in the general population.
  • Only including a white population means these findings may not necessarily apply to other ethnicities.
  • These results are only estimates: though informed by careful analysis of this population and their lifestyle factors and cancer rates, it's possible that the proportion of cancers attributed to poor lifestyle factors is inaccurate, particularly for wider populations.

Despite these limitations, it is well known that unhealthy lifestyle factors could increase your risk of developing cancer, as well as various other health problems. Any small changes you can make to your lifestyle could considerably reduce your risk.

Read more about how to prevent cancer.

Links To The Headlines

HALF of all cancer deaths could be avoided if we simply adopted a healthier lifestyle. Daily Mail, May 19 2016

Links To Science

Song M, Giovannucci E. Preventable Incidence and Mortality of Carcinoma Associated With Lifestyle Factors Among White Adults in the United States. JAMA Oncology. Published online May 19 2016

Categories: NHS Choices

Review calls for global action to tackle antibiotic resistance crisis

NHS Choices - Behind the Headlines - Fri, 20/05/2016 - 01:30

"Superbugs will kill someone every three seconds by 2050 unless the world acts now," BBC News reports.

A review commissioned by the UK government says wide-ranging action is required at a global level to prevent a post-antibiotic future.

The review panel, chaired by economist Jim O'Neill, warns that without global action, antibiotic resistance will become a "devastating problem" by 2050, responsible for an estimated 10 million deaths a year.

Surgery could also carry a much higher risk of complications because of the possibility of infection.

What is antibiotic resistance?

Antibiotics are often used to treat bacterial infections and are a cornerstone of infectious disease care.

However, bacteria evolve in response to their environment. Over time, they can develop mechanisms to survive a course of antibiotic treatment.

This "resistance" to treatment starts as a random mutation in the bacteria's genetic code, or the transfer of small pieces of DNA between bacteria.

If the mutations are favourable to them, they are more likely to survive treatment and be able to replicate, and are therefore more likely to pass on their resistant nature to future generations of bacteria.

When taken correctly, antibiotics will kill most non-resistant bacteria, so these resistant strains can become the dominant strain of a bacterium. This means that when people become infected, existing treatments may be unable to stop the infections.

What recommendations does the review make?

The review makes 10 recommendations, outlined below.

Launch a massive global public awareness campaign

The issue of antibiotic resistance is still not fully appreciated, especially in the developing world, where antibiotics are often sold without prescription.

The review estimates that a successful global campaign could be mounted for around $40 to $100 million a year, a fraction of the advertising costs for products like pet food or chocolate.

Improve hygiene and prevent the spread of infection

Improving access to clean water and sanitation, promoting best practice in hospital infection control, and simply encouraging people to wash their hands will all help prevent infection.

Reduce unnecessary use of antibiotics in agriculture

The US Food and Drug Administration estimates 70% of medically useful antibiotics are actually sold for use in animals.

It argues that critically important antibiotics should be restricted from animal sales.

Improve global surveillance of drug consumption and resistance

Governments need to share data on antibiotic consumption and levels of resistance, and the biological reasons underpinning the two. Poorer countries should be given assistance in gathering data.

Promote new rapid diagnostic tests to reduce unnecessary use of antibiotics

Many antibiotics are prescribed in cases when a bacterial infection hasn't been confirmed, as a precaution. New types of tests could help prevent this.

The review hopes that by 2020, in wealthy countries antibiotics would only be prescribed if a bacterial infection had been confirmed through testing.

Promote the development and use of vaccines and alternatives

Encouraging the take-up of existing vaccines, as well as providing incentives for the creation of new ones, should help reduce the demand for antibiotics.

There also may be alternative interventions that can help prevent infections occurring.

Improve the number, pay and recognition of people working in infectious diseases

Infectious disease health professionals tend to be paid less than their peers working in other fields.

A similar pattern can be seen in both private and public sector workers involved in infection research.

Establish a Global Innovation Fund for early-stage and non-commercial research

The review recommends that a Global Innovation Fund, endowed with $5 billion over the next five years, should be set up to fund "blue sky" research – research that may not have an immediate commercial application, but could lead to breakthroughs in the future.

Better incentives to promote investment for new drugs and improve existing ones

There is currently not a great deal of profit in antibiotic research, so pharmaceutical companies should be encouraged by meaningful incentives, such as a reward for bringing a new drug to market.

Build a global coalition for real action

Antibiotic resistance is a global problem, so it can only be tackled through global action. The review recommends that the G20 countries spearhead action via the United Nations. 

Links To The Headlines

Global antibiotics 'revolution' needed. BBC News, May 19 2016

Blueprint To Tackle Growing Drug Resistance. Sky News, May 19 2016

Antibiotics will stop working at a 'terrible human cost', major report warns. The Independent, May 19 2016

No antibiotics unless doctor runs tests first: Superbugs tsar urges crackdown over fears infections 'will kill more than cancer' by 2050. Mail Online, May 19 2016

Billion dollar rewards for new antibiotics called for to defeat catastrophic rise of superbugs. The Daily Telegraph, May 19 2016

No antibiotics without a test, says report on rising antimicrobial resistance. The Guardian, May 19 2016

Superbugs will kill 10m people a year without new antibiotics claims report. The Sun, May 19 2016

Categories: NHS Choices

Study: 'mini strokes should be treated immediately with aspirin'

NHS Choices - Behind the Headlines - Thu, 19/05/2016 - 15:45

"People should consider taking aspirin immediately after a minor stroke," BBC News reports.

A review of existing evidence found people treated with aspirin after a mini stroke (transient ischaemic attack, or TIA) were less likely to experience a more serious follow-up stroke.

A TIA occurs when a blood clot temporarily blocks blood flow in the brain. It causes problems including numbness or weakness of the face, arms or legs, as well as dizziness and problems with speech and sight.

These usually pass quickly, but are a warning sign of the possibility of a second, more serious stroke in the next few weeks. If you have these symptoms or see someone with them, you should call 999 for an ambulance immediately.

The review found taking aspirin reduced the risk of having another stroke by about 60% in the first six weeks, and of having a disabling or fatal stroke by 70%.

The researchers also suggest people who have symptoms of a stroke should be advised to take aspirin straight away, while waiting for medical help.

But the possible risk of doing this is that if stroke symptoms are caused by bleeding inside the brain, taking an aspirin could make the situation much worse.

The transient symptoms of a TIA are most likely to be caused by a clot, but still, the advice on self-treatment needs to be considered by experts before we can recommend it. The key point is to get medical help immediately by dialling 999. 

Where did the story come from?

The study was carried out by researchers from the University of Oxford, University Medical Centre Utrecht, University Duisburg-Essen and Lund University.

It was funded by the Wellcome Foundation and the National Institute of Health Research Biomedical Research Centre.

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

On the whole, UK media coverage was good, with accurate reporting of the research and the researcher's conclusions.

What kind of research was this?

This was a meta-analysis of randomised controlled trials (RCTs), in which researchers pooled data from a number of studies to get the best summary of the results.

This analysis looked specifically at the effects of the treatment (aspirin) over the course of time.

The researchers wanted to see the effects of aspirin at particular times after a stroke – either a transient ischaemic attack (TIA) or a full stroke caused by a blood clot (ischaemic stroke).

While meta-analyses can provide reliable results, they are only as good as the studies they contain, and there may have been variability in the study design and assessments.

What did the research involve?

Researchers analysed all RCTs that measured the effects of aspirin given after an ischaemic stroke or TIA to prevent a future stroke.

Because many of these trials did not start treatment straight away, they also looked at trials where aspirin was given to people being treated within 48 hours of having a stroke.

They measured the effects of aspirin on repeated stroke and the severity of repeat strokes at up to six weeks after the stroke, between 6 and 12 weeks, and more than 12 weeks.

Most of the studies that established the place of aspirin in the treatment and prevention of stroke were done in the 1980s and 1990s, so some of this research is quite old.

The researchers pooled individual patient data from the studies and stratified it into time periods.

They also looked at studies including the anti-clotting drug dipyramidole, which is sometimes used alongside or instead of aspirin, to see what effect the two drugs had at different time points.

The researchers also assessed the effects of the severity of the first stroke on the results.

What were the basic results?

The risk of having a repeat stroke within six weeks of the initial TIA was cut by about 60% for people taking aspirin.

Just under 1% of people who took aspirin had a repeat stroke within six weeks, compared with 2.3% of people who did not take aspirin (hazard ratio [HR] 0.42, 95% confidence interval [CI] 0.32 to 0.55).

The risk of having a disabling or fatal stroke was cut even more, by about 70% (HR 0.26, 95% CI 0.2 to 0.42). People who'd had a TIA or minor stroke were more likely to benefit from aspirin treatment than those who'd had more severe strokes.

The risk of having a second stroke between 6 and 12 weeks later was also reduced for people taking aspirin.

But after 12 weeks, people who'd taken aspirin were as likely to have a stroke as those who hadn't taken aspirin.

This suggests the effects of aspirin are most important in the weeks immediately after a stroke or TIA, when the risk of another stroke is highest.

When the researchers looked at patients who'd been treated with aspirin immediately after an acute stroke, they again saw a drop in the risk of a repeat stroke, and found this drop in risk was biggest for patients who'd had less severe strokes.

In the trials that compared aspirin with dipyramidole, aspirin alone worked as well as aspirin with dipyramidole to reduce stroke risk in the first 12 weeks, but dipyramidole worked better after 12 weeks.

How did the researchers interpret the results?

The researchers said their results show that the effects of aspirin in reducing the risk of stroke immediately after a first stroke or TIA have been underestimated.

They said that, "It is essential that aspirin is given to patients with suspected TIA or minor stroke immediately."

They went on to suggest that, "Consideration should be given to promoting self-administration [i.e. taking aspirin yourself] immediately after transient stroke-like neurological symptoms."

They also said it would be "prudent" to run a public education campaign to encourage people to seek medical help immediately after having symptoms of stroke, and also to take aspirin.


The study supports current recommended practice that people with a TIA or ischaemic stroke caused by a blood clot are treated with aspirin as soon as possible.

NHS experts are considering whether to recommend that you take aspirin yourself while waiting for medical help.

The reason this isn't recommended at present is that some people will have had a haemorrhagic (bleeding) stroke, and aspirin can make the bleeding worse.

For people who've had a full stroke, an urgent brain scan is usually performed to exclude bleeding as a cause and check it's safe to proceed with anti-clotting treatment. The risk of transient symptoms being caused by bleeding is much smaller, but it is possible.

Until official guidelines are produced – NHS England are reportedly considering the report's findings – current advice still stands. If you are experiencing the symptoms of a stroke, the most important thing is to call for an ambulance immediately. 

The new study included thousands of people from high-quality RCTs, so the results are likely to be reliable, although there are some limitations.

Most of the studies included were conducted 20 or 30 years ago, and the medical treatment of stroke has improved since then, so the results might be different if the trials were run again now.

People who have had a stroke nowadays are more likely to be treated urgently, although too many people with minor strokes or TIAs don't seek help quickly enough.

This analysis would be stronger if the studies included had more people randomised to aspirin treatment within hours or days of their stroke or mini stroke.

However, this would be likely only to strengthen the effects seen with aspirin, and it's unlikely that trials involving more people treated quickly would undermine the main results.

The key point is not to ignore the symptoms of a stroke or TIA, but to treat it as a medical emergency, as you would do a heart attack, and call 999 for help.

Links To The Headlines

'Immediate aspirin' advice for minor stroke. BBC News, May 19 2016

Taking aspirin quickly after minor stroke 'can cut risk of recurrence'. The Guardian, May 19 2016

Take aspirin immediately after a 'funny turn' to cut your risk of stroke. Daily Mail, May 19 2016

Immediate aspirin after mini-stroke substantially reduces risk of suffering a major stroke. The Daily Telegraph, May 18 2016

Taking an aspirin straight after a 'mini stroke' could save your life, say docs. The Sun, May 19 2016

Links To Science

Rothwell PM, Algra A, Chen Z, et al. Effects of aspirin on risk and severity of early recurrent stroke after transient ischaemic attack and ischaemic stroke: time-course analysis of randomised trials. The Lancet. Published online May 18 2016


Categories: NHS Choices

Magic mushroom ingredient tested as depression treatment

NHS Choices - Behind the Headlines - Wed, 18/05/2016 - 17:28

"Magic mushrooms 'promising' in depression," BBC News reports. Magic mushrooms is an umbrella term for fungi that contain psilocybin, a psychoactive substance that can cause intense LSD-like hallucinations, as well as reported feelings of euphoria and "spiritual insight".

Researchers gave two doses of psilocybin to 12 volunteers, all of whom had moderate or severe depression that had not responded to other treatment. As this drug is controlled in the UK, permission from the Home Office was needed for the study, and the participants were closely monitored by psychiatrists.

The intention was to monitor the "intensity" of the experience, as reported by the volunteers, to see if it was feasible to use psilocybin to treat people with severe depression. The researchers also wanted to get an initial impression of its effects.

They found the 12 volunteers tolerated the drug, with minor side effects that did not last long. Eight of them had no symptoms of depression one week after treatment, and five were free from depression after three months.

But because of the type of study this is and its small size, we can't be sure if these results are the result of psilocybin.

The researchers warn that people should not try to treat themselves with mushrooms that contain psilocybin. Aside from their unpredictable effects, magic mushrooms are class A drugs that are illegal to possess – which can carry a seven-year jail sentence – or distribute, which can result in up to life imprisonment.

Where did the story come from?

The study was carried out by researchers from Imperial College London, South London and Maudsley NHS Trust, King's College London, University College London, the Royal London Hospital, and the Beckley Foundation.

It was funded by the Medical Research Council. 

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

While overall the UK media reporting was accurate, The Sun newspaper wins the most inappropriate headline of the month award (and is currently a leading contender for 2016).

Their headline, "Magic mushrooms make you a fun guy", manages to both trivialise the life-limiting and often horrible impact severe depression can have, while simplifying the complex results of this study.

The Sun also used a stock photo of a classic twentysomething cheesy raver with the caption: "Professor Nutt, who worked on the study, was previously sacked as the Government's chief drug adviser in 2009". The distinguished 65-year-old psychiatrist may be a little put out (or possibly amused) by this.

The Daily Mail was also overenthusiastic in its reporting, saying that "Hundreds of thousands of people could benefit from antidepressants derived from magic mushrooms", despite the limited nature of the study.

However, both The Guardian and The Independent give a more measured account of the study and its limitations.

What kind of research was this?

This was an open-label feasibility study designed to test whether the drug psilocybin could be safely given to selected patients with depression, alongside psychological support.

Everyone in the study took the drug, meaning there was no comparison group and everyone knew that they were taking the drug.

That said, it is hard to imagine what could serve as a placebo for a drug (psilocybin) notorious for its hallucinogenic properties.

This type of early-stage trial cannot give us reliable information on efficacy – nor is it set up to do so.

Even if such a trial suggests possible effectiveness, it's hard to be sure whether the results are truly down to the drug or whether they could reflect an "expectation" effect, where people immediately felt better because that is what they expected.

What did the research involve?

Researchers publicised their study, saying they wanted to recruit people with depression that had not responded to other treatments to test psilocybin. Only 12 of the 72 volunteers met the study requirements.

After physical and mental health tests – including checks to make sure the volunteers were not at high risk of psychosis – they were given two doses of psilocybin in hospital, one week apart.

The first was a low dose to check for unexpected reactions, while the second was a high dose aimed at treating depression. The day after treatment, people were asked about their experiences, including the intensity of psychedelic effects (on a scale of 0 to 1) and any unpleasant effects.

Everyone was followed up regularly, by telephone or email, from the day after the high-dose treatment until three months afterwards. Participants filled in questionnaires designed to monitor depression symptoms.

Researchers compared depression scores from before the study began, one week after treatment, and three months after treatment.

What were the basic results?

On average, people rated the intensity of the experience as 0.5 for the low-dose and 0.75 for the high-dose treatment. Psychedelic effects typically appeared from 30 to 60 minutes after taking the dose, peaked after two to three hours, and were no longer detectable after six hours. 

Nobody had to be sedated during the treatment. The main side effects were feeling anxious (which happened to everyone), confusion, nausea and headache. None of these side effects lasted. Average depression scores decreased at one week and remained lower at three months.

Because the study is so small, it may be more useful to look at what happened to the individuals, rather than average depression scores.

After one week, eight people responded to the medicine with reduced depression scores of at least half their previous score, suggesting a big improvement. Seven of them fell into the range that suggested they no longer had depression.

However, most people's depression scores increased over the next three months, and only five of the original 12 volunteers were still free from depression at the end of the study.

At the end of the study, six people had mild or moderate depression, and one person once again had severe depression.

How did the researchers interpret the results?

The researchers said that: "Done with appropriate safeguards, [such as careful screening and therapeutic support] psilocybin can be safely administered" to patients with depression.

They admitted that the study design means "strong inferences cannot be made about the treatment’s therapeutic efficacy" – in other words, we can't be sure that it worked. They went on to say that: "The data do suggest that further research is warranted".

They pointed out that it is rare for people with severe depression to recover spontaneously without treatment, and most of their participants had lived with depression for many years.

They have called for a bigger randomised controlled trial to properly assess how well this treatment works.


Depression is a disabling disease that affects many people in the UK. While antidepressants and therapy work for many people, some people don't fully respond to treatment.

A treatment for depression that uses a drug that works in a different way from existing antidepressants could be very helpful.

Having said that, this study doesn't tell us whether psilocybin is a useful drug for treating depression. This was a very small, early-stage trial that only aimed to see whether the drug was safe and has potential for use – the researchers did not set out to see if the drug is effective for treating severe depression.

Here are some points to consider:

  • Ten of the recruits had referred themselves, rather than being referred by a doctor. This means they actively sought out treatment with psilocybin. Interestingly, five of the 12 had taken psilocybin before, which may mean they joined the study because they already thought the treatment worked for them.
  • There was no control group and no placebo – everyone was given the treatment and knew they were taking the treatment. This means we don't know whether the treatment itself or another factor, such as the intensive therapeutic support from psychiatrists, might have caused the improved depression scores.
  • The chart showing the depression scores for each individual shows that most people (not everyone) had a big initial drop in depression scores by one week after treatment, followed in many cases by a fairly sharp upswing in scores after that. This could mean that the experience of having the treatment has a short-term effect that wears off fairly quickly for most people.

Researchers and funders will review the results of the study and decide whether to build on this with a large randomised controlled trial.

This would give us a better indication of whether this treatment could work for people with depression who are not helped by current treatments – and, most importantly, whether it's safe for use.

The researchers warn that people should not try to treat themselves with mushrooms that contain psilocybin. Aside from their unpredictable effects, magic mushrooms are class A drugs that are illegal to possess or distribute.

We imagine that because of the ongoing political controversies around psychoactive drugs like psilocybin, ketamine and MDMA being used to treat mental health conditions, a larger follow-up phase II trial is not guaranteed to take place.

Links To The Headlines

Magic mushrooms 'promising' in depression. BBC News, May 17 2016

Magic mushrooms make you a fun guy: Tests show shrooms help fight depression. The Sun, May 17 2016

Magic mushrooms 'could help people tormented by incurable depression'. Daily Mail, May 17 2016

Magic mushrooms lift severe depression in clinical trial. The Guardian, May 17 2016

Magic mushrooms could be 'serious breakthrough' for depression treatment, claims drugs expert. The Independent, May 17 2016

Magic mushrooms lifts severe depression in trial. The Daily Telegraph, May 17 2016

Links To Science

Carhart-Harris RL, Bolstridge M, Rucker J, et al. Psilocybin with psychological support for treatment-resistant depression: an open-label feasibility study. The Lancet: Psychiatry. Published online May 17 2016

Categories: NHS Choices

Are broken bones, loneliness and poor sleep really hidden killers?

NHS Choices - Behind the Headlines - Wed, 18/05/2016 - 14:30

"Revealed, the five hidden killers that could send you to an early grave," the Daily Mail reports. These "hidden killers" include loneliness and poor sleep. But this is a simplistic take on complex research aiming to identify new ways of classifying health and wellbeing.

The research assessed the health and lifestyle of 3,000 US adults aged 57 to 85 years, then reassessed how many were incapacitated or had died five years later.

The researchers then compared two models to see which better categorised the participants' health status and risk.

The first mainly looked at the presence of diseases. The second model was more comprehensive, and included wider measures such as psychological wellbeing, mobility and health behaviours.

Overall, two-thirds of the sample was classed as being in "robust" good health when using the medical disease model, but many of these fell into more vulnerable risk groups when using a more comprehensive risk model.

The comprehensive model identified poor mental health, including depression, isolation and memory problems, and frailty and mobility problems as being predictive of mortality – "hidden killers" in newspaper speak – factors that would be largely overlooked if you only focused on physical diseases.

The findings suggest a comprehensive view of a person's health and wellbeing is needed when looking at their risk status and trying to target appropriate medical care and support.

Wellbeing and quality of life is not simply a case of whether or not someone has a physical illness. 

Where did the story come from?

The study was carried out by researchers from the University of Chicago, and was funded by the same institution and the US National Institute of Aging.

It was published in the peer-reviewed journal, PNAS, and the article is openly available for access.

The Daily Mail, The Sun and Metro articles are generally representative of the study's findings on loneliness, fractures and mobility problems.

But none of the papers grasped the point of the study – an attempt to create more complex and subtle models of wellbeing.

What kind of research was this?

This cohort study aimed to look at the best way of defining population health.

The researchers explained how the World Health Organization (WHO) defines health as a "state of complete physical, mental and social wellbeing and not merely the absence of disease or infirmity".

However, despite this there has been little rigorous attempt to use this definition to measure and assess population health. More often, what is described as the "medical model" is used to measure health, which focuses solely on disease diagnoses.

The researchers propose a "comprehensive model" that also considers psychological wellbeing and function as being a better fit to the WHO classification.

The researchers applied both of these models to US survey data to see how population health was defined by the different methods.   

What did the research involve?

The research involved a large, nationally representative sample of 3,005 older US adults aged 57 to 85 years who lived in the community and were taking part in the National Social Life, Health and Aging Project (NSHAP).

The participants were interviewed and completed a questionnaire about their health and lifestyle, as well as having body measures taken.

The researchers then used two different models to categorise the state of a person's health.

The medical model looked at specific diseases:

  • heart disease
  • cancer
  • lung disease
  • stroke
  • diabetes
  • kidney disease
  • liver disease
  • arthritis
  • high blood pressure
  • asthma
  • thyroid disease

The comprehensive model also included 35 additional measures that encompassed five broad dimensions of health and wellbeing:

  • health behaviour – smoking, exercise, sleep
  • psychological health – depression, memory
  • sensory abilities – vision, hearing
  • neuroimmunity – chronic inflammation
  • mobility or frailty – including fractures

The researchers followed these people up five years later. They then identified a few distinct health classes or categories within these models that encompassed several of the disease and wellbeing features, and most reliably indicated a person's health and mortality risk.  

What were the basic results?

The researchers identified five distinct health classes within the medical model that had significant and independent effects on mortality.

The first two classes were people who had undiagnosed high blood pressure (hypertension) and a single non-cardiovascular disease. These were the least vulnerable, or most "robust", health groups.

The intermediate (third) risk group were those with poorly controlled diabetes. The two most vulnerable groups (four and five) were those who had both cardiovascular disease and diabetes, or who had extensive medical illnesses.

People in the first two robust classes had around a 15% risk of being physically incapacitated or dead after five years, compared with 35% in the top extensive illness group.   

In the comprehensive model, six distinct classes arose – again, the first two classes were the least vulnerable, or most robust; classes three and four had an intermediate risk; and five and six were the most vulnerable.

The six classes were:

  1. robust obese – obese but generally in good health
  2. one minor condition – stomach ulcer, thyroid problems, bladder problems
  3. broken bones – people with osteoporosis
  4. poor mental health – depression, poor memory and loneliness
  5. diabetes, hypertension and immobility
  6. extensive medical illnesses and frailty

Almost a quarter of this older US population (22%) were in the first robust obese group. These people often had undiagnosed hypertension as measured by a home device, but, other than this, few other diseases and only a 6% risk of dying after five years.

The second group were not obese and had a minor condition – one not considered to have high mortality risk – and a 16% risk of death.

The two middle classes of the comprehensive model – those with fractures or osteoporosis and poor mental health – included 28% of this US population, despite being, as the researchers say, "largely ignored" by the medical model.   

The last two, most vulnerable, classes had the most compatibility with the vulnerable classes of the medical model, but still more people were reclassified as vulnerable when using the comprehensive model.

People in the most vulnerable sixth group had a 44% risk of dying within five years.

Overall, the medical model classified two-thirds of the older US population as being in robust health. Only half of these people went into the robust classes of the comprehensive model.

These findings suggest that factors such as poor mental health, bone fractures, and sensory and mobility problems are very important to consider when categorising vulnerability and mortality risk.

How did the researchers interpret the results?

The researchers concluded that the comprehensive model identifies new classes of people with mortality risk, such as those with broken bones or poor mental health, who are largely overlooked by medical models that only focus on disease.

They said that: "This approach provides a method for broadly reconceptualising health, which may inform health policy", with implications for medical care, prevention and resource allocation.   


As the researchers say, the WHO definition of health encompasses physical, mental and social wellbeing – not just the presence or absence of disease.

But how often are these extra dimensions taken into account when assessing a person's health status?

In this sample of older adults, just looking at their disease status puts the majority of them into an apparently "robust" health group.

Yet when you consider the additional dimensions of psychological health and wellbeing, you seem to get a much better indication of those who were at higher or lower risk of dying or being incapacitated in the coming five years.

The "hidden killers" the media refer to are factors such as frailty and fractures, and depression and loneliness, which would be overlooked if you looked at disease diagnoses alone.  

This suggests that a comprehensive view of a person's health and wellbeing is needed if you are looking at their risk status, and trying to target appropriate medical care and support.

But you can't say from the results of a study like this that these factors are being overlooked within healthcare.

For example, just because a medical risk model looking at physical diseases alone hasn't looked at these factors as a risk indicator doesn't necessarily mean that the people with these conditions have not been diagnosed in medical practice and are not receiving appropriate care and treatment.

The media term "hidden" in this context is therefore a bit misleading – as is the term "killer".

Of course, factors like loneliness and depression aren't necessarily going to lead to death directly, but could be associated with other poor health factors that together contribute to mortality risk.

Although this is a large, nationally representative sample, these are all older US adults. The six predictive classes the researchers identified to indicate robust, intermediate or vulnerable risk status may not be the same if people from another country were examined, or a population of middle-aged or younger adults.

It would be interesting and useful if researchers carried out a similar analysis on various groups within the UK population.

The study is a valuable contribution to how we define health and wellbeing. However, whether it has any direct implications in terms of health assessment, screening and diagnosis is unknown at this stage.  

Links To The Headlines

Revealed: the five 'hidden killers' that could send you to an early grave. Daily Mail, May 16 2016

Sleeplessness and broken bones: Five hidden killers that could send you to an early grave. The Sun, May 17 2016

The 'hidden killers' that contribute to an early death. Metro, May 17 2016

Links To Science

McClintock MK, Dale W, Laumann EO, Waite L. Empirical redefinition of comprehensive health and well-being in the older adults of the United States (PDF, 984kb). PNAS. Published online May 16 2016

Categories: NHS Choices

Women who regularly attend religious services 'live longer'

NHS Choices - Behind the Headlines - Tue, 17/05/2016 - 16:00

"Going to church could save your life," reports the Daily Mail, adding that, "Women who worship once a week are '25 per cent less likely to die early'."

Perhaps surprisingly, while the first part of the headline is overly simplistic, it may not technically be wrong – according to new research from the US, anyway. Whether or not divine providence is responsible for the increase in lifespan is still up for debate.

A large Harvard study showed that predominantly white Christian nurses who attended religious services more than once a week had a 33% lower relative risk of dying over a 16-year period compared with similar women who did not attend religious services.

A sizeable chunk of the link was explained by social support (23%), smoking rates (23%) and, to a lesser extent, optimism differences (9%) between attenders and non-attenders.

The study was very large, precise, and as robust to bias and confounding as you could reasonably expect, so it can be considered reliable. But the lifestyle and social differences between the groups can't go unnoticed.

It's therefore possible that the regular pattern of social interaction associated with being part of a religious community, and the benefits this brings, is mainly responsible for the outcome seen in this research, rather than any specific religious or spiritual aspects.

Atheists who regularly attend humanist gatherings, or just those who go to weekly bingo sessions, may also experience similar benefits.

Read more about the benefits of connecting with others.

Where did the story come from?

The study was carried out by researchers from the Harvard T. H. Chan School of Public Health in the US.

It was funded by the John Templeton Foundation, which, according to its website, funds research on the "big questions of human purpose and ultimate reality". The foundation has a stated aim of using scientific methods to explore the alleged spiritual aspects of reality.

The study was published in the peer-reviewed Journal of the American Medical Association: Internal Medicine.

Generally, the media covered the story accurately, citing the possible reasons why attending religious services might be good for you in terms of boosting social support, happiness and optimism.

For example, The Independent reported advice from the researchers, who said: "Our results do not imply that healthcare professionals should prescribe attendance at religious services, but for those who already hold religious beliefs, attendance at services could be encouraged as a form of meaningful social participation." 

What kind of research was this?

This cohort study looked at the links between religious service attendance and subsequent death in female nurses.

This type of study is appropriate to investigate this link.

But many factors can influence death rates, and potentially also be linked to church attendance – for example, more resilient social networks can help people cope in times of hardship.

Teasing out any clear causal links from the vast mix of influencing factors is tricky.

What did the research involve?

This study analysed self-reported religious service attendance information from 1996 to 2012 and linked death records from the same time period.

The researchers analysed information from 74,534 female US nurses who had been answering health and lifestyle questionnaires every two years from 1992 to 2012 as part of the Nurses' Health Study, a rich ongoing source of epidemiological research.

From 1992 and every four years thereafter, women were asked how often they go to religious meetings or services. Responses included more than once a week, once a week, one to three times a month, less than once a month, and never (or almost never).

The researchers' main analysis looked at the death rates of women with different frequency of religious attendance, comparing them with those who did not attend.

They adjusted for a lot of confounders to try to isolate the single effect of religious attendance, including:

  • age
  • alcohol consumption
  • physical exercise
  • multivitamin use
  • high blood pressure
  • high cholesterol
  • use of hormonal replacement therapy
  • healthy eating scores
  • smoking status
  • body mass index
  • husband's education level
  • physical impairment
  • social integration score – composite of marriage status, group participation, number of close friends or relatives
  • living alone
  • family income
  • geographic region in the US
  • depression in 1992
  • religious attendance in 1992

The researchers also performed a "mediator" analysis, which helps understand how much each of the confounders is contributing to the main link of interest – in this case, religious service attendance and death.

What were the basic results?

Most women were either Roman Catholic or belonged to other Christian denominations, and 97% or more were white. There was a small minority of Jewish women and no Hindu or Muslim women.

There was a consistent pattern between religious service attendance and lower rates of death from any cause, cardiovascular disease and cancer.

There were 13,537 deaths over the study period, giving a base rate of death of 18.1 %. Compared with women not attending religious services, women who attended a service more than once a week had 33% less risk of dying from any cause during the 16-year study (hazard ratio 0.67, 95% confidence interval [CI] 0.62 to 0.71).

Those attending regularly in both 1996 and 2000 – a sign of long-term, regular attendance – had an even lower relative risk at 45% (95% CI 0.52 to 0.59) less than non-attenders.

Looking at potential mediators, the researchers picked out depressive symptoms, smoking, less social support and optimism as the most important.

Social support explained the highest proportion of the link (23%), with smoking a close second (22%). Optimism accounted for around 9%.

The link appeared consistent over time, as well as for religion (although there wasn't much variety), geography and other potentially influential factors.

How did the researchers interpret the results?

The researchers said that: "Frequent attendance at religious services was associated with significantly lower risk of all-cause, cardiovascular, and cancer mortality among women.

"Religion and spirituality may be an underappreciated resource that physicians could explore with their patients, as appropriate." 


This study showed that white Christian women who attended religious services more than once a week had a lower risk of dying from any cause, cancer, and cardiovascular disease specifically compared with similar women who did not attend religious services.

This link was at least partially explained by social support, smoking rates, and optimism differences between attenders and non-attenders.

As the study was very large, it gives precise estimates of relative risks. The researchers pointed out there are other factors that could potentially mediate the link that they couldn't measure in their study, like psychosocial resilience, religious coping mechanisms, a sense of a purpose in life, and self-discipline.

But their interesting stats also showed that biases from these or other sources would have to be very large to affect the result in a meaningful way, suggesting the study's conclusions are quite solid.

The study mainly involved white women who mostly identified as Christian, so we don't know if the same effects would be seen for men of a similar faith, or adults or children from other religions or with no religion.

Non-religious groups could argue having a purpose in life, self-discipline and many other aspects that potentially mediate the link are not the sole preserve of the religious, but there is no doubt that for many people this comes from practising a faith.

But it's possible the same effect could be achieved in other ways, too. While the researchers tried to account for social factors associated with religious attendance, there could well be other unmeasured, or possibly unconsidered, effects associated with regular social group interaction.

A similar study could have noted reduced mortality among people attending any community activity groups or societies, both for people of all faiths as well as people with none.

As we discussed last month, people with a history of cancer who regularly attended a choir session showed evidence of improved immune function.

Human beings are social animals, so enjoying regular social activities with others is probably a good way, among others, to improve both your physical and mental wellbeing.

Links To The Headlines

Women who go to church more than once a week live five months longer, Harvard study finds. The Independent, May 16 2016

Everlasting life? How going to church could help you live longer. The Daily Telegraph, May 16 2016

Going to church could save your life: Women who worship once a week are '25 per cent less likely to die early'. Daily Mail, May 16 2016

One religious step that could extend your life. Metro, May 16 2016

Links To Science

Li S, Stampfer MJ, Williams DR, VanderWeele TJ. Association of Religious Service Attendance With Mortality Among Women. JAMA Internal Medicine. Published online May 16 2016

Categories: NHS Choices

Dad's age, diet and lifestyle may cause birth defects

NHS Choices - Behind the Headlines - Mon, 16/05/2016 - 16:45

"Men are being warned to become fathers by 40 or face a greater risk of having children with serious illnesses," the Daily Mail reports after a new review looked at some of the evidence about paternal influences on the risk of childhood diseases.

The review discusses several research findings found previously, including some reports that children born to fathers over the age of 40 have higher rates of conditions like autism spectrum disorder – and that stress, smoking and alcohol may also cause heritable changes.  

But this is an opinion piece. We don't know how the researchers selected the evidence they reviewed, and it is possible that not all relevant research was considered.

The review should not be taken as firm evidence that there is such a thing as a "male biological clock" and fathers are putting their children at risk by delaying fatherhood until middle age.

Still, men trying for a baby should avoid smokingexcessive alcohol consumption and eating a poor diet. It may not boost your sperm's health, but it will definitely improve your health.  

Where did the story come from?

The study was carried out by researchers from Georgetown University Medical Centre in the US, and was funded by the US National Institutes of Health.

It was published in the peer-reviewed American Journal of Stem Cells. This is an open-access journal, so the study can be downloaded for free as a PDF.

Neither the Daily Mail nor The Times recognise the important limitations of this review: namely, that is it is not a systematic review, so it carries far less weight in terms of evidence.

Also, the Mail talks about men being "warned" about delaying fatherhood – but, as far as we can tell, the only people actually issuing any warning based on this review is the Mail itself.

What kind of research was this?

This appears to be a narrative review discussing whether how a man's age and environmental exposures may alter his genes and so be passed on to his offspring.

The article centred on epigenetics, the idea that, though a person's DNA sequence may not change, their exposures over the course of a lifetime may lead to changes in their gene activity and expression that can be passed on to their children.

This happens through mechanisms such as DNA methylation, where methyl groups (types of molecules) are added to the building blocks of the DNA, or where small RNA molecules (miRNA) are added to the DNA – both of which alter gene activity.

This review discusses how epigenetics in the father have an effect on the offspring, focusing on age and environmental exposures. The researchers discuss these theories, referencing various publications, but this does not appear to be a systematic review. 

The research team did not provide any information about how they identified and selected the evidence they reviewed. As such, it is possible that not all relevant research has been examined and so this must largely be considered to be an opinion piece.      

What does the research say about a father's age?

The researchers say that past research has shown that a father's age has a significant effect on a child's characteristics and the likelihood of them having congenital abnormalities.

Some studies have linked increasing paternal age (over 40 or so years) with higher rates of conditions like autism and schizophrenia. Others have observed increased rates of birth abnormalities, such as heart defects, musculoskeletal abnormalities, and Down's syndrome.

Mouse studies also support this. Studies have shown that mice born to "old" fathers (over two years old) performed poorly on tests of learning and memory, and also had a reduced lifespan and less reproductive success themselves. Mice with slightly younger fathers (10 months old) were less social.

The researchers say that although the mechanism behind this is not established, most evidence points in the direction of DNA methylation. Animal studies have shown higher rates of DNA methylation in the sperm cells of older rats compared with younger rats.

What does the research say about environmental exposure?

The effect of environmental exposures on offspring is less clear, although there is some evidence of this. Some studies have shown that people with little available food have demonstrated some changes that can be passed on to their children, though not necessarily bad ones.

It's reported that children born to fathers who had low food availability during pre-adolescence were less likely to die from cardiovascular disease. And those whose grandparents had little food were less likely to have diabetes.

Other studies have suggested stress induces DNA changes that could be passed on. Mouse fathers who were subject to the stress of food deprivation before mating had offspring with lower blood glucose levels.

Mice exposed to other psychological stressors – such as cage changes and fox smell – had offspring that displayed blunted stress responses, indicating some form of behavioural defect.

Smoking and alcohol may also have effects. Smoking has been shown to alter the DNA in sperm.

And three-quarters of babies with foetal alcohol syndrome – birth defects normally associated with maternal consumption of alcohol during pregnancy – are reported to have fathers with alcohol use problems.

Chronic alcohol use in the father is said to again affect DNA methylation. In rats, offspring from fathers given alcohol were more likely to have a low birthweight or spatial learning problems when put in a maze test.

Studies in mice also found those whose fathers were given alcohol were more likely to have cognitive and mobility problems. 

How did the researchers interpret the results?

The researchers say their review findings support the concept of the epigenetic inheritance of paternal experiences across generations.

They say their review highlights "the possible links between birth defects and paternal age, environmental factors, and alcohol consumption" and the need for future research in this area.


This narrative review summarises past research on DNA changes that may occur as a result of a father's age and exposures that could be passed on to his children.

In particular, the review discusses animal and human studies that have linked changes in offspring with increasing paternal age, stress and substance use.  

But this review must largely be considered to only be an opinion piece. We don't know how the researchers identified, appraised and selected the studies they discussed.

As such, there is a strong possibility that not all animal and human research relevant to the issue of paternal epigenetic inheritance will have been reviewed and discussed here.  

There are also no clear methods or results provided for the studies that are discussed, with only a few brief sentences given for each study. We are not able to critique the quality and strength of evidence linking a father's age or any other exposure with the outcome reported. 

For example, people would likely be concerned by reports that increased rates of autism or congenital defects have been observed in children born to fathers over the age of 40. But we have nothing more to go on than this – no firm risk figures are given.

And the observational studies themselves are likely to have been influenced by various unknown sources of bias and confounding, like the report that three-quarters of babies with foetal alcohol syndrome have a father with alcohol use problems.

This doesn't tell us anything about what the mother is doing. It could be that many of these babies had a mother who also had alcohol use problems – alongside her partner – and used alcohol during pregnancy, and has directly exposed the developing baby.

This study will add to the research on how parental exposures may be passed on to a child through epigenetics.

However, given the limitations of this review and the lack of methods given, this opinion piece should not be taken as firm evidence that fathers are putting their children at risk by delaying fatherhood.

These limitations aside, advice that men hoping to become fathers should avoid known bad lifestyle behaviours, such as smoking, drinking too much, not exercising and eating a poor diet seems sensible.

Read more about what both men and women can do to protect their fertility.

Links To The Headlines

Men's biological clock kicks in after 40, too: Warning to start a family early to cut risk of fathering sick children. Daily Mail, May 16 2016

Drinking dads can harm babies just as much as mums who drink alcohol. Metro, May 15 2016

Older fathers can raise risk of birth defect in children. The Times, May 16 2016 (subscription required)

Links To Science

Day J, Savani S, Krempley BD, et al. Influence of paternal preconception exposures on their offspring: through epigenetics to phenotype (PDF, 243kb). American Journal of Stem Cells. Published online May 15 2016

Categories: NHS Choices

Immune system 'plays a role in dementia'

NHS Choices - Behind the Headlines - Fri, 13/05/2016 - 14:30

"Scientists have identified a new cause of devastating neurological conditions," the Mail Online reports – but this is entirely inaccurate.

A review of existing evidence makes the case that the innate immune system may be involved in neurodegenerative conditions, which are associated with progressive damage to brain cells, like Alzheimer's and Parkinson's. However, no new evidence was provided.

The innate immune system is designed to prevent the spread of infection by identifying foreign bodies such as viruses that may have infected cells and, if needs be, killing these cells so the infection doesn't spread.

The review argues that the innate immune system initially activates to eliminate a perceived threat of brain cell abnormality. But by remaining active over time, it causes low-level prolonged damage to normal brain cells, ultimately leading to their death.

The idea that immune responses may play a role in dementia is nothing new. A study published earlier this year tried using immunosuppressant drugs on rats with symptoms of dementia, with some degree of success.

This review doesn't pretend to be anything other than a collection of evidence supporting a hypothesis. It provides a useful range of evidence-based points exploring potential trigger molecules, genetic susceptibility, and how the underlying biology might work.

As any reputable scientist will tell you, a hypothesis needs to be tested by experimentation before it can advance into a credible theory.

Where did the story come from?

The review was carried out by researchers from the University of Adelaide in Australia, and was funded by the Australian National Health and Medical Research Council, and a grant from the National Ataxia Foundation.

It was published in the peer-reviewed journal, Frontiers in Neuroscience. The study is open access, so it is free to view online and download as a PDF.

The Mail Online's headline, "Scientists discover new trigger for devastating brain diseases", is not accurate and the quality of its reporting is poor.

The study in question was a review, meaning it brought together research already published. There is no new laboratory or human study involved here, which isn't most people's idea of a "discovery". 

What kind of research was this?

This was a review of evidence to support the idea that a common disease-causing mechanism for neurodegenerative disease exists, and that "surveillance" by the innate immune system mediates cell death.

The innate immune system helps protect your body – inside and out – from threats like bacteria, viruses and cell damage. It's like a surveillance system keeping an eye on your body.

When foreign bacteria enters your blood, when you cut yourself and have dirt in your wound, or even if some of your cells are behaving abnormally, your innate immune system kicks in to attack and destroy the threat.

This often involves mobilising the immune system to trigger abnormal cells – those possibly infected by viruses or bacteria – to self-destruct, taking the bacteria or other offending organism with it. This process is called programme cell death or, in biological vernacular, apoptosis.

The immune system has innate and acquired components, which recruit different cells and processes to detect and neutralise health threats.

The innate immune system is largely what you are born with, whereas the acquired immune system varies from person to person, depending on what sorts of bacteria, viruses and other micro-organisms you come across in your life.

What did the research involve?

The review reports no methods, only stating that the researchers intended to "present evidence to support the hypothesis that a common pathogenic mechanism for neurodegenerative disease exists, and is mediated by innate surveillance-cell death".

As such, we cannot assume they used systematic review methodology in their search for relevant material. This means some relevant evidence may have been missed.

The review openly looked for evidence in support of one theory, so was not concerned with alternative theories or the relative strength of evidence behind each study.

What were the basic results?

The review itself describes the function of the innate immune system, how it triggers cell death and molecules for the immune system to attack, and different pathways whereby it can damage our bodies.

The researchers explain that many neurodegenerative diseases like Alzheimer's and Parkinson's diseases involve the gradual damage and death of brain cells called neurones.

But it isn't clear whether many disease-specific mechanisms are involved or whether they share a common disease-causing mechanism.

The review argues there is an increasing body of evidence that suggests the innate immune system is activated across a number of neurodegenerative conditions, so might be the obvious candidate for a common underlying mechanism.

Delving more into specifics, the researchers suggest that the innate immune system is initially activated to eliminate a perceived threat of brain cell abnormality in neurodegenerative diseases.

But it cannot remove the threat, meaning the immune system remains active, causing low-level prolonged damage and, ultimately, progressive brain cell death.

The review also identifies possible genetic susceptibility markers, identifying those more likely to have a larger innate immune response to brain cell damage in this way.

A lot of research on neurodegenerative diseases has focused on disease-specific features of the disease – in Alzheimer's, for example, the damaging bundles of amyloid protein that gather in the brain.

The review's authors argue that while these are important, we shouldn't ignore the possibility of a generic component across diseases, which in their view is driven by the innate immune system.

How did the researchers interpret the results?

The researchers concluded that, "Here we have assembled evidence in favour of the hypothesis that neurodegenerative disease is the cumulative result of chronic activation of the innate surveillance pathway, triggered by endogenous or environmental danger or damage associated molecular patterns in a progressively expanding cascade of inflammation, tissue damage and cell death." 


This review presents evidence supporting the idea that the innate immune system is involved in a range of neurodegenerative conditions, such as Alzheimer's and Parkinson's.

Reviews like this are very useful at summarising the current state of science in an area, but may miss important research, unless they are systematic.

This review was openly one-sided, transparently exploring the evidence behind one hypothesis.

While there is nothing wrong with that, a more systematic and balanced review would add the extra value of being able to discuss alternative ideas and find out how much evidence stacks up behind each one, aiding comparisons. 

Despite news coverage suggesting this is a radical new theory, the idea that the immune system might be involved in neurodegenerative conditions has been around for a while.

A study from earlier this year in mice tentatively suggested that inflammation might be involved in the progression of Alzheimer's disease, and can be reduced by targeting it. 

Any potentially promising avenue of research into neurodegenerative diseases is worth exploring, and this review provides some interesting ideas that other researchers may want to follow up. 

Links To The Headlines

Have we been getting it all wrong about dementia? Scientists discover new trigger for devastating brain diseases. Mail Online, May 13 2016

Links To Science

Richards RI, Robertson SA, O'Keefe LV, et al. The Enemy within: Innate Surveillance-Mediated Cell Death, the Common Mechanism of Neurodegenerative Disease. Frontiers in Neuroscience. Published online May 10 2016

Categories: NHS Choices

No evidence probiotics are beneficial for healthy adults

NHS Choices - Behind the Headlines - Thu, 12/05/2016 - 16:28

"Probiotic goods a 'waste of money' for healthy adults, research suggests," The Guardian reports. A new review of previously gathered data found no evidence that probiotics improved the balance of gut bacteria in healthy adults.

Probiotics are live bacteria and yeasts, often added to yoghurt or taken as a supplement, that are promoted as helping stimulate the growth of "friendly bacteria" in the gut.

Supporters claim they can help treat a wide range of conditions, from eczema to irritable bowel syndrome (IBS), but there's little evidence to support many of these claims.

It has also been claimed that healthy people should take probiotics to improve their digestive health, a claim assessed in this latest review.

The review found seven trials, all with vastly different designs, methods and assessment of outcomes. As such, trial results could not be pooled in any meaningful statistical way.

Four of the trials found the probiotic had no different effect on gut bacteria from inactive placebo. Three of the trials reported some effect, but the overall quality of reporting for all trials was poor.

Given the limitations of the studies – including the variety of probiotics examined – it is not possible to conclude with certainty that all probiotics are ineffective.

Absence of good-quality evidence is not evidence of there being no effect. Better-designed studies may yet find some benefit from taking probiotics. 

Where did the story come from?

The study was carried out by researchers from the University of Copenhagen and was funded by the Novo Nordisk Foundation.

It was published in the peer-reviewed journal, Genome Medicine.

The UK media's reporting takes a very black and white attitude towards the review, concluding that probiotics "don't work" and are "a waste of time".

But they would benefit from considering the limitations of the small number of diverse trials included in this study. It would have been more accurate to say that based on the current evidence, we don't know whether they work or not.

It should also be noted that photos of yoghurt drinks – including Tesco own-brand – are misleading. Only one of the seven trials assessed a milk-based drink and we don't know what brand it was. Considering these were all non-UK studies, though, it is very unlikely to have been a UK supermarket brand.

What kind of research was this?

This systematic review aimed to gather the evidence from randomised controlled trials (RCTs) that have looked at the effect of probiotic supplements on gut bacteria.

As the researchers say, in recent years the composition of bacteria in the human gut has received considerable attention as a possible modifiable risk factor for various digestive and metabolic diseases.

This has led to a surge in the use of probiotic supplements to try to boost the health of the gut, through ways such as improving the intestinal lining and introducing more "friendly" bacteria to compete against the "bad" bacteria.

However, the effect of probiotic supplements – particularly in healthy individuals – is poorly understood.

This review therefore aimed to compile the evidence, looking at RCTs that have compared supplements with inactive placebo and used molecular approaches to measure gut bacteria. 

A systematic review is the best way of seeing if the evidence to date shows whether they are effective. But reviews are only as good as the studies they include.

Because of the vastly different designs of the various studies, the researchers were unable to perform a meta-analysis of the results.

What did the research involve?

The researchers searched three literature databases up to August 2015 to identify RCTs of any duration that:

  • included healthy adults only
  • compared probiotics with placebo
  • assessed gut bacteria composition using specific molecular techniques and reported this as the main outcome

They excluded studies where other interventions were combined with supplement use, such as antibiotics or other medications.

Two reviewers separately assessed trials for eligibility, and carried out quality assessment and data extraction from the trials included.

Seven trials met eligibility criteria: two from Italy, two from Denmark, and one trial each from the US, Germany and Finland.

All were conducted in healthy adults aged 19 to 88 years, and the sample size of the individual studies ranged from 21 to 81.

Most supplements included Lactobacillus, in one trial combined with Bifidobacterium, and one trial used Bacillus. These were provided as capsules in four trials or in biscuits, drinks or sachets in one trial each. The length of the trials was typically one to two months.

The main source of potential bias in the studies was the lack of blinding of researchers assessing outcomes. 

What were the basic results?

The results of the seven studies are not pooled and are only reported study by study.

Essentially, none of the studies provided evidence that probiotics had a beneficial effect on gut bacteria.

The results were as follows:

  • Four studies reported no difference in the diversity of, composition of, or stability of bacteria between probiotic and placebo groups.
  • One study reported that the probiotic reversed the age-related increase in certain disease-causing bacteria (such as C. difficile and Campylobacter), but did not compare between groups.
  • One study reported some difference in the diversity of bacteria, with increased abundance of certain bacteria (such as Proteobacteria) in the probiotic group.
  • One study also reported some differences in the abundance of certain bacteria, but did not directly compare between groups.
How did the researchers interpret the results?

The researchers concluded that, "Overall, this systematic review demonstrates that there is no convincing evidence for consistent effects of probiotics on faecal microbiota composition in healthy adults."


This review finds no evidence that probiotic supplements have beneficial effects on the composition of gut bacteria in healthy adults.

The review has strengths in that it pre-specified exactly which trials would be eligible – that is, only RCTs in healthy adults, comparing probiotics with placebo, that assessed changes in gut bacteria levels as the main outcome.

This should aim to reduce diversity between the trials and try to find a definitive answer on the effect in a specific population.

However, despite this, the seven trials were still highly variable in their methods and design, such as the type of probiotic given and how gut bacteria were assessed.

This variability is demonstrated by the fact they are only reported narratively and the results could not be pooled to give an overall quantitative effect, as would be the case in a meta-analysis.

The trials also contained several quality limitations. In most, the researchers were not blinded to the assigned group, which may have biased their assessment of outcomes.

Only one of the seven trials had calculated beforehand how many participants they would need to recruit to detect whether the treatment had a significant effect. This is a notable limitation, given that all had sample sizes of less than 100.

Also, several of the trials had not statistically assessed, or not clearly reported, whether there was a difference between the probiotic and placebo groups. 

As the researchers say, future studies would benefit from clearly specifying the main outcome they're looking at, giving transparent results with statistical analyses, and clearly distinguishing within-group treatment effects – such as changes from study start to end – and between-group effects.

Further points to bear in mind:

  • These trials only included healthy adults with no known diagnoses or conditions. This means the study can't tell us whether probiotics are effective in IBS or for "rebuilding" the gut bacteria in people who have had an illness. However, even though they were healthy adults, the trials included quite variable populations – for example, one was in elderly people, another specifically in postmenopausal women. We also do not know the effectiveness in children.
  • There were only seven trials, and these used different probiotics containing different "friendly" bacteria, in different forms, from capsules to yoghurt drinks and biscuits. As such, there is not enough evidence to definitely conclude that all probiotics are ineffective, particularly given the limitations of the trials. It could be that certain bacteria in particular formulations could have different effects.
  • None of the trials were from the UK, so the formulations used may differ from those on the UK market. 
  • The trials were only of a couple of months' duration, so we don't know what longer-term use might have.
  • The trials only looked at direct effects on gut bacteria level. We don't know whether taking the probiotic increased the person's sense of health and wellbeing, for example. If probiotics help some people in this way, that can only be a good thing – even if it is just a placebo effect.

Overall, the current state of the evidence does not demonstrate that probiotics have any effect on gut bacteria in healthy people.

Given the limitations of these studies, that is not to say that all probiotics definitely have no effect. Further high-quality research in their use is needed.  

Links To The Headlines

Probiotic goods a 'waste of money' for healthy adults, research suggests. The Guardian, May 10 2016

Probiotic drink 'myth': No evidence that yoghurt products boost healthy bacteria, say scientists. Daily Mail, May 10 2016

Healthy people who drink probiotic drinks full of 'good bacteria' wasting their time, according to report. Daily Mirror, May 10 2016

Links To Science

Kristensen NB, Bryrup T, Allin KH, et al. Alterations in fecal microbiota composition by probiotic supplementation in healthy adults: a systematic review of randomized controlled trials. Genome Medicine. Published online May 10 2016

Categories: NHS Choices

Is a pint of beer a day good for the heart?

NHS Choices - Behind the Headlines - Thu, 12/05/2016 - 15:28

"Pint of beer a day could protect you from heart attacks," The Independent reports. A new review on the alleged protective effects of moderate beer drinking has been warmly welcomed by the UK media – but nobody reported that it was funded by an Italian beer trade association.

Researchers reviewed the existing evidence about beer and health, including the effects on heart and circulation, cancer, liver disease, dementia and overall length of life. They say that much research has been done on the effects of wine on health, but less on beer. 

The research team claims that, based on the result of their review, men who drink the equivalent of around two 330ml cans of beer a day, and women who drink one can, will receive "some benefit against cardiovascular disease".

This recommendation equates to around 2.5 units of alcohol a day for men and 1.25 for women, or 17.5 units a week for men and 8.75 units for women.

For men, this advice contradicts recent advice issued by UK Chief Medical Officers that "you are safest not regularly drinking more than 14 units per week".

So, who's right? Well, the methods the researchers used to identify and select the evidence are not clearly reported.

This means it's possible that this review may not have considered all relevant research and, playing devil's advocate, could have ignored evidence countering the researchers' hypothesis.

What we do know is that there are safer, well-validated methods to reduce your risk of cardiovascular disease.

Where did the story come from?

The study was carried out by researchers from 10 research centres in Italy, Spain, Luxembourg and the US.

It was funded by the Italian Association of the Beer and Malt Industries, Assobira. The researchers say Assobira had no role in designing or writing the study.

Several of the researchers declared conflicts of interest in working for Assobira or other industry bodies linked to alcoholic drinks.

The study was published in the peer-reviewed journal Nutrition, Metabolism and Cardiovascular Diseases.

Disappointingly, not one single UK media outlet managed to report this arguably significant conflict of interest.

The study was met with enthusiasm by the UK media, although the quantities of alcohol recommended seemed to confuse some, and little mention was made of the downsides of this approach.

For example, The Daily Telegraph said, "drinking up to two 1.4 pints of beer a day for men and half of that for women" could benefit heart health.

However, the researchers define a healthy limit as "up to" one drink a day for women and two for men.

They say that one drink is approximately 330ml of 4% beer. That is equivalent to 0.58 of a pint – so the limit for men would be just over one pint, while the limit for women is just over half a pint.  

What kind of research was this?

This was a consensus document, which means a group of experts were brought together to review evidence on the topic and agree a statement outlining their conclusions.

It is not clear from the document who chose the experts in the group, or whether they used standard systematic review methods to review published evidence.

The problem with non-systematic evidence reviews is that researchers might cherry-pick the research that suits them and ignore anything that doesn't fit their theory. We're not saying that happened in this case, but it's unclear how the studies were chosen.

What did the research involve?

A group of doctors were asked to review the evidence on the effect of the consumption of moderate amounts of beer on human health.

Each doctor carried out a search of the published literature before writing one section of the review, which was then shared for comments by other doctors. They arrived at a final version after meeting to discuss their findings.

While the study does tell us the search terms and the reasons for excluding studies from the review, it is unclear whether this was a formal systematic review.

The researchers did ask two external experts to review the manuscript as part of the process before meeting to prepare their final version.

They did not carry out a meta-analysis of their findings, but summarised the findings of the evidence they reviewed.

What were the basic results?

Low to moderate consumption of beer seems to have the same effect of reducing the chances of cardiovascular disease as wine.

This was the clearest finding from the review, based on a meta-analysis published in 2011 that pooled the results of 16 studies in almost 290,000 healthy adults.

The maximum protection against cardiovascular disease observed in that study – a 33% risk reduction – was seen at a consumption level of 25g of alcohol a day (about one pint of beer).

As with all alcohol, beer increases the risk of cancer, even at low levels. The paper says that "most alcohol-related cancers (85-90%) are in fact due to heavy drinking", which they define as more than two drinks a day.

However, light and moderate drinking were linked to increased risk of breast, mouth and throat cancers.

Importantly, the chances of alcohol causing cancer seem higher in Asian people. This is said to possibly be because there are genetic differences in many people of Asian origin that mean they are less able to process the toxins produced by alcohol.

There was insufficient evidence to show the effect of beer on the liver, apart from the known effects of consuming too much alcohol, which increases the chance of liver disease.

It is unclear whether beer increased or decreased the chances of getting dementia, as the studies reviewed gave conflicting results.

The effects of beer on length of life are also unclear, although the report's authors say they are likely to be in line with the known effects of drinking any alcohol.

These show a "J-shaped curve", with non-drinkers being slightly more likely to die than those who drink a small or moderate amount of alcohol, but those who drink a large amount of alcohol being more likely to die.

As the authors said, "Heavy alcohol (and beer) consumption increases the risk of total mortality, ranking eighth place among the causes of attributable deaths all over the world." 

How did the researchers interpret the results?

The researchers said that, "Unless they are at high risk of alcohol-related cancers, there is no reason to discourage healthy adults who are already regular light-moderate beer consumers from continuing to follow the same pattern.

"On the other hand, we do not recommend that adult life-long abstainers begin drinking for health reasons as, up to now, there is no direct evidence that adult abstainers who start drinking beer or other alcoholic beverages (also in moderation) reduce their risk of chronic diseases."

In other words, if you don't drink beer, there's no reason to start – but if you're healthy and drink a small amount of beer, there's no need to stop.


Perhaps the most important message from this study is that low to moderate drinking may have health benefits, but binge drinking or heavy drinking is very bad for your health. The other message seems to be that beer has similar effects to wine.

Whether wine is good or bad for us has been debated for many years. Some have pointed to a reduction in the risk of cardiovascular disease, perhaps because of the phenols produced by fermented grapes, or perhaps because of alcohol itself. It seems that any benefits from wine are also seen in beer – as long as this is in moderation.

However, even drinking in moderation raises the risk of some cancers. Overall mortality figures suggest that the benefits may outweigh harms at low to moderate levels of drinking.

The researchers included 150 papers for their review, which suggests they carried out a careful study of the evidence.

However, without knowing if the review was carried out systematically, it's hard to know how rigorous the evidence-gathering process was. It is possible that some research relevant to the issue has not been considered.

A review's findings are only as strong as the underlying studies. The consistent themes identified suggest these are likely to be true effects associated with low to moderate beer consumption.

However, the underlying studies are only observational, so introduce the possibility of many sources of bias and confounding. For example, there could be inaccurate recall of the type of alcohol consumed or its quantity.

It is also possible that other health and lifestyle factors are influencing the results. Several of the studies adjusted their analyses for common ones such as age, smoking and body mass index, but otherwise there was considerable inconsistency in the factors that were taken into account.  

The study's conclusions – that there's no need to stop drinking moderate amounts of beer if you're healthy and already do so, but no need to start if you don't drink already – seem sensible. It's worth reiterating that pregnant women and those with certain conditions are advised to avoid alcohol altogether.

Because of this review's lack of rigour, we would recommend that you ignore the advice that if you are a man, you can safely drink 17.5 units a week, and stick to the recent official UK guidance that both men and women should drink no than 14 units a week.

This is equivalent to a bottle-and-a-half of wine or five pints of export-type lager (5% abv) over the course of a week. 

Read more about the new guidance and get tips on how to cut down on alcohol if you find yourself drinking too much on a regular basis.  

Links To The Headlines

Pint of beer a day could protect you from heart attacks, scientists say. The Independent, May 11 2016

A beer a day keeps a heart attack at bay: Even one can reduces risk of disease by a quarter. Mail Online, May 11 2016

Beer is good for you! A pint a day could protect your heart. The Daily Telegraph, May 11 2016

Links To Science

de Gaetano G, Costanzo S, Di Castelnuovo A, et al. Effects of moderate beer consumption on health and disease: A consensus document. Nutrition, Metabolism and Cardiovascular Diseases. Published online March 30 2016

Categories: NHS Choices

BMI categories may need adjusting, argue researchers

NHS Choices - Behind the Headlines - Wed, 11/05/2016 - 14:30

"Being overweight may not be as unhealthy as it was 40 years ago," BBC News reports.

New research has found a body mass index (BMI) of 27 is linked to the lowest rate of death – but someone with a BMI of 27 is currently classed as being overweight.

BMI is a score calculated by dividing your weight (usually in kilograms) by the square of your height (usually in metres and centimetres). Currently, a BMI of 25 to 25.9 is classified as being overweight.

Researchers looked at 120,528 people from Copenhagen, recruited from 1976 to 2013, and separately compared those recruited during the 1970s, 1990s and 2000s. They were followed up until they died, emigrated, or the study finished.

The BMI linked to the lowest risk of having died from any cause was 23.7 in the 1970s group, 24.6 in the 1990s group, and had further risen to 27 in the 2003-13 group.

It may be the case that the suggested upward shift in optimal BMI is the result of improvements in preventative treatments for weight-related conditions such as type 2 diabetes.

But this is just an estimate based on averages – it doesn't mean that having a "healthy" BMI is bad for you. Similarly, it shouldn't be assumed that it's now best to be in the overweight category. People often gain weight as they age, so there is the risk you could move from being overweight to obese.

Where did the story come from?

The study was carried out by researchers from Copenhagen University Hospital.

It was funded by the Danish Heart Foundation, the Danish Medical Research Council, Copenhagen County Foundation, Herlev and Gentofte Hospital, and Copenhagen University Hospital. 

The study was published in the peer-reviewed Journal of the American Medical Association (JAMA).

The study was covered by the UK media with a certain amount of glee, with the Daily Mail suggesting that the BMI system was a "blunt instrument".

It also said this study showed that, "Millions of Britons who are currently classed as overweight, actually have the optimal BMI and the lowest chance of death."

However, the study was reported on accurately, and the reports included expert views saying that people still need to keep an eye on their weight.

What kind of research was this?

This cohort study compared results from three large previous cohort studies in the same part of Denmark, starting at different times.

Researchers wanted to see if there had been a change over time in the optimal BMI score – that is, the BMI shared by people with the lowest rate of death from any cause.

While this type of study can show trends of this nature, it cannot explain why the changes happen.

What did the research involve?

Groups of adults in Copenhagen had their height and weight measured as part of three studies carried out in the city in 1976-78, then 1991-94, and the final study in 2003-13.

Researchers followed them up, then looked to see at which BMI people had the lowest chance of dying. They compared the numbers for the three studies to see if that number changed over time.

The first two studies were linked. Participants for the first study were invited back for a second round of measurements over the period from 1991-94, although younger people were recruited to add to the numbers. People in the third study had not taken part in either of the first two.

As well as weight and height, researchers checked whether people smoked, how much exercise they did, whether they'd been diagnosed with any medical conditions, including cancer or heart disease, and how much alcohol they drank.

They carried out sensitivity checks by including or excluding people with different risk factors to see whether any of them explained the overall results.

The researchers also looked at whether length of follow-up made a difference. They did this by carrying out their calculations with a much shorter follow-up period to see if the longer follow-up from the older studies distorted the results.

What were the basic results?

The average BMI at which fewest people in the studies died from any cause increased by three points over the three decades:

  • 23.7 (95% confidence interval [CI] 23.4 to 24.3) in 1976-78
  • 24.6 (95% CI 24 to 26.3) in 1991-94
  • 27 (95% CI 26.5 to 27.6) in 2003-13

The results showed a similar shift when researchers looked at just deaths from cardiovascular disease for non-smokers who had not been diagnosed with diabetes, cardiovascular disease or cancer, as well as for shorter periods of follow-up. None of the sensitivity analyses explained the trend.

In addition, researchers found the increased risk of death linked to being obese – a BMI of 30 or above – compared with a "healthy" BMI has gradually decreased to zero.

In the 1970s obese people had a 31% increased risk of death. By the 1990s it had reduced to a 13% increased risk, and by 2003-13 there was no longer a statistically significant link (adjusted hazard ratio 0.99, 95% CI 0.92 to 1.07).

How did the researchers interpret the results?

The researchers say their findings were "robust" and cannot be explained by confounding factors such as age, sex, smoking status and disease at the start of the study.

They said that, "If this finding is confirmed in other studies, it would indicate a need to revise the World Health Organization (WHO) categories presently used to define overweight."

They also said cohort studies cannot address the causes of the results, but speculated that their finding may reflect improvements in treatments for diseases affecting people with higher BMIs, such as heart disease and diabetes.

This would make it less risky to be overweight than in the 1970s, when more people died of these diseases. The reduction in smoking and increase in exercise they found could also have helped mitigate the effects of being overweight, they said.


The link between weight and health is not straightforward. We've known for years that if you plot death rates against BMI categories on a graph, you get a U-shaped curve, where people who are very underweight or very overweight are at higher risk of dying, while people in the middle have a lower risk.

This makes sense: extremes of weight are linked to illness, both as a cause or result. Many people with cancer or lung disease, for example, are underweight, which is one reason why lower BMIs are linked to higher death rates. That's why doctors talk about people having a "healthy" BMI.

What this study seems to show is that the lowest point of that U-shaped curve has shifted to the right, towards higher BMIs. But it doesn't mean that slimmer people are at a higher risk of death.

The study shows that in the period 2003-13, there was no difference between the death rates of people with a BMI of 18.5 to 24.9 (healthy) and those with a BMI of 25 to 29.9 (overweight), which were 4 per 1,000 per year for both groups.

The rate for obese people was 5 per 1,000 per year, despite this being a non-significant increased risk of death. There's certainly no need to try to put on weight if you are already at a healthy weight for your height.

The potential reasons for the shift are interesting. It may be, as the researchers suggest, that the diseases which killed more overweight people in the 1970s are now better treated and controlled, meaning that the risks of being overweight are smaller than they once were.

It's possible that the risks associated with being underweight have not decreased in the same way, which would automatically shift the "optimal" point towards overweight.

Also, despite a general increase in the population's BMI over the decades, health awareness has improved. Though the results have taken smoking status into account in the analyses, other factors, such as improvements in physical activity and alcohol moderation, could be having an influence.

However, this study has some limitations. Importantly, it was only carried out among white Danish people, which means it may not apply to other ethnic groups.

We know that some groups, such as people of south Asian origin, are more likely to have problems such as diabetes at lower BMIs than white people, so this study might not apply to everyone. And the follow-up for the most recent group studied was, on average, four years, so we don't yet know if this is a long-term trend.

The criticisms of the BMI system are not unfounded, though. BMI doesn't take into account the increased weight of muscle compared with fat – some athletes have high BMIs, despite being very fit, for example.

Waist circumference and waist-to-hip ratio can give a good indication of body "fatness". Regardless of your height or BMI, you should try to lose weight if your waist is:

  • 94cm (37in) or more for men
  • 80cm (31.5in) or more for women

You are at very high risk and should contact your GP if your waist is:

  • 102cm (40in) or more for men
  • 88cm (34in) or more for women

Read more about why waist size is important.

Links To The Headlines

Being overweight 'may be less unhealthy'. BBC News, May 10 2016

Got a high BMI? It doesn't mean you are unhealthy: People categorised as overweight after being given a rating of 27 found to have the lowest risk of dying. Daily Mail, May 11 2016

Overweight people less likely to die early than the slim, study shows. The Daily Telegraph, May 10 2016

Links To Science

Afzal S, Tybjærg-Hansen A, Jensen GB, et al. Change in Body Mass Index Associated With Lowest Mortality in Denmark, 1976-2013. JAMA. Published online May 10 2016

Categories: NHS Choices

33,000 deaths 'linked to failings in NHS heart attack care'

NHS Choices - Behind the Headlines - Tue, 10/05/2016 - 14:28

"Thousands of heart victims killed by poor care," claims the Daily Mail.

A review of clinical data from the last 10 years in England and Wales looked at patients with a history of what are known as non-ST segment elevation myocardial infarction (NSTEMI) heart attacks.

NSTEMIs describe a class of heart attack that are serious enough to warrant hospitalisation, but don't pose as big a threat as typical heart attacks.

Data from almost 390,000 people who had an NSTEMI was included in the review. It found around 87% of patients did not receive one or more internationally agreed recommended interventions.

It has been estimated that if all patients had received all of the interventions recommended to them, 32,765 (28.9%) deaths may have been prevented over the 10-year period.

But an important consideration is that some of the interventions consisted of lifestyle advice, such as quitting smoking or changing diet. This means we cannot assume that all the people given such advice after a heart attack would follow it.

These findings are also limited by the possibility that data was missing or had been recorded incorrectly. The design of the study is not able to prove cause and effect, and there are a number of other factors beyond the recommended interventions that may have had an effect on survival.

The data is certainly worth considering – one preventable death is one too many – but it doesn't prove that "thousands of heart victims [were] killed by poor care", as reported by the media. 

Where did the story come from?

The study was carried out by researchers from a number of institutions, including the University of Leeds and University College London.

Funding was provided by the British Heart Foundation and the National Institute for Health Research.

It was published in the peer-reviewed European Heart Journal: Acute Cardiovascular Care.

This study has been reported widely in the UK. And, while these reports have been accurate, none mention the inherent limitations of the study.

The Daily Mail and The Daily Telegraph both quote Professor Peter Weissberg, Medical Director at the British Heart Foundation, who said: "This study shows that many people in the UK are receiving suboptimal care after a heart attack and that lives are being lost as a consequence.

"Applying clinical guidelines in heart disease costs little, and in the long term saves money and, most importantly, saves lives." 

What kind of research was this?

This cohort study used data from the UK national heart attack register to see whether guidelines for the care of patients who have had a non-ST elevation myocardial infarction (NSTEMI) is being followed.

An NSTEMI is a type of heart attack where the person has the symptoms of a heart attack and associated blood test results (raised heart enzymes), but they don't have the typical signs of heart attack (ST elevation) on an ECG monitor.

Typically, in an NSTEMI the blood supply to the heart is only partially, rather than completely, blocked. As a result, a smaller section of the heart is damaged. However, NSTEMI is still regarded as a serious medical emergency.

They are managed slightly differently from a typical heart attack, usually with medications and a coronary angiography to identify any blocked blood vessels that may need treating. 

This type of study is a good way of investigating whether the best care is being provided to people with this type of heart attack.

But as the data collected in this registry was not specifically for the study, it is possible that it is not entirely fit for purpose – not all relevant detail may have been recorded, for example – and so may introduce bias.

What did the research involve?

The researchers used European Society of Cardiology guidelines for the management of NSTEMIs and mapped this to UK registry data to see whether guideline-indicated interventions were being followed.

The registry data included adults admitted to one of 247 hospitals in England and Wales with an NSTEMI attack between January 1 2003 and June 30 2013.

NSTEMI cases were identified using the recorded hospital discharge diagnosis. Exclusions were those who died in hospital, where pharmacological therapies were uncertain, or if there was missing data on death.

The data contained information corresponding to 13 interventions, some of which were:

  • electrocardiogram (ECG)
  • aspirin
  • blood pressure medications – such as beta-blockers and ACE inhibitors
  • anti-clotting medications – grouped as P2Y12 inhibitors in this study
  • statins
  • echocardiogram
  • advice to quit smoking
  • dietary advice
  • cardiac rehabilitation programme
What were the basic results?

A total of 389,057 adults were included in the analysis, with an average age of 70.9 years. Researchers found 86.9% were not recorded as receiving one or more recommended interventions.

Some of the ones frequently missed were:

  • advice to quit smoking (87.9%)
  • dietary advice (68.1%)
  • P2Y12 inhibitors (66.3%)
  • coronary angiography (43.4%)

Of the missed interventions, the ones estimated to have the strongest effect on reducing survival were:

  • coronary angiography
  • cardiac rehabilitation
  • advice to quit smoking
  • statins

By modelling the collected data, it was found that if all eligible patients in the study had received all of the interventions recommended to them, 32,765 (28.9%) deaths may have been prevented during the 10-year period.

How did the researchers interpret the results?

The researchers concluded that: "The majority of patients hospitalised with NSTEMI missed at least one guideline-indicated intervention for which they were eligible. This was significantly associated with excess mortality.

"Greater attention to the provision of guideline-indicated care for the management of NSTEMI will reduce premature cardiovascular deaths." 


This study aimed to investigate whether adults who have had a non-ST elevation (NSTEMI) heart attack were offered all of the guideline-recommended interventions they were eligible for.

The researchers used guidelines set out by the European Society of Cardiology and found almost 87% of patients were not recorded in the registry as receiving one or more of the 13 interventions reviewed.

This study has both strengths and a number of limitations. This is a large dataset that has been designed to assess the quality of care given for this type of heart attack in the UK.

But the findings are limited by a number of factors:

  • Findings from data analysis studies are always limited by the possibility that the recording of data was not complete and there may be some misclassification. For example, interventions such as advice for stopping smoking or about diet may have been classified in the registry as cardiac rehabilitation rather than counselling.
  • Reasons for not giving interventions such as contraindications for use or patient refusal were recorded in the registry. However, reasons were not given for those simply recorded as not having received the intervention.
  • The researchers excluded more than 31,000 people who died in hospital because they had incomplete information on the medications they received, as well as more than 21,000 who had missing mortality data. The missing cases may have pushed the findings in either direction.
  • The design of the study is not able to prove cause and effect. There are a number of other factors beyond the recommended interventions that may have an effect on survival.
  • Improvements were seen in the interventions offered over the course of the study – if we are just considering present day data, the picture may therefore be quite different.
  • Perhaps most importantly, it is unclear why the researchers compared UK practice against the European Society of Cardiology guidelines, rather than the guidelines on management of NSTEMI issued by the UK guideline body, the National Institute for Health and Care Excellence (NICE). This may have given slightly different results.   

Guideline -ecommended interventions for managing heart attacks are usually backed by good-quality research. It is important that the best care is offered to all people, regardless of hospital trust or the severity of their illness.

If you have had this or another type of heart attack, you should take all medicines as prescribed and follow the advice given by your doctors.

Steps to take yourself include making lifestyle changes such as having a healthy diet, maintaining a healthy weight, taking regular physical exercise within your limits, and stopping smoking

Links To The Headlines

Thousands of heart victims killed by poor care: More than 33,000 people died needlessly over the past few years because of shocking flaws in NHS treatment. Daily Mail, May 10 2016

One third of heart attack deaths could be avoided. The Times, May 10 2016 (subscription required)

33,000 heart attack deaths could have been prevented if NHS had followed guidelines. The Daily Telegraph, May 10 2016

Heart attack care failings 'leading to tens of thousands of deaths'. ITV News, May 10 2016

33,000 heart attack victims killed by 'failings in care' study claims. Daily Mirror, May 10 2016

Heartbroke: 3,000 Brits die each year due to poor care after cardiac arrest. The Sun, May 10 2016

Links To Science

Dondo TB, Hall M, Timmis AD, et al. Excess mortality and guideline-indicated care following non-ST-elevation myocardial infarction. European Heart Journal: Acute Cardiovascular Care. Published online May 3 2016

Categories: NHS Choices

Are we sleepwalking into a 'global sleep crisis'?

NHS Choices - Behind the Headlines - Mon, 09/05/2016 - 14:30

"We are facing a global sleep crisis because we don't go to bed early enough, say scientists," the Mail Online reports.

The warning comes from a study produced by a research team using a smartphone app (Entrain) to track sleep patterns from around the world.

The findings reveal that as people age, they tend to go to sleep earlier and wake later, and women tend to sleep more than men.

The researchers also found the timing of sunrise and sunset does influence sleep, but less than you might think.

Worldwide, there is a lot of variability in people's bedtime and the researchers believe this is down to social influences.

The researchers warn of a "global sleep crisis", but it is difficult to assess exactly what evidence this warning is based on.

The big stumbling block for this research is it can't provide us with any conclusive answers. It may be that factors such as using technical devices are disrupting our sleep, but we can't say anything about that based on this research.

Another drawback is that people chose to download this app. It could be that people with troubled sleep patterns would be more motivated to download the app than people with healthy sleep patterns.

Signs you may not be getting enough sleep include irritability and problems with concentration and memory. Persistent lack of sleep can make you more prone to accidents and chronic diseases.

Read more about why lack of sleep can be bad for your health.

Where did the story come from?

The study was carried out by researchers from the University of Michigan, and was funded by the Biomathematics Program at the Army Research Laboratory and the Human Frontier Science Program.

It was published in the peer-reviewed journal Science Advances on an open access basis, so it is free to read online or download as a PDF.

The Mail's headline, which says "we are facing a global sleep crisis", probably goes too far – the study provided no evidence to support the claims of an impending "sleep crisis". But, to be fair, this term was used in the study itself, but the researchers didn't elaborate on this.

What kind of research was this?

This cross-sectional study aimed to validate the use of mobile technology to collect information on sleep patterns worldwide, and explore the possible influences that social pressures have on sleep.

Sleep is known to be driven by our internal body clock. Naturally, sunrise and sunset would regulate this rhythm, but our modern lives are controlled by social factors, work obligations and artificial lighting, meaning we can't follow this natural rhythm.

As the researchers say, understanding the factors that control how much sleep we get is important as this can have a direct effect on human health.

In 2014 the researchers released a free app for iOS and Android devices – Entrain – that recommends optimal lighting schedules for adjusting to new time zones.

Users input data on their normal sleeping times, home time zone and typical lighting, sleep schedules and experience of jetlag.

In this study, the researchers analysed sleep habits from those who submitted data.   

What did the research involve?

In 2014, the first year of the app's release, 8,070 users submitted data.

The researchers explained that when the app is loaded, the opening screen asks users their normal wake time and bedtime to the nearest hour, home time zone, and typical amount of light exposure.

The options for typical light were:

  • low indoor (200 lux)
  • bright indoor (500 lux)
  • low outdoor (1,000 lux)
  • bright outdoor (10,000 lux)

For the purposes of this study, the researchers combined the indoor categories into a single group and did the same for the outdoor ones.

Users were also asked to give data on age, gender and travel frequency (from several times a week to less than once a year). They could also record data on travel dates and experiences of jet lag.

The main countries contributing data were the US (45%), Australia (9%) and Canada (5%). The UK, France, Spain, the Netherlands, Denmark and Germany jointly contributed 15% of the data, and China, Japan and Singapore made up 5%.

The researchers excluded "outlier" data that was far from the norm: for example, those who woke before 3am or after 11am, who went to bed before 7pm or after 3am, or who had less than 4 or more than 12 hours' sleep a night. This means most shift workers would have been excluded.

They also excluded those aged under 18 or above 85. This left 5,450 people for analysis. 

What were the basic results?

The adults analysed (majority male) represented a wide range of time zones, and more commonly reported indoor rather than outdoor light.

The researchers observed a relationship between age and sleep schedule, where in general increasing age was associated with less sleep and earlier waking times.

They found age has the strongest influence on the timing of midpoint of sleep, while gender had the strongest influence on duration of sleep, with women getting more sleep at nearly all ages.

Prior mathematical models suggested a later sunset and sunrise influence both bedtime and wake time, and the app data supported this. Sunrise after 6.30am and later sunset were both associated with later wake time and bedtime.

Later sunset was also associated with more sleep, particularly in the group who reported spending more time in outdoor light.

In general, women, older people and those with more outdoor light exposure seemed more sensitive to changes in sunset and sunrise than men, younger people and those with mostly indoor light exposure.

However, sunset timing had a weaker effect on bedtime than models may have predicted. The researchers considered that solar cues do influence sleep but may be ignored in the real world, particularly around bedtime.

The country the person resided in had an influence on their bedtime, suggesting that people are more responsive to social cues at night.

And sleep duration goes down as bed time becomes later. While average bedtime varied across countries, average wake time remained fairly consistent.

No results are reported for the influence of travel and reports of jet lag.

How did the researchers interpret the results?

The researchers noted that the trends they identified agree with previous large-scale surveys and laboratory studies, and validate the use of this mobile technology for assessing sleep.

They said that, "This work better defines and personalises 'normal' sleep, produces hypotheses for future testing in the laboratory, and suggests important ways to counteract the global sleep crisis." 


These findings show that the app works, and it is possible for people to input data on the timing and duration of their sleep for researchers to get a global picture of sleep patterns worldwide.

The researchers noticed a number of themes, including that age, gender and the amount of time we spend outdoors are factors that can influence the timing and duration of sleep.

Timing of sunrise and sunset do seem to have an influence on our sleep, but less than may be expected. Across countries worldwide there is most variability in the time we go to bed, and this directly influences our sleep duration.

The researchers also considered that social influences are causing us to go to bed later and ignore the natural influences of sunset.

However, this is the big stumbling block of this research – it can't provide us with any answers, and we can only speculate as to why this is the case.

It may be that factors such as late-night working, socialising or using technical devices are influencing our sleep, but we can't say anything about that based on this research.

Another limitation of the study is that excluding people with outlying sleep patterns – very late bed times or waking times – automatically excludes shift workers. This is often the group in which previous research has speculated disrupted sleep patterns could have an adverse effect on health.

There is also the potential for misclassification when people are asked to categorise their typical light exposure as indoor or outdoor. There is likely to be wide variation in the amount of natural daylight that people in these two broad categories are exposed to.

A final important limitation is that the population were self-selecting. People actively chose to download and use the application, meaning the study could be at risk of selection bias.

Arguably, people with sleep problems are more likely to download a sleep app than people without sleep problems, so the results may not be truly representative.

It is also worth noting that only a fraction of the data analysed comes from the UK, so the study can't give any great insight into this country's sleep patterns and influences.

Overall, the findings are undoubtedly of interest in furthering understanding of the world's sleep patterns. However, they raise more questions than answers on how our social and working lives are affecting our sleep and health.    

Links To The Headlines

We are facing a global sleep crisis because we don't go to bed early enough say scientists who used smartphone app to find out how much shut-eye everyone is getting. Mail Online, May 8 2016

Global sleeping patterns revealed by app data. BBC News, May 7 2016

Scientists warn of 'global sleep crisis' from data collected on smartphone app. Daily Mirror, May 7 2016

Global sleeping study reveals women get more than men. The Independent, May 7 2016

Links To Science

Walch OJ, Cochran A, Forger DB. A global quantification of "normal" sleep schedules using smartphone data. Science Advances. Published online May 6 2016

Categories: NHS Choices

Study finds no link between mobile phones and brain cancer

NHS Choices - Behind the Headlines - Mon, 09/05/2016 - 13:00

"Mobile phones don't increase the risk of brain cancer, 30-year study concludes," the Mail Online reports.

The Australian study found the massive increase in mobile phone use over the past 30 years was not matched by a similar rise in brain cancer cases.

The first official mobile phone call in Oz took place in 1987 by the then Minister of Communication, Michael Duffy. Now, mobile phone ownership rates are estimated to be around 94%.

Despite the explosion in Australian mobile phone ownership, the researchers found no corresponding spike in brain cancer rates. They therefore concluded there was no evidence that mobile phones cause brain cancer.

But the researchers only had the number of Australians with mobile phone contracts to play with – they didn't have any individual data, for example, with information about how often or for how long people had their phones to their heads or, increasingly in the smartphone era, held over their faces.

The study tells us that at a population level, it's unlikely mobile phone ownership is responsible for any moderate or larger increase in brain cancer in Australia. But it doesn't tell us about individual risk patterns.

Despite this uncertainty, when it comes to other risk factors for cancer, such as smoking, poor diet, drinking too much alcohol and lack of exercise, mobile phone ownership is probably not a significant risk to your health.

If you are concerned, read more about the potential risks of mobile phone use.

Where did the story come from?

The study was carried out by researchers from the University of Sydney and the University of New South Wales, Australia. No funding source was mentioned.

It was published in the peer-reviewed journal, Cancer Epidemiology.

The Mail Online coverage was accurate and contains a link to an article by the lead author, which may be of interest to those wanting more information about the background to the study and its possible implications.

What kind of research was this?

This ecological study set out to look for a link between mobile phone ownership and brain cancer incidence since the first mobile phone call in Australia in 1987.

Since the 1980s, mobile phone use has rocketed in most countries, including Australia, where more than 90% of the adult population use them today.

But mobile phones have been dogged by consistent and high-profile concerns that the electromagnetic radiation they give off might cause or contribute to cancer.

The researchers reference several reports showing an alleged link between mobile phone radiation and cancer, but say they had problems with the methods used in these studies, which meant the results were inconsistent and hard to replicate, and so may be wrong.

In an attempt to clear up the controversy, they set out to do a large, long-term study assessing the alleged link, bypassing many of the methodological flaws of previous research.

This sort of study is the most appropriate type to uncover any link between mobile phone ownership and cancer at a country level.

But as it is an ecological study, we need to resist the natural temptation to apply the country-level findings to individuals. We are dealing with averages of large groups, not individual cases.

What did the research involve?

All cases of cancer are recorded in Australia and have been for many decades. The percentage of Australians with mobile phone accounts was obtained from large mobile phone companies and governing bodies.

Putting these two pieces together, the researchers had mobile phone accounts dating between 1987 and 2014, and brain cancer diagnoses of 19,858 male and 14,222 females between 1982 and 2012. 

Their analysis looked at whether the rise in mobile phone ownership was linked to a rise in new cases of brain cancer, and they did this separately for different age groups and genders.

The researchers then probed the alleged link in more detail. Assuming a 10-year lag between phone radiation exposure and resulting cancer, they calculated the number of cancer cases they would expect to see if phone radiation caused cancer in a 20-year period, using the best estimates of risk increase from recent studies.

Their assumption was that mobile phones raised the risk of brain cancer 1.5 times for "ever-users" – those who'd used a mobile phone at any point in their lives – and 2.5 times for "heavy users", defined as more than 896 hours of total life use, which represented around 19% of Australians. These risk estimates were informed by previous research.

Using these assumptions, they were able to calculate an expected number of brain cancer cases if mobile phones caused brain cancer and compare it with the number of cases actually observed.

What were the basic results?

Mobile phone use in Australia rose from 0% in 1987 to 94% in 2014. Over a similar time period, 19,858 males and 14,222 females aged 20 to 84 were diagnosed with brain cancer from 1982 to 2012.

Age-adjusted brain cancer incidence rates over this time rose slightly in men but not at all in women. The rise in men was not attributed to mobile phone use.

Assuming mobile phones caused brain cancer, the researchers expected to see much higher rates of cancer than they did.

For example, the actual rate of brain cancer in men was 8.7 cases per 100,000 men, which should have been around 11.7 per 100,000 if the causal theory was true.

Combining men and women of all ages, they expected around 1,867 cases of brain cancer in 2012 if mobile phones were part of the cause (ever-users), but found significantly less: 1,434. The difference was even larger for heavy users: 2,038 expected compared with 1,434 actually observed.

One age group, 70 to 84 years, did show up as having similar expected and observed cases, but the rise in cases started in 1982, before the introduction of mobile phones, leading the researchers to conclude it couldn't be caused by mobiles. 

They thought it was probably the result of more access to better cancer diagnosis over time – picking up more cancer cases than in the past – leading to higher rates of cancer overall.

How did the researchers interpret the results?

The researchers concluded that: "After nearly 30 years of mobile phone use in Australia among millions of people, there is no evidence of any rise in any age group that could be plausibly attributed to mobile phones."


This ecological study found an explosion in Australian mobile phone ownership since the 1980s coincided with relatively little change in brain cancer rates, suggesting mobile phone ownership is unlikely to cause brain cancer.

This conclusion is based on assuming there would be a 10-year lag between mobile phone use and cancer, and 1.5 and 2.5 times risk increases due to mobile phone use. Using different assumptions may lead to different conclusions.

The study has many strengths, including its large size, comprehensive information on brain cancer rates over many decades, and research-based assumptions when modelling the expected number of cancer cases – assuming mobile phones do raise the risk of cancer.

What might be less obvious is that the study was more about mobile phone ownership rather than use. While you'd expect the two to be closely linked, it's important to spot the difference. 

The data the researchers had was about having a mobile phone contract – they didn't have individual patterns of use in terms of how often the phone was pressed up against users' heads emitting different strengths of radiation, for example.

As such, it's probably wise to use the term phone ownership, rather than phone use – used in the media – when talking about this study.

The study's conclusions are in line with other research quoted by this study, which showed no link between mobile phones and brain cancer.

The big problem with ecological studies are that they don't tell us about individual risk patterns, only about averages of large groups, in this case Australians. This is really useful for public health professionals who deal in population level issues, but less relevant for you and I.

For example, we can't infer from this study, however tempting, that mobile phone use doesn't contribute to brain cancer in some way, as the data simply isn't individualised or detailed enough to find out.

These caveats aside, it would be surprising, given the now massive ownership of mobile phones across the globe, if there was a strong cause and effect association, such as that between tobacco use and lung cancer.

If you are concerned, read more about the potential risks of mobile phone use

Links To The Headlines

Mobile phones DON'T increase the risk of brain cancer, 30-year study concludes. Mail Online, May 6 2016

No link between mobile phones and brain cancer, according to 29-year study. Daily Mirror, May 6 2016

Links To Science

Chapman S, Azizi L, Luo Q, Sitas F. Has the incidence of brain cancer risen in Australia since the introduction of mobile phones 29 years ago? Cancer Epidemiology. Published online May 5 2016

Categories: NHS Choices