Medical News

Claims cannabis 'rewires the brain' misleading

Medical News - Tue, 11/11/2014 - 10:26

"Cannabis use 'shrinks and rewires' the brain," reports The Daily Telegraph, with much of the media reporting similar "brain rewiring" headlines.

The headlines are based on a study that compared the brain structure and connections of cannabis users with those of non-users.

The researchers identified several differences between cannabis users and non-users in a region of the brain called the orbitofrontal cortex.

This is part of the reward network, and is enriched with cannabinoid 1 receptors. These bind THC, the active ingredient in cannabis.

Some of the differences seen by the researchers were associated with how long people had used cannabis or the age they started using the drug.

However, although brain differences were found, it is not clear they were caused by cannabis use. It is possible that brain differences mean it is more likely that certain people use cannabis.

 

Where did the story come from?

The study was carried out by researchers from the University of Texas, The Mind Research Network and the University of New Mexico.

It was funded by the US National Institute on Drug Abuse.

The study was published in the peer-reviewed medical journal PNAS. This article was open access, so is free to read online.

The media generally reported the results of this study along the lines of The Guardian's headline: "Smoking cannabis every day 'shrinks brain but increases its connectivity'." But these headlines are misleading.

This study did find differences between the brains of cannabis users and non-users, but because it was only a snapshot in time, we can't tell if the brain differences were caused by cannabis.

It is possible that brain differences mean it is more likely that certain people use cannabis. These could be pre-existing differences in the parts of the brain associated with feelings of reward, and people with this brain structure are more likely to try or persist in using cannabis.

 

What kind of research was this?

This was a cross-sectional study that compared the brain structure and connections of people who used cannabis with the brain structure of non-users to see if there were any differences.

Although this type of study can identify differences in brain structure and connections between cannabis users and non-users, it cannot show that the differences were caused by cannabis use: people with different brain structures may be more likely to use cannabis, for example.

 

What did the research involve?

The researchers used magnetic resonance imaging (MRI) scans to look at the brains of 48 cannabis users, who were using cannabis at least four times a week over the previous six months, and 62 non-users.

The cannabis users varied in age, and the non-users were chosen because they were the same sex and age as the users.

The researchers also used the marijuana problem survey to assess the negative psychological (such as feeling bad about marijuana use), social (such as family problems), occupational (such as missing work), and legal consequences of marijuana use over the previous 90 days.

 

What were the basic results?

The researchers identified several differences between the brains of cannabis users and non-users.

These differences were in a region of the brain called the orbitofrontal cortex. This is part of the reward network of the brain, and is enriched with cannabinoid 1 receptors that bind THC (the "active" ingredient in cannabis).

The researchers found the orbitofrontal cortex was smaller in cannabis users, but there was more connectivity.

Some of the brain differences were correlated with behaviour related to cannabis. Some brain differences varied with duration of use, and some of the differences were associated with the age a person had started using cannabis.

 

How did the researchers interpret the results?

The researchers say that their findings "suggest that chronic marijuana use is associated with complex neuroadaptive processes, and that onset and duration of use have unique effects on these processes".

 

Conclusion

Links To The Headlines

Smoking cannabis every day ‘shrinks brain but increases its connectivity’. The Guardian, 10 November 2014

Cannabis use 'shrinks and rewires' the brain. The Daily Telegraph, 10 November 2014

Smoking cannabis every day 'warps your brain and shrinks grey matter', scientists warn. Daily Mail, 10 November 2014

Links To Science

Filbey FM, et al. Long-term effects of marijuana use on the brain. PNAS. Published 10 November 2014

Categories: Medical News

Are pollution and attention problems related?

Medical News - Mon, 11/10/2014 - 14:47

“Could ADHD be triggered by mothers being exposed to air pollution while pregnant?,” asks the Mail Online.

Pregnant women have enough to worry about, without going round in a gas mask or moving to the country. Fortunately, the study that this news relates to doesn’t find a connection between exposure to pollution while pregnant and attention deficit hyperactivity disorder (ADHD).

In fact, the study looked at just 250 African-American and Dominican children in three suburbs of New York. It looked at whether symptoms of ADHD (rather than diagnoses) at the age of nine were associated with their pregnant mother’s exposure to environmental pollution, derived from traffic fumes and domestic heaters. The pollution – polycyclic aromatic hydrocarbons (PAHs) – was measured by levels of PAH DNA in maternal and cord blood samples taken at birth.

The researchers found there to be an association between PAH levels in maternal blood and ADHD symptoms. The mothers with high PAH levels had increased odds of being categorised as having “moderately to markedly atypical” scores on “inattentive” and “total symptom” scales.

However, there is no evidence that the association between symptoms and PAHs in the mothers’ blood was caused by environmental pollution. The researchers found no association between maternal blood PAH levels and air-measured PAH levels, nor estimations of dietary PAH intake. 

This relatively small study of a specific population sample demonstrates an association, but does not provide conclusive evidence of a link between exposure to pollution during pregnancy and a child’s chances of developing ADHD.

 

Where did the story come from?

The study was carried out by researchers from Columbia University in New York, and was funded by the National Institute for Environmental Health Sciences and the US Environmental Protection Agency. The study was published in the open access, peer-reviewed medical journal PLOS One.

The media appears to have taken these results at face value, but not considered the various limitations of this small study, which make the results far from conclusive.

 

What kind of research was this?

This was a US cohort study that investigated whether there is an association between childhood symptoms of ADHD and maternal exposure to PAHs during pregnancy

PAHs are toxic air pollutants released during incomplete combustion of fossil fuels. They are produced by traffic and residential heating, among other sources. As the researchers say, urban minority populations often have much higher exposure to air pollution than other populations.

This is a health concern because foetuses and developing children are potentially susceptible to PAHs and other pollutants. Previous laboratory studies have suggested a range of neurodevelopmental and behavioural effects from PAH exposure. Results from this cohort of mothers has already found that exposure to PAH before birth is associated with developmental delay at three years old, reduced IQ at five, and symptoms of anxiety or depression and attention problems at six to seven years old.

As ADHD is the most common behavioural disorder in childhood, the researchers also wanted to see if it was associated with ADHD at nine years of age.

However, a cohort study such as this can only demonstrate an association – it can’t prove cause and effect, as the relationship may be influenced by other factors.

 

What did the research involve?

This cohort study recruited a sample of African-American and Dominican women from antenatal clinics in three suburbs of New York City between 1998 and 2006. The women were all aged 18 to 35, non-smokers and did not use any other drug substances.

The researchers measured PAH exposure by levels of PAH-modified DNA in maternal and umbilical blood samples taken after delivery. They also measured air PAH levels during pregnancy, and questioned the women about their exposure to passive smoke and dietary PAH consumption (through grilled, fried or smoked meat).

Child ADHD behaviour problems were assessed when the children were nine years old using two validated parent-reported rating scales: 

  • the CBCL: a screening instrument assessing various child functioning problems
  • the CPRS-Revised: a focused assessment of ADHD

The CBCL and CPRS-revised scales also assessed child anxiety and depression symptoms.

The researchers analysed the association between PAH metabolites and ADHD symptoms, adjusting for other measured health and environmental factors, such as child age, sex, mother’s educational level and her own ADHD symptoms. The researchers also measured levels of PAH breakdown products detected in the child’s urine samples when aged three and five years, so that they could adjust for PAH exposure after birth.

The final sample included 250 children with complete data.

 

What were the basic results?

The researchers found that all CPRS subscales scores were significantly associated with levels of PAH-modified DNA in maternal blood.

The researchers then analysed the information to see whether there was an association with “moderately to markedly atypical” scores. Compared to those whose maternal blood was categorised as having low PAH levels, those with high levels had increased odds of being categorised as having “moderately to markedly atypical” scores on the “inattentive” and “total” DSM-IV subscales of the CPRS, but not the hyperactive-impulsive subscale.

There was some association between maternal blood PAH and the ADHD problems on the CBCL checklist scores, but this did not reach statistical significance.

Levels of PAH DNA in umbilical cord blood were available for fewer participants. There were no significant associations between PAH cord blood levels and CPRS or CBCL scores.

 

How did the researchers interpret the results?

The researchers conclude that their results, “suggest that exposure to PAHs encountered in New York City air may play a role in childhood ADHD behaviour problems”.

 

Conclusion

Overall, this relatively small cohort study demonstrates an association, but does not provide conclusive evidence, that exposure to pollution (in the form of PAHs) before birth is associated with the development of ADHD.

There are a number of limitations to consider. These include the fact that the study includes a relatively small sample of 250 children, with all of them from two specific ethnic groups (African-American and Dominican), and from three suburbs of New York City. The findings may not be generalisable to other populations.

While the researchers used valid assessment scales, it has not focused on examining actual diagnoses of ADHD.

Importantly, the only association identified by the researchers was between ADHD symptoms and levels of PAH DNA in maternal blood at the time of birth. There was no association between maternal blood PAH levels and environmentally-measured PAH levels or dietary PAH intake. Therefore, the source of this exposure is not known, and it cannot be reliably assumed to be due to environmental causes. Levels of PAH-modified DNA not only reflect exposure, but also an individual’s uptake, detoxification and DNA repair rates.  

Finally, there remains the possibility that if there is an association between maternal levels of PAH and child ADHD symptoms, it could be influenced by a variety of unmeasured health, lifestyle and socioeconomic factors.

While the findings are undoubtedly worthy of further research, there does not appear to be firm evidence from this study to support the media conclusion that exposure to environmental pollutants during pregnancy could lead to the development of ADHD.

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

Links To The Headlines

Could ADHD be triggered by mothers being exposed to air pollution while pregnant? Mail Online, November 7 2014

Links To Science

Perera FP, et al. Early-Life Exposure to Polycyclic Aromatic Hydrocarbons and ADHD Behavior Problems. PLOS One. November 5 2014

Categories: Medical News

Anxiety affects children in different ways

Medical News - Mon, 11/10/2014 - 14:47

"Teenage anxiety: Tailored treatment needed," BBC News reports, saying a "one-size-fits-all approach to treating teenagers with anxiety problems may be putting their futures at risk."

The news is based on research that looked at the diagnoses of a group of children and a group of adolescents – it did not look at how they were treated or how effective any treatment was.

But this research highlighted potential problems with assuming that "children" – defined as being aged 5 to 18 years – are affected by anxiety in the same way.

This study looked at different diagnoses among 100 children (aged six to 12 years) and 100 adolescents (aged 13 to 18 years) with anxiety problems referred to a specialist mental health service in England.

The findings showed that, despite children and adolescents often being considered as one group, their specific diagnoses – and therefore treatment needs – can differ.

In this sample, children more often had separation anxiety disorder, while adolescents were marginally (but not significantly) more likely to have generalised anxiety disorder and social anxiety disorder. Adolescents were also more likely than children to have mood disorder and have problems with school attendance.

However, as this study looked at a single consecutive sample of children and adolescents, it may not be representative of all young people with anxiety disorders: different results may be obtained from a different sample.

And this study does not provide evidence that children or adolescents are being incorrectly diagnosed or are receiving inadequate treatment.

 

Where did the story come from?

The study was carried out by researchers from the University of Reading and was supported by a Medical Research Council Clinical Research Training Fellowship awarded to one of the authors.

It was published on an open access basis in the Journal of Affective Disorders, a peer-reviewed medical journal.

The BBC News coverage is generally representative of this research.

 

What kind of research was this?

This was a case series reporting the diagnoses of 100 children (aged six to 12 years) and 100 adolescents (aged 13 to 18 years) who were consecutively referred to a specialist UK mental health service for anxiety problems.

The researchers report how little is known about the clinical characteristics of children and adolescents who are routinely referred for anxiety disorders.

And, when considered in studies, children and adolescents with anxiety disorders are often treated as one very similar (homogenous) group with an age range of five to 18 years, although they may differ in meaningful ways.

The researchers wanted to examine a series of cases of anxiety disorders to see whether there are key characteristics that distinguish children from adolescents referred for these conditions.

They expected that adolescents would have a higher anxiety severity, more social anxiety, disturbed school attendance and more frequent co-existing mood disorders.

 

What did the research involve?

The children and adolescents were consecutive referrals from general practice and secondary care to the care services at the Berkshire Healthcare NHS Foundation Trust Child and Adolescent Mental Health Service (CAMHS) Anxiety and Depression Pathway based at the University of Reading. CAMHS accepts referrals of children and adolescents with anxiety disorders from across the UK.

The child and adolescent assessments were conducted at one point in time, and involved separate diagnostic assessments or questionnaires with the child and their "primary caregiver" (usually a parent).

Child and adolescent diagnoses of anxiety disorders were determined using a structured interview called the Anxiety Disorders Interview Schedule for DSM IV – Child and Parent Version (ADIS-C/P). This assesses anxiety and other mood and behaviour disorders according to standard diagnostic criteria.

If the child or adolescent met diagnostic criteria, a clinician severity rating (CSR) was given from 0 (absent or none) to 8 (very severely disturbing or disabling), where 4 would be the score indicating a diagnosis.

The Spence Children's Anxiety Scale (SCAS-C/P) assesses symptoms reported by parents and the children themselves. These symptoms related to six domains of anxiety, rated on a scale from 0 (never) to 3 (always):

  • panic attacks or agoraphobia
  • separation anxiety
  • physical injury fears
  • social phobia
  • generalised anxiety
  • obsessive-compulsive symptoms

Other assessments include the Short Mood and Feelings Questionnaire (SMFQ-C/P) to assess self-reported depression, and the Strengths and Difficulties Questionnaire (SDQ-P) to assess parent-reported behavioural disturbance.

Caregivers' own psychological symptoms were assessed using the short version of the Depression Anxiety Stress Scales (DASS).

 

What were the basic results?

The majority of children and adolescents (84%) met a primary (main) diagnosis of anxiety disorder on the ADIS. Ten per cent of the children and 7% of adolescents did not meet any diagnostic criteria.

Six per cent of children and 9% of adolescents had non-anxiety primary diagnoses, including oppositional defiant disorder, attention deficit hyperactivity disorder (ADHD), and depression.

The results were based on the 84 children and 84 adolescents who met the criteria for a main diagnosis of anxiety disorder.

Children were significantly more likely than adolescents to have a diagnosis of separation anxiety disorder (affecting 44% of children versus 18% of adolescents).

Social anxiety disorder and generalised anxiety disorder were slightly more common in adolescents (affecting 52% and 55%, respectively) than children (affecting 45% and 49%, respectively), but the difference between children and adolescents was not statistically significant.

Although most children and adolescents had moderate severity anxiety, adolescents tended to have more severe diagnoses than children. The mean CSR score for anxiety was 5.33 for adolescents and 4.93 for children.

Mood disorders were also significantly more common in adolescents than children (affecting 24% of the total adolescent sample and 6% of children). School refusal was also significantly more frequent in adolescents (18%) than children (7%).

 

How did the researchers interpret the results?

The researchers conclude that, "The finding that children and adolescents with anxiety disorders have distinct clinical characteristics has clear implications for treatment.

"Simply adapting treatments designed for children to make the materials more 'adolescent friendly' is unlikely to sufficiently meet the needs of adolescents."

 

Conclusion

This is a useful exploratory study, which should give a good indication of the range of diagnoses among children and adolescents referred for anxiety disorders to specialist mental health services in England.

Children and adolescents, particularly in research, can often be placed into one homogenous group, and this study shows specific diagnoses can differ significantly between the groups. For example, this study showed that children more often had separation anxiety disorder.

And adolescents were marginally (but not significantly) more likely to have generalised anxiety disorder and social anxiety disorder. Adolescents were also more likely than children to have mood disorder and to have problems with school attendance.

The researchers warn they have considered childhood and adolescence as two distinct developmental periods, with age 13 being the turning point.

In reality, as they say, differences between diagnoses and treatment needs would be unlikely to occur in the same way in every growing child. They suggest that further studies focus on narrower age bands.

As the researchers also acknowledge, the people in this study were from a predominantly white British ethnic background and from relatively high socioeconomic backgrounds.

The study also did not include those with autism spectrum disorders, obsessive compulsive disorders, or post-traumatic stress disorder.

This study is likely to give a good indication of the proportion of children and adolescents with different anxiety diagnoses referred to this specialist mental health service, but we cannot be certain it is entirely representative of young people with anxiety disorders. Different results may be obtained from a different sample.

As the researchers say, their results highlight that children and adolescents with anxiety disorders are likely to have different treatment needs.

But this case study does not show that children and adolescents are being incorrectly diagnosed or are receiving inadequate treatment.

The present study focused solely on diagnosis, and not treatment. As the research did not look at treatments, it should not be assumed that children and adolescents are not receiving the appropriate treatment targeted at their diagnosis.

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

Links To The Headlines

Teenage anxiety: Tailored treatment needed. BBC News, November 8 2014

Links To Science

Waite P, Creswell C. Children and adolescents referred for treatment of anxiety disorders: Differences in clinical characteristics. Journal of Affective Disorders. Published June 25 2014

Categories: Medical News

Stem cells could repair Parkinson's damage

Medical News - Fri, 11/07/2014 - 14:30

"Stem cells can be used to heal the damage in the brain caused by Parkinson's disease," BBC News reports following the results of new Swedish research in rats.

This study saw researchers transplant stem cells into rats' brains. These cells then developed into dopamine-producing brain cells.

Parkinson's disease is a neurological condition associated with the loss of dopamine-producing brain cells. This leads to the symptoms characteristic of the condition, such as tremor, stiff, rigid muscles, and slow movements.

Parkinson's is currently treated with medication that attempts to compensate for the loss of these cells, but it cannot replace them.

This new research demonstrated it may be possible to use stem cell-derived dopamine nerve cells to treat the condition, giving long-term functional results.

Up to six months after the cells were grafted into the brains of the rats, brain scans and functional tests showed the transplanted cells had proliferated and matured, reinnervated the brain tissue, and were producing dopamine.  

The next step would to be to try to follow on from this research with clinical trials in humans.

 

Where did the story come from?

The study was carried out by researchers from Lund University in Sweden and other research institutions in France.

The research and individual authors received various sources of financial support, including the European Community's 7th Framework Programme.

The study was published in the peer-reviewed journal, Cell Stem Cell on an open access basis, so it is free to read online.

Both BBC News and ITV News gave a good representation of the research.

 

What kind of research was this?

In this laboratory study, researchers aimed to produce dopamine neurones (nerve cells) from human embryonic stem cells and graft these into a rat model of Parkinson's disease. They wanted to see if this had the potential to be used as a treatment for the disease.

Parkinson's is a neurological disease with an unknown cause, which sees a loss of the nerve cells in the brain that produce the chemical dopamine.

Loss of dopamine causes the three classic Parkinson's symptoms of tremor, stiff, rigid muscles and slow movements, as well as a range of other effects, including dementia and depression. There is no cure, and current drugs aim to try to control symptoms by treating this dopamine imbalance.

Human embryonic stem cells have the potential to develop into any type of cell in the body. Using these stem cells to replace dopamine nerve cells seems a promising area for research, and this study is the first step in investigating whether this type of treatment could one day be possible.

 

What did the research involve?

The researchers developed dopamine nerve cells from human embryonic stem cells (hESC) in the laboratory.

They then needed to see whether these cells would survive and function in the long term when grafted into brain tissue.

They transplanted these hESC-derived dopamine neurones into a rat model of Parkinson's disease, where the rats' brains were injected with a toxin to stop dopamine production.

The researchers followed the rats for six months after the cells were transplanted into their brains, carrying out various brain scans and tissue examinations to see how the cells had developed and were functioning.

They then carried out a behavioural test in the rats to see whether the transplanted cells had caused a recovery of their motor function (movement).

 

What were the basic results?

One to five months after the hESC-derived dopamine neurones had been grafted into the brains of the rats, MRI scans showed the transplanted cells had increased in volume, indicating that they were proliferating and maturing.

Further imaging was carried out using PET scans to detect a radiolabeled chemical marker that targets dopamine receptors.

Before grafting, the brains of the Parkinson's rats demonstrated a high level of binding of this chemical to the dopamine receptors, indicating that dopamine was lacking and that this marker was taking dopamine's place in the receptors.

Five months after grafting, binding of this chemical was reduced to normal levels, which indicated there was an active release of dopamine from the transplanted cells and dopamine was therefore now binding to these receptors.  

Examination of the rats' brain tissue confirmed these imaging findings, showing that the tissue was rich in dopamine neurones and that the transplanted cells had reinnervated the brain tissue.

The behavioural test also gave positive results, indicating that the transplanted hESC-derived dopamine neurones led to functional motor recovery in the rats.

 

How did the researchers interpret the results?

The researchers concluded they have "performed a comprehensive preclinical validation of hESC-derived [dopamine] neurons that fully supports their functional efficacy and capacity for long-distance, target-specific reinnervation, predictive of their therapeutic potential".

 

Conclusion

This is promising early-stage research that demonstrates it is possible to manufacture dopamine-producing nerve cells from human embryonic stem cells in the laboratory.

The cells were then transplanted into a rat model of Parkinson's disease (the rats were given a toxin that destroyed their dopamine-producing cells).

Up to six months after the cell transplant, brain scans and functional tests showed that the transplanted cells had proliferated and matured, reinnervated the brain tissue, and were producing dopamine.  

The next step is to follow on from this research with the first clinical trials in humans. The researchers say they hope they will be ready for the first clinical trial in about three years' time.

But there are several technical obstacles that need to be overcome first. Although the results indicate the transplanted cells were functioning well in the rat model at five months, as the researchers say, it is important to verify that these functional effects are robust and stable over significantly longer time periods.

Also, the rat brain is much smaller than the human brain. It would therefore need to be demonstrated that the transplanted cells have the capacity to grow nerve fibres that can reinnervate distances relevant to the size of the human brain.

This research holds promise for a future stem cell treatment that could restore the dopamine-producing nerve cells lost in people with Parkinson's disease. The next stages in this research are awaited eagerly.

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

Links To The Headlines

Parkinson's stem cell 'breakthrough'. BBC News, November 7 2014

Major breakthrough puts scientists on path to first ever stem cell transplantations in people with Parkinson's disease. ITV News, November 7 2014

Links To Science

Grealish S, Diguet E, Kirkeby A, et al. Human ESC-Derived Dopamine Neurons Show Similar Preclinical Efficacy and Potency to Fetal Neurons when Grafted in a Rat Model of Parkinson's Disease. Cell Stem Cell. Published online November 6 2014

Categories: Medical News

Norovirus returns: advice is to stay away from GP

Medical News - Fri, 11/07/2014 - 13:29

After Halloween and Bonfire Night, we have the return of another, much less welcome, winter tradition: the norovirus. Or, as The Times reports, “Tis the season for winter vomiting bug”.

The body responsible for public health in this country, Public Health England, has issued a bulletin reminding everyone experiencing symptoms of norovirus to stay at home and to telephone 111 for advice, if necessary. Symptoms of norovirus typically include forceful vomiting and watery diarrhoea.  

It's vital that people don’t visit GP surgeries, hospitals, schools and care homes if they think they may be infected. For the vast majority of people, the norovirus is self-limiting (it gets better by itself) but vulnerable groups, such as the elderly and people with a pre-existing illness or weakened immune system could be at risk of complications if exposed to the virus.

 

What is norovirus?

Norovirus is the most common stomach bug in the UK, and has a peak season during the winter months (roughly around October/November to March/April). It causes vomiting and diarrhoea, with symptoms lasting around one to two days, though the severity and duration of symptoms can vary between individuals.

Norovirus is a highly contagious virus, meaning that only a few viral particles are required to cause infection. It is passed on by virus particles picked up on the hands being transferred to the mouth (e.g. through touching contaminated surfaces or eating contaminated food). It can also be spread by inhaling small airborne particles of the virus (e.g. if someone nearby has profuse vomiting).

As it is so contagious, it’s frequently the cause of outbreaks in places where people are gathered together, such as schools, childcare centres, care homes and hospital wards.

It is a self-limiting virus, meaning that symptoms will clear up by themselves and no specific treatment is effective, or needed. However, as with any diarrhoea and vomiting bug, dehydration is the main risk, particularly for vulnerable people, such as the young or elderly. Therefore, regular fluids are very important.

 

What are the main ways to prevent norovirus spreading?

As norovirus is highly contagious, the key ways of stopping the virus spreading centre on:

  • effective hand washing
  • isolation or exclusion of the infected individual (e.g. from school or work)
  • effective cleaning and disinfection of environmental surfaces (e.g. bathrooms and toilets)

Effective hand washing is a key measure. Hands should be washed at all appropriate times, such as before eating and preparing food, and after using the toilet or helping others (e.g. changing nappies).

Effective hand washing includes:

  • wetting hands under running water
  • applying soap and rubbing this in thoroughly, over all hand surfaces; the length of time spent washing your hands is recommended to last as long as it takes to sing the “Happy Birthday” song
  • rinsing
  • drying hands thoroughly, ideally with disposable paper towels (reusable towels or flannels should not be shared between people)
  • using the paper towel to close the tap, so not to re-contaminate hands

Even if gloves are worn (e.g. when cleaning up spillages of vomiting), hands still need to be washed after removing the gloves.

If hand sanitiser/alcohol gel is used instead of hand washing, sufficient gel (e.g. the size of a 10p coin) needs to be applied to all hand surfaces and rubbed in for about 30 seconds. If hands are visibly soiled, they need to be washed with soap and water.

People with diarrhoea and vomiting should be sent home from work or school (or isolated if in a care home, for example) and should not return until 48 hours after symptoms have resolved.

This includes not visiting public places where people are gathered, such as GP surgeries, hospital wards or care homes. Public Health England has highlighted the risk in hospitals.

 

What does Public Health England say?

Public Health England says there were 18 outbreaks of norovirus in hospitals across England in November 2013, 17 of which led to ward closures. Data for July 2013 to June 2014 indicated that there were 610 reported hospital outbreaks over this one-year period, 94% of which led to ward closures. As Public Health England says, closures are necessary to stop the contagious virus spreading, but are also highly disruptive.

John Harris, an expert in norovirus at Public Health England, advises: “October usually marks the start of the norovirus season and the bulk of cases will occur between now and April next year.

“No two norovirus seasons are the same, and there is no way of predicting how busy a season will be. What we do know is that many people will be affected across the country and they will probably feel very unwell for a couple of days, but will get better.

“For patients already ill in hospital, this virus could cause further health complications, making it vital to prevent introducing the virus into the hospital environment.

“We strongly urge anyone affected to stay at home and to telephone NHS 111 for advice.”

 

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

Links To The Headlines

If you've got winter vomiting bug, stay at home: Health officials warn patients NOT to visit their GP or hospital as norovirus spreads through wards. Mail Online, November 6 2014

Norovirus: What are the symptoms of the winter vomiting bug and how do you avoid it? The Independent, November 6 2014

‘Tis the season for winter vomiting bug. The Times, November 7 2014

NHS crisis warning over killer winter bug. Daily Express, November 7 2014

Categories: Medical News

Fruit chemical may prevent organ damage

Medical News - Thu, 11/06/2014 - 15:00

"Could fruit help heart attack patients? Injection of chemical helps reduce damage to vital organs and boosts survival," reports the Daily Mail – "at least in rodents," it should have added.

When tissues are suddenly deprived of oxygen-rich blood (ischaemia), which can occur during a heart attack or stroke, they can suffer significant damage. Further damage can occur once blood supply is restored. Until now, scientists did not know the exact cause of this damage.

Through a set of animal experiments, researchers may have now identified the cause. It could be the result of an increase in a chemical called succinate. Succinate appears to interact with the returning oxygen molecules, creating harmful molecules (reactive oxygen species) that can damage individual cells.

The researchers were able to reduce the amount of succinate produced during periods of mouse heart ischaemia and brain ischaemia by injecting a chemical called dimethyl malonate, which is found in some fruits. This in turn reduced the amount of tissue damage that occurred when the blood supply was returned to the heart and brain.

Although the potential uses are wide ranging, including the use of dimethyl malonate as a potential preventative treatment during heart attacks, stroke or surgery, it will need to be shown to be both effective and safe through human trials.

 

Where did the story come from?

The study was carried out by researchers from the University of Cambridge, St Thomas' Hospital, University College London, the University of Glasgow, and the University of Rochester Medical Centre, New York.

It was funded by the Medical Research Council, the Canadian Institutes of Health Research, the Gates Cambridge Trust, and the British Heart Foundation.

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

The study was accurately reported by the Daily Mail, although the headline was misleading – dimethyl malonate has not yet been used to improve survival in humans. It has only been used in experiments involving mice and rats.

Also, although dimethyl malonate is found in some fruit, the chemical itself has been used, rather than the mice and rats being treated with pieces of fruit.

 

What kind of research was this?

This was an animal study looking at the mechanism behind the injury that occurs to tissues when blood supply is returned after a period of ischaemia (no blood supply).

It was previously believed that tissue injury in these cases, particularly seen after a heart attack, was a non-specific response to the cells regaining oxygen.

The researchers wanted to test the hypothesis that a specific metabolic process causes the injury. And, if so, they wanted to see whether they could develop a drug to limit the process and thereby prevent the injury.

 

What did the research involve?

The researchers looked at chemicals produced in mouse kidneys, livers and hearts, and rat brains after the animal had suffered from ischaemia and had then been reperfused (had their blood and oxygen supply returned).

After identifying one chemical, called succinate, which was increased in all of the tissues studied, the researchers performed a variety of experiments on mouse hearts to investigate the metabolic pathways responsible for the increased level and tissue damage.

They then tested a chemical, dimethyl malonate, that prevented the accumulation of succinate in mouse hearts and rat brains during ischaemia to mimic a stroke.

 

What were the basic results?

The chemical succinate was increased in all of the animal tissues by 3 to 19 times normal levels, and the level of succinate increased with longer periods of ischaemia. It returned to normal levels by five minutes after reperfusion.

Infusing mice with the chemical dimethyl malonate, which can act as an inhibitor of one of the enzymes that can make succinate, significantly reduced the succinate accumulation in the ischaemic heart.

It also stopped the accumulation of succinate in rats' brains during ischaemia (similar to a stroke), and reduced the amount of tissue damage and neurological disabilities.

Succinate is a chemical present in what is known as the citric acid cycle. This cycle is the series of chemical reactions used by all aerobic (oxygen using) organisms to produce energy from fats, carbohydrates and proteins. Interestingly, none of the other chemicals in this pathway were increased during the ischaemia.

Dimethyl malonate is a naturally occurring substance and has been detected in a number of fruits, such as pineapples, bananas and blackberries. It is also widely used in pharmaceuticals, agrochemicals, vitamins, fragrances and dyes.

 

How did the researchers interpret the results?

The researchers concluded they have shown how the chemical succinate accumulates during ischaemia, and that this drives the tissue injury seen when blood supply is returned in a range of rat and mouse tissues.

They found they can reduce the amount of accumulation and damage by using an infusion (injection of a solution) of dimethyl malonate. This research will now pave the way for human trials.

 

Conclusion

This exciting set of experiments has identified the metabolic driver of tissue injury seen when blood supply is returned after a period of ischaemia. The researchers have also shown this process can be limited by using an injection of dimethyl malonate in mice and rats.

It is likely the same increased metabolic processes occur in humans, so there are wide implications for the future, including the potential use of dimethyl malonate injections to prevent tissue damage during surgery.

At present it is unclear how this could be used practically during a heart attack or stroke, and this will be one of many issues that will be explored when human trials are initiated, along with the safety of this treatment.

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

Links To The Headlines

Could FRUIT help heart attack patients? Injection of chemical helps reduce damage to vital organs and boosts survival. Daily Mail, November 5 2014

Links To Science

Chouchani ET, Pell VR, Gaude E, et al. Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS. Nature. Published online November 5 2014

Categories: Medical News

Does having a hobby help you live longer?

Medical News - Thu, 11/06/2014 - 14:00

"Having a hobby can add YEARS to your life," The Daily Express reports. The headline is prompted by an international study that looked at ageing and happiness.

The study found older people who reported the greatest sense of purpose in life survived longer than those who reported having little sense of purpose, suggesting that having a meaning in life might play a role in protecting people's health.

But this study cannot prove having a hobby or other purpose in life increases the chances of surviving longer.

As the authors point out, there are many other factors involved that might have an effect on survival, including ill health and material income.

Other studies show a two-way connection between health and wellbeing. Being affected by common illnesses such as arthritis or heart disease, for example, can make it difficult to maintain a zest for life.

That said, it's obviously sensible for people to stay active as they grow older and to maintain their social activities and relationships. Having something to live for, whether it's as noble as eradicating world poverty or a little more down to earth, such as maintaining an attractive garden, could help you live longer.

Research shows people who regularly give up their time to help others, stay activelearn new things and connect with others tend to have higher reported feelings of wellbeing.

 

Where did the story come from?

The study was carried out by researchers from University College London, as well as Princeton University and Stony Brook University, which are both in the US.

Funding came from a variety of sources, including the US National Institute on Aging and several UK government departments.

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

Press coverage reported the study's findings uncritically and took some liberties in extrapolating the results. It would be simplistic to say – as the Express did – that, "having a hobby can add YEARS to your life", as many other confounding results are likely to be involved.

The Daily Telegraph's claim that, "pensioners with sense of purpose live two years longer than cynics" is overstating the study's findings. Cynicism was not even mentioned in the study.

BBC News took a slightly different take on the study, focusing on the global variations in happiness and how this changes over the course of a lifetime.

 

What kind of research was this?

This study is part of a Lancet series on ageing, which drew on various sources to look at the relationship between wellbeing, health and ageing.

It did not present any new evidence, but analysed findings from existing sources, such as an ongoing international poll on wellbeing and an English study of ageing.

According to the researchers, there are three different aspects to wellbeing:

  • evaluative wellbeing – or life satisfaction
  • hedonic wellbeing – feelings of happiness, sadness, anger, stress and pain
  • eudemonic wellbeing – sense of purpose and meaning in life

The researchers say subjective wellbeing is becoming a focus of intense debate in public policy and economics, with improvement in wellbeing a key aspiration.

Research suggests subjective wellbeing might even protect health, reduce the risk of chronic illness and promote longevity. Their paper summarises the present evidence linking subjective wellbeing with health in an ageing population.

 

What did the research involve?

The researchers searched online databases for relevant evidence, and included all articles published in English between January 2000 and March 2012.

For their analysis of the link between wellbeing and age in different parts of the world, they mostly drew on large-scale international surveys such as the Gallup World Poll, an ongoing survey taking place in more than 160 countries.

To look at the association between wellbeing and survival, they carried out a new analysis of an existing study, the English Longitudinal Study of Ageing (ELSA), relating eudemonic wellbeing to mortality. 

In this analysis, 9,040 people with an average age of 64.9 years were followed for an average of 8.5 years, with 1,542 deaths analysed. Eudenomic wellbeing was assessed by questionnaire on issues such as sense of control, purpose in life and self-realisation. The cohort was divided into quartiles of wellbeing and were analysed for the relationship between wellbeing and survival. 

 

What were the basic results?

The researchers' analysis of the ELSA found eudemonic wellbeing is associated with increased survival:

  • 29.3% of people in the lowest quartile of wellbeing died during the follow-up period of 8.5 years, compared with 9.3% of those in the highest quartile
  • after adjustment for factors such as education, health and income, the highest quartile had a 30% lower risk of dying within the study period

They also reported on other data, which shows:

  • a U-shaped relation between life satisfaction (evaluative wellbeing) and age in high-income English-speaking countries, with the lowest levels of wellbeing in those aged 45-54, after which levels start to rise
  • this pattern is not universal – for example, respondents from the former Soviet Union, Eastern Europe and Latin America show a large progressive reduction in wellbeing with age, while wellbeing in Sub-Saharan Africa shows little change with age

They also found studies that showed how the relation between physical health and subjective wellbeing is "bidirectional".

Older people with common illnesses of ageing, such as coronary heart disease, arthritis and chronic lung disease, show both increased levels of depressed mood and impaired wellbeing.

 

How did the researchers interpret the results?

The researchers concluded that the wellbeing of elderly people is an important objective for both economic and health policy.

"Even though the results do not unequivocally show that eudemonic wellbeing is causally linked with mortality, the findings do raise intriguing possibilities about positive wellbeing being implicated in reduced risk to health," the authors conclude.

They also concluded that the U-shaped curve in wellbeing in high-income English-speaking countries – with life satisfaction at its lowest in the 45-54 age group – is because this is the period for working and earning the most at the expense of wellbeing.

The findings about wellbeing in former Soviet Union and Eastern European countries is attributed to the recent transitions and resulting political and economic instabilities in these countries. Similar, if not as extreme, instabilities can be seen in the Caribbean and Latin America.

The flatlining of happiness in Sub-Saharan Africa, while not explicitly discussed by the researchers, is possibly a result of the high levels of poverty, and corresponding lack of opportunities to build a better life as a person grows older.

 

Conclusion

This is an interesting paper on the important issue of wellbeing and its potential effect on health and survival. However, as the authors point out, it does not prove that wellbeing protects health and increases the chance of living longer.

The association they found could be a result of both measured and unmeasured confounders, such as ill health. Wellbeing could be a marker for underlying biological processes that are responsible for the effect on survival.

There are likely to be bidirectional effects at work. Some people with poor health become unhappy, while others who are unhappy become physically unwell.

That said, it's sensible for people to stay active as they grow older, and maintain their social activities and relationships. Eating well, exercising regularly and maintaining a healthy lifestyle are also advised.

Read more about how to be happier.

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

Links To The Headlines

How you can add years to your life: Major lifestyle changes can combat killer diseases. Daily Express, November 6 2014

Pensioners with sense of purpose live two years longer than cynics. The Daily Telegraph, November 6 2014

Happiness 'dips in midlife in the affluent West'. BBC News, November 6 2014

Here's Where People Are Happiest Growing Old. Time, November 5 2014

Links To Science

Steptoe A, Deaton A, Stone AA. Subjective wellbeing, health, and ageing. The Lancet. Published online November 6 2014

Categories: Medical News

Smoking 'increases risk of chronic back pain'

Medical News - Wed, 11/05/2014 - 15:00

"Smokers are three times more likely to suffer from back pain," the Mail Online reports. The headline was prompted by the results of a recent study, which involved observing 68 people with sub-acute back pain (back pain lasting for 4 to 12 weeks with no back pain in the previous year) over one year.

The participants completed repeated questionnaires about their level of back pain and had four functional MRI brain scans over the course of the year.

Smokers were three times more likely to develop chronic back pain. They were also more likely to have increased activity in the brain pathways implicated in addiction (between the nucleus accumbens and the medial prefrontal cortex).

The researchers speculate this increased activity may also increase the risk of chronic pain developing. This increase in activity reduced in a small number of people who stopped smoking.

As this was an observational study, it cannot prove that the increased brain pathway activity or smoking caused the back pain to become chronic, but it does indicate they may be linked in some way.

Even if you don't suffer from back pain, there's no excuse not to try to quit smoking. It can cause lung cancer and heart disease, and increase your risk of a stroke – all of which can be fatal.

 

Where did the story come from?

The study was carried out by researchers from the Feinberg School of Medicine in the US, and was funded by the US National Institutes of Health.

It was published in the peer-reviewed medical journal, Human Brain Mapping.

The study was generally reported accurately by the Mail Online, although it didn't emphasise that the findings were only based on 68 people.

Similarly, the study was about how smoking influenced the risk of people moving from experiencing sub-acute back pain to chronic back pain, but this subtlety seemed to be lost.

Based on the headlines, readers may get the wrong impression that the study was about developing back pain full stop.

Also, the Mail's claim that "quitting can ease symptoms" – while well meaning – is unsupported by the evidence of this study.

 

What kind of research was this?

This was a longitudinal study looking at the potential relationship between developing chronic back pain and smoking tobacco.

Previous research suggested the brain pathways involved in addiction are also related to those implicated in the development of chronic pain.

The researchers aimed to test the theory people with new-onset back pain would be more likely to develop chronic back pain if they were smokers.

As this was a type of observational study, it cannot prove smoking causes a transition to chronic back pain, but it can show potential links that can be tested in more rigorous studies in the future.

It is often difficult to tease out the precise relationship between smoking and chronic back pain. Smokers tend to be unhealthy in other ways, such as not taking very much exercise, so this could also have a confounding effect.

 

What did the research involve?

The year-long study involved participants completing well-validated questionnaires about:

  • pain (McGill short form)
  • depression (Beck's Depression Inventory)
  • positive or negative feelings and emotions (Positive Affective Negative Affect Score, PANAS)
  • demographic information, including smoking status

After an initial visit, participants were assessed on four more occasions during the year using further questionnaires. They also had their brains scanned using functional MRI scans, which can – at least to a certain extent – measure brain activity.

Three groups of people were included in the research. The first and largest group consisted of 160 people with sub-acute back pain, defined as back pain lasting for 4 to 12 weeks with no back pain in the previous year. Of these, 123 were recruited to the study and 68 people completed follow-up after one year.

The second group included 32 people with chronic back pain for more than five years, of whom 24 completed the study. The third group of 33 people was considered to be the control group. These people had no back pain, and 19 completed the study.

For all groups, the researchers analysed whether smoking was linked to their back pain.

 

What were the basic results?

Of the 68 people with sub-acute back pain, 31 were considered to be recovering according to a pain decrease of at least 20% after one year (six of these were smokers and 25 were non-smokers). The other 37 had persistent pain (16 smokers and 21 non-smokers).

Those with persistent pain were three times more likely to be smokers than those who recovered, (odds ratio [OR] 3.17, 95% confidence interval [CI] 1.05 to 9.57) despite having similar levels of initial back pain.

They were also more likely to have increased activity in the brain pathways implicated in addiction (between the nucleus accumbens and the medial prefrontal cortex).

In nine participants with sub-acute back pain or chronic back pain, this brain pathway activity reduced after they quit smoking, but it is unclear what effect this had on their back pain.

Smoking also did not appear to relieve pain, as smokers did not have reduced back pain intensity either at baseline or after one year compared with non-smokers, and back pain did not increase when people stopped smoking.

At baseline, people with sub-acute back pain and chronic back pain were more likely to be smokers than controls. And the pain was also likely to have a negative impact on their mood, according to higher scores on the Beck Depression Inventory and negative PANAS scores.

 

How did the researchers interpret the results?

The researchers concluded that, "Smoking increases risk of transitioning to CBP [chronic back pain], an effect mediated by corticostriatal circuitry involved in addictive behaviour and motivated learning."

 

Conclusion

This longitudinal study found sub-acute back pain was three times more likely to progress to persistent back pain in smokers.

The researchers presented functional MRI findings, which indicated brain pathways that could be involved in this process. But further research will be required to fully understand the mechanisms at play.

The study did not find that smoking provided any pain relief, and indeed the pain intensity did not increase for those people who stopped smoking.

The study sample was quite small, meaning the results may not be applicable to larger and more diverse groups of people. As such, the results are not conclusive and should not be taken at face value.

The general advice for the early management of lower back pain is:

  • to continue normal activities as far as possible
  • to stay physically active and exercise within your capabilities
  • if medication is required, start with paracetamol and then consider other options, such as non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, with appropriate stomach protection

While this research is not conclusive, there are many health benefits associated with stopping smoking that have a large and robust evidence base, such as a reduced risk of lung cancer and heart disease.

Read more advice about effective methods known to help many smokers quit.

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

Links To The Headlines

Smokers are three times more likely to suffer from back pain - but quitting can ease symptoms. Mail Online, November 4 2014

Links To Science

Petre B, Torbey S, Griffith JW, et al. Smoking increases risk of pain chronification through shared corticostriatal circuitry. Human Brain Mapping. Published online October 12 2014

Categories: Medical News

'Elite controllers' may provide clues for HIV cure

Medical News - Wed, 11/05/2014 - 14:50

“Scientists have uncovered the genetic mechanism which appeared to have led two HIV-infected men to experience a 'spontaneous cure’,” the Mail Online reports.

The men are what is known as “elite controllers”: people thought to have high levels of immunity against the virus, as they do not develop any symptoms of HIV, despite going untreated.

Both men had no trace of HIV in blood tests that are normally used to detect the virus, but did have the virus in their DNA. This study found that there had been a mutation in the virus, meaning it was unable to replicate. This mutation may have been caused by the increase of an enzyme called APOBEC, which is usually inhibited by HIV infection.

Current treatment of HIV involves taking anti-viral medication to keep the spread of the virus (viral load) minimised, so it doesn’t cause any symptoms. This treatment regime has actually been remarkably successful – one of the great achievements of modern medicine. However, the major drawback is that the person has to take drugs every day. This research may offer the possibility of modifying the HIV virus, making it harmless – thus achieving, to all extents and purposes, a complete cure.

The researchers now wish to determine if this same mutation is present in other people who appear to have immunity to HIV infection.

  

Where did the story come from?

The study was carried out by researchers from Aix-Marseille University, hospitals in Marseille, the University of Paris Est, and the Vaccine Research Institute in Créteil. The study was reported to be funded internally and the authors declare no conflicts of interest.

The study was published in the peer-reviewed medical journal Clinical Microbiology and Infection.

The Mail Online’s reporting of the study was accurate and provided useful insights from the study authors.

 

What kind of research was this?

This was a case study of two people who were HIV positive, but with no symptoms. These people are known as “elite controllers” as they seem to have an innate immunity against infection.

It's difficult to estimate exactly how common elite controllers are as, by their very nature, they remain free of symptoms, so they often go undiagnosed. They usually only come to light if a sexual partner or fellow drug user contracts HIV, so they are offered testing. The current best guess is that less than 1 in a 100 people have this immunity.

The researchers aimed to study the immune response of these two elite controllers to HIV infection, to understand why they have been asymptomatic.

 

What did the research involve?

The researchers investigated the DNA of two men who had been diagnosed with HIV in 1985 and 2011, but who had no HIV-related disease and no HIV detection in their blood after undertaking routine tests.

They performed laboratory tests to investigate how the HIV had been incorporated into the host DNA without it replicating. They also looked at the individual’s immune response to the HIV.

 

What were the basic results?

Viruses isolated from both men were inactive, meaning they could not spread in the men’s bodies, causing illness. This was due to a change in the genetic code of the virus, which effectively stopped it from replicating. For the geneticists out there, this involved many transformations of tryptophan codons into stop codons.

This transformation causes problems for the virus, as it can’t make the proteins it needs correctly. A specific enzyme called APOBEC makes this change, and this enzyme is usually inhibited by HIV infection.

The researchers speculated that, in these individuals, APOBEC might have been stimulated when they were first infected.

 

How did the researchers interpret the results?

The researchers concluded that their, “findings, which warrant further confirmation, are a first step in understanding the resistance to retroviruses. They may allow us to figure out the endogenisation [internal development] of retroviruses and detect resistant patients, as well as to initiate strategies of imitations of these patients to cure or prevent AIDS”. In other words, they suggest a new strategy for HIV treatments that does not require full eradication of the virus; instead, it allows incorporation of the virus into the DNA, but inactivating it. This is a new way of thinking.

 

Conclusion

This interesting research has found a likely reason for the apparent immunity of two men to HIV infection. This was through a transformation of an amino acid in the genetic code of the virus that stops it from replicating. The researchers now wish to reproduce their findings by looking at samples from other people who appear to be resistant to HIV infection. The next step in the quest for a cure would be to determine how to replicate this genetic switch in amino acids in people without natural resistance.

The results of the study have no immediate treatment implications, but do increase understanding of the virus and the disease, so could aid development of future treatments.

While current anti-viral treatment is effective, it usually requires a person to take drugs for the rest of their life, which can sometimes cause unpleasant side effects.

Therefore, a drug that could achieve a complete cure by stopping the HIV virus replicating would have a significant positive impact for people living with HIV.

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

Links To The Headlines

Scientists uncover the secret of the 'elite controllers' who can spontaneously 'cure' HIV - and say it could lead to new treatments. Mail Online, November 4 2014

Links To Science

Colson P, Ravaux I, Tamalet C, et al. HIV infection en route to endogenization: two cases. Clinical Microbiology and Infection. Published online November 4 2014

Categories: Medical News

Short height 'linked to dementia death risk'

Medical News - Tue, 11/04/2014 - 14:50

"Short men more likely to die from dementia," The Daily Telegraph reports, though the results of the study it reports on are not as clear cut as the headline suggests.

Researchers combined the results of 18 surveys, which included more than 180,000 people. They aimed to see whether reported height was associated with deaths from dementia over 10 years of follow-up.

They found decreasing height was associated with higher rates of death from dementia. Each standard deviation decrease in height was associated with a 24% increase in risk of dementia death for men, and a 13% increase for women. This was after adjustment for factors such as age and smoking.

However, there are important limitations to consider. Despite the large cohort size, only 0.6% of the cohort died from dementia. These are small numbers on which to base any analysis.

Also, despite the trend, none of the smaller height categories were associated with a significantly increased risk of dementia death.

So, for both men and women, the smallest people in the study did not have a significant increased risk of dementia when compared with the tallest.

This means the association seen between height and dementia death isn't entirely convincing.

 

Where did the story come from?

The study was carried out by researchers from the University of Edinburgh, University College London, and the University of Sydney.

The Health Survey for England is part of a programme of surveys commissioned by the UK NHS Health and Social Care Information Centre.

Other surveys have been carried out since 1994 by the Joint Health Surveys Unit of the National Centre for Social Research, and the Department of Epidemiology and Public Health at University College London.

A number of other funding sources are also acknowledged. No conflicts of interest were reported.

The study was published in the peer-reviewed British Journal of Psychiatry.

The UK media took the reported results at face value without considering the limitations of this research. That said, all news sources that reported on the study took pains to emphasise that shortness in itself is very unlikely to cause dementia.

 

What kind of research was this?

This was a meta-analysis of data collected from participants as part of English and Scottish health surveys. It aimed to investigate the association between height and death as a result of dementia.

A meta-analysis aims to summarise the evidence on a particular question from multiple related studies.

The researchers say height is a marker of early-life illness, adversity, nutrition and psychosocial stress, and that these characteristics influence brain development, which may then affect dementia risk.

As this study is based on observational data, it cannot prove cause and effect. Its limitations include the inability to adjust for all possible confounders that may be influencing the results.

Also, deaths as a result of dementia were identified through the use of death certificates, which have not always clarified the type of dementia or whether it was directly involved in a person's cause of death. As it is primarily a disease of ageing, many people die with dementia rather than of dementia.

 

What did the research involve?

The researchers performed a meta-analysis of 181,800 participants from the Health Survey for England for the years 1994 to 2008, and the Scottish Health Survey for 1995, 1998 and 2003.

As part of the health surveys, participants were visited by a trained interviewer, who measured their height and weight. Participants were also asked about their:

  • occupation
  • age on leaving full-time education
  • ethnic group
  • smoking status
  • whether they suffered from a longstanding illness

They were subsequently visited by a nurse, who measured their blood pressure and took a blood sample to measure their cholesterol levels.

Each participant was linked to the UK NHS death register. Researchers reviewed death certificates to look for International Classification of Diseases (ICD) codes related to dementia.

In their analyses, they considered any mention of dementia on the death certificate (it may not always have been the direct cause of death). 

The researchers looked at the association between height and death from dementia, controlling for age, gender and the other factors they had information about.

 

What were the basic results?

Increasing height was generally associated with a more favourable risk factor profile in both men and women.

Taller study members were younger, from higher socioeconomic backgrounds, had slightly lower body mass index, a lower prevalence of longstanding illness, and lower blood pressure and serum cholesterol levels. Taller men were also less likely to smoke, but the reverse was true of women.

During an average follow-up of 9.8 years, there were 17,533 deaths, of which 1,093 (0.6% of the cohort) were dementia related (426 men and 667 women).

Overall, there was a 27% increased risk of dementia death per standard deviation decrease in height in men (corresponding to 7.3cm; hazard ratio [HR] 1.24, 95% confidence interval [CI] 1.11-1.39) and a 13% increased risk of dementia death in women (corresponding to 6.8cm; HR 1.13, 95% CI 1.03-1.24).

These results show the association was stronger in men than women. This overall trend for increasing dementia risk with each standard deviation decrease in height was significant for both men and women.

However, when comparing the tallest height category with each of the three smaller height categories, none were associated with a significantly increased risk of dementia compared with the tallest – in other words, for both men and women, the smallest people in the study did not have an increased risk of dementia when compared with the tallest.

 

How did the researchers interpret the results?

The researchers concluded that, "early-life circumstances, indexed by adult height, may influence later dementia risk."

 

Conclusion

This study has combined the results of 18 health surveys for England and Scotland involving more than 180,000 people.

They found, overall, each standard deviation decrease in height was associated with an increased risk of death from dementia, with the trend slightly stronger for men than for women.

But this study has important limitations to consider. Despite the large cohort size, only 0.6% of the cohort (426 men and 667 women) died from dementia, as identified by documentation on their death certificate. These are small numbers on which to base analyses, particularly when further subdividing by gender and height category.

Though there was an overall trend for increasing risk with each standard deviation decrease in height, none of the smaller height categories were associated with a significantly increased risk of dementia death for either men or women, when compared with the tallest. Therefore, the association between height and dementia death isn't as clear cut as the media reporting implied.

The researchers considered dementia deaths to be any mention of dementia on the death certificate. We don't know from this study what the specific type of dementia was (Alzheimer's or vascular dementia, for example).

We also don't know that this was necessarily the direct cause of death. It could be the case that the person with dementia died from other causes. It is also possible the results are being influenced by confounding.

As the researchers consider, it is unlikely that height itself is a risk factor for dementia. It is more likely that decreased height could be a marker of other exposures, such as socioeconomic circumstances, nutrition, stress and illness during childhood.

This study did adjust for various factors, such as age, smoking, BMI, socioeconomic status and long-term illness, but the researchers would not have been able to take into account all the factors that could be influencing the relationship.

Overall, people with a shorter stature should not be too concerned by this study. The causes of dementia – in particular Alzheimer's, the most common type – are not clearly established.

Improving your cardiovascular health (keeping the flow of blood to your brain and heart well regulated) is probably the most effective step you can take to reduce your dementia risk.

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

Links To The Headlines

Short men more likely to die from dementia, Edinburgh University finds. The Daily Telegraph, November 3 2014

Men shorter than 5ft 6ins are '50% more likely to die from dementia than those over 5ft 10ins'. Daily Mail, November 3 2014

Shortness can increase the risk of dementia. Daily Express, November 4 2014

Links To Science

Russ TC, Kivimäki M, Starr JM, et al. Height in relation to dementia death: individual participant meta-analysis of 18 UK prospective cohort studies. British Journal of Psychiatry. Published online November 3 2014

Categories: Medical News

Shift work 'ages the brain', study suggests

Medical News - Tue, 11/04/2014 - 14:25

“Shift work dulls your brain,” BBC News reports. In a French study, researchers assessed 3,232 adults using a variety of cognitive tests and compared the results between people who reported they had never performed shift work for more than 50 days per year with those that had. They analysed the results, comparing the number of years of rotating shift work performed and how long ago the shift work had stopped.

They estimated that working shifts for 10 years or more "aged" the brain by 6.5 years. They also estimated that it takes at least five years of non-shift working to reverse the effects, though this was not based on individuals' recovery of cognitive abilities. It was based on a snapshot comparing people who had stopped shift work more than five years before with people who were currently doing shift work or had never done shift work.

The study did not prove shift work causes cognitive decline, as it did not take into account people’s baseline cognitive ability.

It is also unknown whether the small, observed differences in cognitive performance scores would have had any meaningful difference in terms of daily life and functioning.

So if you are reading this on a break during your night shift, you should not be overly concerned.

 

Where did the story come from?

The study was carried out by researchers from the University of Toulouse, Swansea University, Stockholm University, the Université Paris Descartes and the University of Monaco. It was funded by several French national organisations and the UK Institute of Occupational Safety and Health.

The study was published in the peer-reviewed medical journal Occupational and Environmental Medicine.

The UK media reported the findings accurately. However, what was not made clear in reports was that, although the participants were assessed on three occasions, the analysis of recovery was based on only one time point. Therefore, this does not prove that an individual will recover their cognitive abilities after stopping shift work. Media reports also did not made it clear that the differences seen could have been due to natural abilities, rather than shift work.

 

What kind of research was this?

This was a cohort study that aimed to assess the impact of shift work on mental ability. As it was a cohort study, it is useful to look for associations; however, it cannot prove causality as it does not take all other factors into account.

 

What did the research involve?

In 1996, 3,232 adults aged 32, 42, 52 or 62 years old were randomly recruited from French registries of salaried or retired workers. They completed questionnaires, had a clinical examination and performed a variety of well-validated cognitive tests, such as being asked to read 16 words three times and then immediately reciting the list from memory.

The results of these tests were pooled to provide a score for global cognitive performance, memory and processing speed on a scale of 0 to 100, with 100 indicating a higher performance. They were invited to have similar tests five and 10 years later. A total of 1,197 people attended on all three occasions.

The participants were also asked if their work involved any of the following types of shift work for more than 50 days per year, with responses categorised as either "current", "past" or "never":

  • rotating shift work (for example, alternating morning, afternoon and night shifts)
  • schedules that did not allow them to go to bed before midnight
  • work requiring them to get up before 5am
  • work preventing them sleeping during the night (night work)

The researchers also calculated the amount of exposure to rotating shift work and analysed whether longer duration of this type of shift work had any effect on the cognitive test scores. They grouped the participants according to:

  • never worked rotating shifts
  • 10 years or less
  • more than 10 years

Finally, they analysed whether the scores differed between people who were currently doing rotating shift work or those who had stopped more or less than five years before and people who had never done shift work.

They performed statistical analyses to take into account the following confounders:

  • age
  • gender
  • socioeconomic position
  • sleep problems
  • perceived stress
  • alcohol consumption
  • tobacco consumption

 

What were the basic results?

At baseline, the 1,635 people who reported never having done shift work for more than 50 days per year had higher average global cognitive performance scores compared to 1,484 people who had experienced shift work (56.0 compared to 53.3). This difference remained the same at each time point in the study. They also had slightly better memory scores (50.8 versus 48.5) and speed processing scores (78.5 versus 76.5).

The global cognitive performance scores were highest in the group aged 32 (59.6) and lowest in the group aged 62 (47.7).

People with more than 10 years of exposure to rotating shift work had poorer cognitive scores compared to those who had never worked rotating shifts. They compared the figures with the difference seen by age group at baseline and concluded that more than 10 years of rotating shift work was equivalent to 6.5 years of age-related decline. A similar difference was seen for the memory score, but not the speed processing score.

There were no significant differences in cognitive scores for people with 10 years or less exposure to rotating shift work compared to those who never had worked rotating shifts.

People who were currently working rotating shifts had an equivalent of 5.8 years of age-related decline, and people who had left within the past five years had an equivalent of 6.9 years of age-related decline compared to those who never had worked rotating shifts.

In contrast, those who had left rotating shifts more than five years before had no difference in cognitive tests compared to those who had never worked rotating shifts.

 

How did the researchers interpret the results?

The researchers concluded that, “exposure to shift work was associated with a chronic impairment of cognition; the association was highly significant for exposures to rotating shift work exceeding 10 years (with the exception of the speed scores among non-executive participants) and the recovery of cognitive functioning after having ceased any form of shift work took at least five years (with the exception of speed scores”. They also say, “the current findings highlight the importance of maintaining a medical surveillance of shift workers, especially of those who have remained in shift work for 10 years or more”.

 

Conclusion

The researchers conclude that, “shift work was associated with impaired cognition”, but as this was found at the start of the study, it cannot prove that shift work was the cause. It is possible that people who performed shift work differed in baseline cognitive ability from those who didn’t, which may be related to various other factors (such as educational attainment). To prove cause and effect, the study would need to assess cognitive ability in individuals before any exposure to shift work.

Further limitations of this study include that in each analysis, the control group considered never to have been exposed to shift work may actually have had up to 50 days of shift work per year. A more rigorous criteria for the control group, such as working no days of shift work per year, may have been more useful. 

It's not possible to draw firm conclusions about the cause of the association seen, as there was such a wide range of shift work patterns grouped together. It is also not known the type of shift work undertaken (for example, whether in a professional or more manual occupation).

The conclusion that cognitive function recovers five years after stopping rotating shifts is also not proven by this study. The researchers performed this section of the analysis using the information obtained at baseline only. They did not compare the cognition of individuals during periods of rotating shift work with their cognition five years after stopping. They compared people who had stopped with people who were still doing rotating shifts. Therefore, this analysis does not take into account their natural cognitive abilities.

Finally, it is not known whether the small differences in cognitive functioning, memory and processing scores observed between shift workers and day workers, would have actually made any meaningful difference in terms of the person’s daily life and functioning.

Overall, this study demonstrates an association between shift work and poorer cognitive function scores, but it did not prove that shift work was the cause.

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

Links To The Headlines

Shift work dulls your brain – report. BBC News, November 4 2014

Shift work could be affecting your mental ability, scientists claim. The Independent, November 4 2014

Long-term shift work ages the brain: More than a decade 'knocks six years off memory and thinking skills'. Mail Online, November 4 2014

Long-Term Shift Work Ages Brain, Study Finds. Sky News, November 4 2014

Links To Science

Marquié J, Tucker P, Folkard S, et al. Chronic effects of shift work on cognition: findings from the VISAT longitudinal study. Occupational & Environmental Medicine. Published online November 3 2014

Categories: Medical News

Weight loss surgery cuts diabetes risk in very obese

Medical News - Mon, 11/03/2014 - 14:55

“Weight loss surgery can dramatically reduce the odds of developing type 2 diabetes,” BBC News reports.

The underlying research identified a group of 2,167 obese adults without diabetes, the majority of whom were severely obese, with a body mass index (BMI) of 40 or above.

This group had undergone weight loss surgery, so researchers compared them with a comparison group matched for age, sex and BMI, who did not have surgery. They looked at the development of type 2 diabetes in both groups.

Using the maximum follow-up period in the study (seven years), they found that the “surgery group” had an 80% reduced risk of developing diabetes compared with the “no surgery” group.

These findings are mainly applicable to those with a very high BMI (over 40). Results at lower BMIs (30 to 35) were still positive, but did not have statistical significance.

It's important to stress that weight loss surgery is no magic bullet and is associated with both short- and long-term risks and complications, such as unsightly excess skin.

Regardless, the results are consistent with current English guidelines, which recommend offering weight loss surgery to people with a BMI of 40 or more if a number of additional conditions are fulfilled. People with a BMI of 35 to 40 can also be offered weight loss surgery if they have other medical conditions that are compounded by obesity. 

Read more about who is eligible for weight loss surgery on the NHS.

 

Where did the story come from?

The study was carried out by researchers from London-based University and Hospital Departments, and was funded by the UK National Institute for Health Research.

The study was published in the peer-reviewed medical journal The Lancet – Diabetes & Endocrinology. The study has been made available on an open access basis, so is free to read online.

Both the BBC and the Daily Express reported the study accurately.

 

What kind of research was this?

This was a (matched) cohort study in a large group of obese individuals, assessing the effect of weight loss surgery (also called bariatric surgery) on the risk of developing type 2 diabetes.

Cohort studies have the ability to give an indication of cause and effect, but not direct proof. Common limitations of such a study design include high dropout rates, and the possibility of confounding – that there are other differences between the people with the different exposures that are influencing the outcomes.

That said, due to the size of the reduction in relative risk in the surgery group, it would be surprising if surgery did not have at least some influence on the study's outcomes.

 

What did the research involve?

The research team recruited two groups of closely matched obese adults: one group underwent weight loss surgery and one group didn't. They then analysed whether the surgery influenced if they went on to develop type 2 diabetes over the following seven years.

The study recruited adults (age 20 to 100 years) identified from a UK-wide database of family practices, who were obese (BMI ≥30 kg/m2) and did not have diabetes.

They enrolled 2,167 patients who had undergone weight loss surgery between Jan 1 2002 and April 30 2014 and matched them according to BMI, age, sex, index year and a blood glucose measure for diabetes (HbA1c) with 2,167 controls who had not had surgery. Weight loss surgical procedures included:

  • laparoscopic gastric banding (n=1053)
  • gastric bypass (795)
  • sleeve gastrectomy (317)

In two people, procedures were undefined.

The main outcome the team were interested in was development of clinical diagnosis of diabetes, which was extracted from electronic health records.

 

What were the basic results?

The group reported that they found a reduction in diabetes risk in both men and women due to surgery, across age groups, and after different types of surgical procedures.

The average BMI for both groups was 43 – well above the minimum threshold level for obesity (30). People who had bariatric surgery were more likely to have high blood pressure or cholesterol, and to be treated with medications for these conditions.

Maximum follow up was seven years after surgery; however, most were followed up for less. The average (median) follow up was 2.8 years (interquartile range: 1.3 to 4.5 years).

By the end of the maximum seven-year follow-up period, 4.3% (95% confidence interval (CI) 2.9 to 6.5) of the weight loss surgery group had developed diabetes, compared with 16.2% (13.3 to 19.6) in the matched control group. This analysis took into account the time between surgery and diabetes, so gives different figures from the above.

This meant that the number of newly diagnosed diabetes cases (incidence) was significantly lower in the weight loss group compared with the controls, giving a hazard ratio of 0.20 (95% CI 0.13 to 0.3). This analysis was adjusted for confounders, including comorbid cardiovascular disease and depression, smoking, high blood pressure, and cholesterol and their associated treatments. This means that the surgery reduced the relative risk of developing diabetes by 80% compared to not having surgery.

 

How did the researchers interpret the results?

Their interpretation was that, “bariatric surgery [weight loss surgery] is associated with reduced incidence of clinical diabetes in obese participants without diabetes at baseline for up to seven years after the procedure".

 

Conclusion

This research suggests that weight loss surgery may reduce the risk of developing diabetes in people who are morbidly obese (with an average BMI of 43) compared with no surgery. The beneficial effect appeared to increase over time and at the maximum follow-up period assessed in the study (seven years), the relative risk of developing diabetes had reduced by 80%.

There was variation in the risk reduction depending on age, BMI and the type of procedure, but all were beneficial.

The study had many strengths, but also some key limitations.

The obese participants were sampled from a database that indicated whether or not they had surgery. The comparison group was only matched for age, sex and BMI, so it is likely that there is some other differences between these people which influenced their selection for surgery. For example, it could have been for reasons such as personal choice, inadequate trial of non-surgical measures, or being unsuitable for anaesthesia and surgery.

Despite the results being adjusted for various medical confounders that could have an influence, these other unknown and unmeasured differences may have meant the groups had different diabetes risk to begin with.

This could make it harder to be certain how much of the difference in diabetes risk is specifically down to the effect of surgery, and how much is due to other influences.  

It is also important to recognise that the results do not apply to all people who are categorised as obese. The average BMI of recruits was high overall, at 43, meaning the results may be less applicable to people with BMIs at the lower end of the obesity scale. Further evidence of this came from a sub-analysis by BMI category. They found significant risk reductions in BMI groups 35 to 39.9, and 40 and above. At BMI levels 30 to 34.9, there was still a 60% or so reduction in risk reported, but this failed to meet statistical significance, meaning it may be a chance finding.

However, in any case, most people with BMIs below 35 are not currently eligible for bariatric surgery on the NHS, in line with UK guidance.

A further factor to bear in mind is that the control group were not offered any intervention at all, such as an intensive weight loss programme. Hence, the results tell us how much surgery is better than doing nothing, rather than if it is better than specific non-surgical alternatives, such as the NHS Choices diet and exercise plan.

The results are consistent with current English guidelines, which recommend offering weight loss surgery to people with a BMI of 40 or more if a number of additional conditions are fulfilled. People with a of BMI 35 to 40 can also be offered weight loss surgery if they have other medical conditions. For full details, see Weight Loss Surgery – who can use it?

As with any surgery, weight loss surgery has risks. The balance of risks and potential benefits would need to be discussed between doctor and patient on a case-by-case basis. Information from studies like this may inform the conversation.

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

Links To The Headlines

Weight loss surgery reduces diabetes risk. BBC News, November 3 2014

New research says surgery could be key to beating diabetes. Daily Express, November 3 2014

Links To Science

Booth H, Khan O, Prevost T, et al. Incidence of type 2 diabetes after bariatric surgery: population-based matched cohort study. The Lancet – Diabetes & Endocrinology. Published online November 3 2014

Categories: Medical News

Sadness 'lasts longer' than other emotions

Medical News - Mon, 11/03/2014 - 14:30

"Sadness lasts 240 times longer than other emotions, study claims," is the somewhat sobering news on the Mail Online.

Researchers surveyed 233 young adults from a Belgian high school with an average age of 17, and found emotions vary widely in duration.

Of the 27 emotions studied, sadness lasted the longest, whereas shame, surprise, fear, disgust, boredom, feeling touched, irritation and relief were the shortest-duration emotions. 

Emotions that lasted longer were associated with more important event triggers, as well as more reflection about the feelings and the consequences of the event that prompted the emotion.

While the study is intriguing, it has a number of limitations to consider. Chiefly, the sample size (233) was small for a cross-sectional study and recruited a relatively homogenous (similar) group of students, who were aged around 17 years.

Young students who are coming out of the emotional turmoil that is puberty, as well as facing exam stress, may be more likely to report feeling sad for longer periods than other groups. This means it is uncertain whether similar findings would be seen in other populations.

While the results give us a tentative estimate of the duration of different emotions in a group of young adults, this can't be generalised to other age and demographic groups at this stage.

 

Where did the story come from?

The study was carried out by researchers from the faculty of psychology and educational sciences at the University of Leuven in Belgium.

It was funded by the University of Leuven Research Fund, the Interuniversity Attraction Poles Programme, which is financed by the Belgian government, and a postdoctoral research fellowship from the Fund for Scientific Research, Flanders.

The study was published in the peer-reviewed medical journal, Motivation and Emotion. This is an open-access study, meaning anyone can read it free online.

Generally, the Mail Online reported the study results accurately, although it tended to take the findings at face value, without discussing any of the limitations inherent in the research.

However, the Mail did include a useful infographic showing the duration of all the different emotions tested, with sadness being noticeably higher.

 

What kind of research was this?

This was a cross-sectional study investigating which emotions last longest and why.

The researchers wanted to describe any differences in the duration of different emotions and attempt to explain what might be behind these differences.

From a health perspective, the researchers suggested this might be useful because the duration of emotional disturbances are symptoms of some mental health conditions, such as depression.

The researchers specifically looked at emotions, which they outlined were distinct from moods, because emotions start in response to an external or internal event.

For example, you may wake up in a grumpy mood, whereas receiving an unexpected tax bill stimulates emotions such as anxiety and anger.

 

What did the research involve?

The research team asked a small group of young adults to recall the duration of past emotions, their triggers and coping strategies.

The team recruited 233 high school students (112 women, 118 men, three no gender reported) with an average age of 17 years. Participation in the study was a compulsory part of their high school course.

Using a long questionnaire, participants were asked to recollect emotional episodes, report their duration, and answer questions regarding their appraisal of the emotion-eliciting event, as well as any strategies they used to regulate the emotion.

Each questionnaire had nine emotions to prompt recall from a larger set of 27.

These included admiration, anger, anxiety, feeling touched, boredom, compassion, contentment, desperation, disappointment, disgust, enthusiasm, fear, gratitude, guilt, hatred, hope, humiliation, irritation, jealousy, joy, pride, relaxation, relief, sadness, shame, stress and surprise.

Each questionnaire had a different set of nine questions. The different questionnaires were then randomly distributed to participants.

Participants were asked to rate the emotion-eliciting event using a number of appraisal dimensions. One of the main ones asked participants to indicate to what extent the event that elicited the emotion was important to them (importance).

They were also asked to report on a number of coping strategies, including to what extent they "kept on thinking about their feelings and the consequences of the event that elicited the emotion (rumination)".

To see whether the findings depended on the way emotion duration was defined, half of the participants were told that an emotion ends as soon it is no longer felt for the first time, whereas the other half were told that an emotion ends as soon as one has fully recovered from the event. All participants had the difference between emotions and moods explained to them.

 

What were the basic results?

Out of 27 emotions assessed, sadness lasted the longest, whereas shame, surprise, fear, disgust, boredom, feeling touched, irritation and relief were the shortest-lived emotions.

One appraisal dimension and one regulation strategy accounted for almost half of the variability in duration between emotions.

Compared with short emotions, persistent emotions were elicited by events of high importance and were associated with high levels of rumination (reflection or musing on an event).

The study group reported these broad findings held true across the two different emotion duration definitions, as well as when taking into account how recent and intense the emotion being recalled was.

 

How did the researchers interpret the results?

The research team summed up that their "present study revealed that meaningful differences in duration between emotions exist and that these differences can be partially explained by differences in one appraisal dimension (event importance) and one regulation strategy (rumination)".

 

Conclusion

This small cross-sectional survey of young adults suggests emotions vary widely in duration. Of the 27 emotions the researchers looked at, sadness lasted the longest by far.

Emotions that lasted longer were associated with more important event triggers, as well as more rumination about the feelings and the consequences of the event that elicited the emotion.

The study is intriguing, but has a number of limitations to consider. The sample size, for example, was small for a cross-sectional study at just 233.

It also recruited a relatively homogenous group of students aged around 17 years, so emotional duration may be very different for other age groups and groups from other educational backgrounds.

The accuracy of recalling emotions may be a further source of error, as some emotions may be far easier to recall than others: consider recalling instances of hatred, compared with hope.

This was partly addressed by the researchers by adjusting for the intensity of the emotion, but may not have completely eliminated a potential recall bias.

The results are also perhaps only as would be expected. For example, it makes logical sense that sadness is likely to be a more persistent emotion.

Sadness is likely to be influenced by a particular situation or trigger and, if there is no immediate resolution to this situation, continuing to reflect on it or being troubled by it is likely to result in a longer-lasting emotional effect.

Meanwhile, emotions such as surprise or disgust are likely to be the result of more transient events that would not have longer-term effects on the person, so they would be expected to be much shorter-term emotions.

Overall, the results give us some indication of the emotional duration of a group of young adults, but limited wider implications can be drawn from this research.

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

Links To The Headlines

Feeling sad? It could take up to FIVE DAYS to shift your mood: Sadness lasts 240 times longer than other emotions, study claims. Mail Online, October 31 2014

Links To Science

Verduyn V, Lavrijsen S. Which emotions last longest and why: The role of event importance and rumination. Motivation and Emotion. Published online October 31 2014

Categories: Medical News

Brain differences linked to chronic fatigue syndrome

Medical News - Fri, 10/31/2014 - 14:00

"Scientists find three differences in the brain [of people with chronic fatigue syndrome]," the Mail Online reports.

Chronic fatigue syndrome (CFS) affects around a quarter of a million people in the UK and causes persistent symptoms, such as fatigue, that can have a significant adverse impact on people's quality of life. The cause of CFS is unknown and the condition continues to be researched. 

The study behind this headline used a specialised type of MRI scan to examine whether there were any differences in the brain volume and structure of 15 people with CFS, compared with 14 people without.

The researchers found the volume of white matter (brain cell nerve fibres) was lower in the group with CFS. There were also some differences on the right side of the brain in the nerve fibres that connect the temporal to the frontal brain regions.

These are interesting developments in furthering our understanding of CFS. However, the study only involved a very small sample of 15 people, and we don't know how representative they are of all people with the condition.

The design of the study is able to demonstrate brain features that may be associated with the condition, but it cannot show cause and effect. We also don't know the order in which events happened.

It's not known whether these differences could have led to the development of CFS (and if so, whether they were always present, or whether some other unknown factors caused them to occur), or whether these are new changes that have occurred since the people developed CFS.

The next step would be to try to understand how these differences are associated with the condition's development.

 

Where did the story come from?

The study was carried out by researchers from Stanford University School of Medicine in California.

Financial support was provided by the Division of Infectious Disease Chronic Fatigue Syndrome Fund, and one of the authors received support from GE Healthcare.

The study was published in the peer-reviewed medical journal, Radiology.

The Mail Online's headline, "Is this proof chronic fatigue DOES exist?", casts doubt upon whether CFS actually exists. It's known CFS affects many thousands of people, with often severely debilitating consequences, so its existence is not in doubt.

However, the causes of CFS remain poorly understood. This study has tried to further understanding of the condition by examining brain features that may be associated with it. This study provides a starting point, but not the whole picture.

 

What kind of research was this?

This was a cross-sectional study that took brain scans of 15 people with CFS and a comparison group of age and sex-matched people without CFS. It aimed to research differences in the brain structure.

As the researchers explain, CFS is a debilitating condition characterised by six or more months of persistent or relapsing fatigue without any associated medical or mental health disorder.

The researchers consider that brain imaging may help inform diagnosis and prognosis, though conventional scan findings to date have been inconsistent and of limited help in any further understanding of the condition.

This study used a special MRI technique called diffusion tensor imaging (DTI). DTI measures the diffusion (movement or spread) of water through the brain tissues, which provides 3D images of the size, shape and microscopic structure of tissues.

 

What did the research involve?

The researchers scanned the brains of 15 people with CFS and compared them with 14 age- and gender-matched people without CFS. They were looking for any brain volume and structure differences between the two groups that may be linked to the condition.

People with CFS had to meet two inclusion criteria:

  • a clinical diagnosis of CFS made up of fatigue for six months or longer, with at least four other symptoms from: impaired memory or concentration, sore throat, tender lymph nodes, headaches, muscle pain, joint pain, unrefreshing sleep and malaise after exertion
  • ongoing memory or concentration problems causing severe enough impairment that a doctor thought brain imaging was necessary to confirm no other disease process was occurring

The group with CFS had an average age of 46 years. Eight people in the group were female (55%) and the average duration of their CFS symptoms was 12 years.

The age- and sex-matched comparison group were people without CFS, depression or substance use in the past year. Of 28 recruited, 14 chose to participate.

All participants completed a 20-item Multidimensional Fatigue Inventory (MFI-20), which assesses general, physical and mental fatigue, reduced motivation and activity. It is said to be a well-validated tool for assessing CFS, with higher MFI-20 scores indicating increased severity.

They also assessed whether each person was right- or left-handed or ambidextrous, as this is linked to differences in structure and volume in some brain areas.

The main analysis compared differences in brain volume and structure between the two groups using MRI (DTI) brain scans. This took into account variations in age, handedness and total brain volume.

 

What were the basic results?

The researchers found, on average, people with CFS had a lower total volume of white matter (nerve cell fibres) in their brain than people without.

They took a measure known as fractional anisotropy (FA), which gives a value between zero and one indicating the degree of diffusion of water, and whether there are any restrictions in any direction. A value of zero would mean that diffusion is the same in all directions.

They found significant differences in the FA of people with and without CFS in one particular region of the brain on the right side, called the right arcuate fasciculus. This is a nerve fibre tract that links the temporal region on the right side of the brain with the frontal region.

Most right-handed people with CFS had a maximum FA in the right arcuate fasciculus above 0.6, while those without CFS had a FA value below 0.6. They noticed that in people with CFS, FA of the right arcuate fasciculus tended to increase with disease severity.

The researchers also observed that people with CFS had areas of thickening in parts of the grey matter connected by the right arcuate fasciculus.

 

How did the researchers interpret the results?

The researchers concluded there is a loss of white matter in people with CFS. They also suggest the fractional anisotropy of the right arcuate fasciculus might be a biological indicator for CFS.

 

Conclusion

This study used a specialised type of MRI to examine whether there were any differences in the brain volume and structure of 15 people with CFS, compared with 14 people without.

They found the volume of white matter (nerve fibres) appeared to be lower, on average, in the people with CFS. There were also differences in the magnitude of water diffusion (a measure known as fractional anisotropy) in one particular white matter tract on the right side of the brain, which connects the temporal with the frontal brain regions.

These are interesting developments in furthering our understanding of CFS. But there are points to bear in mind when considering the meaning of these findings.

It must be remembered this research only used a very small sample of 15 people with CFS from the US, who may not be representative of the many thousands of people affected by this condition in the UK or elsewhere.

For example, these were people who had severe and persisting memory or concentration problems, such that their doctor thought brain imaging was required to make sure no other disease process was going on. The differences seen between these 15 people with CFS and 14 without may not be identical to differences that may be seen in a different sample.

Also, as this is a cross-sectional study, it cannot prove cause and effect: it can't tell us the order in which events happened. For example, it can't tell us whether these are structural features that occurred before people developed CFS, which may have been involved in the development of the condition, or whether these are changes that happened after the people developed CFS.

Further imaging studies in larger samples of people with this condition may reveal whether these results are consistent observations in the brain structure of people with CFS. The next step would then be to try to understand how these differences are associated with the condition's development.

These findings have no immediate treatment or preventative implications for CFS.

Analysis by Bazian. Edited by NHS Choices

Follow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

Is this proof chronic fatigue DOES exist? Scientists find three differences in the brain that suggest condition may not just be 'in the mind'. Mail Online, October 30 2014

Chronic fatigue syndrome is real, researchers say. CNN, October 30 2014

Links To Science

Zeineh MM, Kang J, Atlas SW, et al. Right Arcuate Fasciculus Abnormality in Chronic Fatigue Syndrome. Radiology. Published online October 30 2014

Categories: Medical News

Genes may play a role in Ebola survival chances

Medical News - Fri, 10/31/2014 - 14:00

"Genetic factors could play an important role in whether people survive the Ebola virus," BBC News reports. Researchers found around one in five mice remained unaffected by the infection.

Researchers investigated how mice with a different genetic make-up responded to Ebola infection. The research involved eight research strains of mice said to represent the majority of genetic variation seen across major mouse species. They were infected with Ebola and had their disease response examined.

The researchers found mice with different genetic profiles show variable disease response, ranging from complete resistance to infection with full recovery, to the disease being fatal.

Mice with resistance and those who died from the disease tended to have differences in the activity of certain genes, which was associated with differences in their immune and inflammatory response.

But the findings do not necessarily mean a similar pattern will be seen in humans, who have quite different genetics to mice.

Environmental factors such as access to good healthcare and hygiene standards (which, sadly, are of a low standard in West Africa), as well as the age, health and fitness of the person, are also likely to play a significant role in how infection with Ebola affects any individual.

Nevertheless, learning more about the genetic and immune responses to the Ebola virus could help contribute to the future creation of an effective anti-viral treatment.

Experts believe Ebola is highly unlikely to spread within the UK. To understand why, read Why Ebola risk is low for people in the UK.

 

Where did the story come from?

The study was carried out by researchers from the University of Washington and other research institutions in the US.

It was funded by grants from the US National Institute of Allergy and Infectious Diseases, the National Institutes of Health, and the Intramural Research Program of the National Institute of Allergy and Infectious Diseases, National Institutes of Health. 

The study was published in the peer-reviewed scientific journal Science Express on an open access basis, so it is free to read online.

The UK media's stories generally provide an accurate summary of the research, with most stating early on that the study was in mice.

However, the Mail Online's headline, "Will Ebola kill you? It depends on your genes," is overly conclusive and does not take account of the uncertainty of the research or its unproven applicability to people.

 

What kind of research was this?

This was an animal study investigating how mice with a different genetic make-up responded to Ebola infection in different ways.

The researchers explain how most animal studies examining the disease development of Ebola, or looking at the effectiveness of vaccines or treatments, have had to use primates or small mammals.

This is because when mice have been infected with Ebola in the laboratory, they don't demonstrate the same haemorrhagic syndrome (for example, complete dysfunction of the clotting system in the body) that occurs in humans.

This study specifically examined the role of host genetics in determining the severity of disease caused by Ebola infection.

 

What did the research involve?

This study involved infecting genetically diverse mice with different strains of Ebola to see if their genetics influenced the symptoms they developed, and whether they ultimately lived or died.

The study used mice from what is called the Collaborative Cross (CC) resource, a genetically diverse group of inbred mice obtained from the cross of eight mouse strains – five said to be classic laboratory strains, and three wild-type (found in nature) strains.

The eight "founder" mice strains are said to represent 90% of the common genetic variation seen across three major mouse species.

The researchers infected the eight CC founder strains with two strains of Ebola virus – a mouse strain and the wild-type strain, which doesn't normally cause haemorrhagic syndrome in mice.

They carried out a detailed analysis of the disease symptoms and the disease response in the mice.

 

What were the basic results?

When infected with the mouse strain of Ebola virus, the researchers observed different disease responses across the mice, ranging from complete resistance to infection to fatal disease. Some of the fatal cases developed disease changes consistent with haemorrhagic syndrome, while others did not.

The researchers performed more detailed analysis on two of the mouse lines – those resistant to disease and those that developed Ebola haemorrhagic fever.

Mice from both of these lines lost about 15% of their body weight in the five days following infection. The susceptible mice died on day five or six, while resistant mice fully recovered two weeks after infection.

Those that died demonstrated disease features consistent with Ebola haemorrhagic fever, including internal bleeding, prolonged blood coagulation times, spleen enlargement and liver discolouration. The resistant mice had no disease changes or alteration in their liver.

On further study, the researchers found differences in the inflammatory and immune response of mice susceptible or resistant to infection. This difference in response seemed to be mediated by differences in gene expression.

In particular, expression of the Tek gene in the liver was lower in the susceptible mice, and this was associated with onset of haemorrhagic disease. 

When infected with the wild-type Ebola strain, however, neither the susceptible nor resistant mice developed clinical disease. The animals had very low levels of the virus in their liver and spleen – up to 1,000 times lower than their levels when infected with the mouse strain.

At five days after infection, there was no longer any virus detectable, indicating that the wild-type Ebola virus is not able to replicate in mice.

 

How did the researchers interpret the results?

The researchers concluded that their results indicate genetic background determines susceptibility to Ebola hemorrhagic fever.

 

Conclusion

This research across mouse strains demonstrates that mice with different genetic profiles show variable disease response after infection with the Ebola virus. Responses ranged from complete resistance to infection with full recovery, to fatal disease, with or without changes consistent with Ebola haemorrhagic fever.

When comparing the mice that were resistant with those that developed fatal Ebola haemorrhagic syndrome, they found differences in the activity of certain genes, which was associated with different immune and inflammatory response.

However, these results in mice should not be extrapolated too far at this stage. The findings that different genetic strains of mice respond to Ebola infection in different ways does not mean the case will be exactly the same in people, who have quite different genetics to mice.

Genes may play a more or less important role in Ebola symptoms and survival in people, but at this stage we simply don't know.

Similarly, the different infection responses were seen only when mice were infected with the mouse strain of Ebola. The wild Ebola strain was not able to replicate in mice, further demonstrating the dissimilarities to human disease.

As BBC News reports, Andrew Easton, Professor of Virology at the University of Warwick, said the study "provided valuable information, but the data could not be directly applied to humans because they have a much larger variety of genetic combinations than mice".

Even if in humans (as in mice) our genetics play a role in how we respond to Ebola infection, it is unlikely to provide the whole answer. Factors such as the environment we live in – such as healthcare and hygiene standards – and our own underlying age, health and fitness are likely to play a large role in how we respond to Ebola infection.

Nevertheless, this study contributes to the wider understanding of Ebola, and may help direct further research examining the causes and effects of this devastating disease, as well as effective treatments at some point in the future.

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

Links To The Headlines

Ebola virus: Genes 'play significant role in survival'. BBC News, October 31 2014

Ebola outbreak: Ebola may not be a deadly disease for everyone, scientists find. The Daily Telegraph, October 31 2014

Will Ebola kill you? It depends on your genes: Scientists discover DNA could determine if victims live or die. Mail Online, October 31 2014

Links To Science

Rasmussen AL, Okumura A, Ferris MT, et al. Host genetic diversity enables Ebola hemorrhagic fever pathogenesis and resistance. Science. Published online October 30 2014

Categories: Medical News

Does paracetamol ease pain of decision making?

Medical News - Thu, 10/30/2014 - 14:45

"Paracetamol could make difficult decisions less of a headache," the Mail Online reports. The story follows a US study that looked at whether taking paracetamol could reduce the pain of making difficult decisions.

Researchers tested their theory in two experiments where young, healthy adults were given either paracetamol or an inactive placebo.

The first experiment tested the theory that being asked to choose between two equally attractive things can cause mental discomfort.

Participants were asked to rate seven mental tasks and choose one of two they rated positively. People who took paracetamol were less negative about the rejected task than those who took a placebo, suggesting they experienced less pain in decision making.

The second experiment tested the theory of "loss aversion" – where people put greater value on personal possessions they own than those they do not. Participants were given a coffee mug – half were told it was theirs, while the other half were told it was the property of the laboratory.

All were asked to give a selling price for the mug. Those who took paracetamol set lower selling prices than those taking a placebo, presumably because they experienced lower levels of loss aversion.

This small study proves very little about the effect of paracetamol on the pain of decision making. The suggestion that we should take paracetamol every time we face a difficult decision in life is certainly not advisable. Sustained regular use is not recommended, and even a small overdose can cause potentially fatal liver damage.

 

Where did the story come from?

The study was carried out by researchers from the University of Kentucky. There is no information about external funding.

It was published in the peer-reviewed Journal of Experimental Social Psychology.

The study was covered uncritically by the Mail Online, with no comments from independent experts.

 

What kind of research was this?

This US study involved two experiments carried out in the laboratory setting, testing the theory that taking paracetamol can reduce the pain of certain types of decision making.

The researchers say people often talk of decisions being "painful". They specifically explored the theories of "cognitive dissonance" and "loss aversion".

Cognitive dissonance is the theory that if we have to choose between two equally attractive things (such as paying for a luxury holiday or buying a new car) it can cause mental discomfort.

To make this less painful, the researchers say, we rationalise the decision by adopting a negative attitude towards the choice we rejected ("I don't really need a new car" or "Sitting on the beach all day would have been boring").

Loss aversion is the theory that people endow their personal possessions with greater value than things they do not own.

The researchers say both cognitive dissonance and loss aversion involve regions of the brain associated with physical pain (the dorsal anterior cingulate cortex [dACC] and anterior insula), and hypothesise that paracetamol may reduce the pain of decision making.

 

What did the research involve?

In the first experiment, researchers recruited 112 undergraduates, three-quarters of whom were women, with an average age of 19.

They were screened for conditions that might have affected the results, including dependence conditions such as alcohol misuse or daily paracetamol consumption. They were randomised to consume 1g of paracetamol (one standard dose) or an inactive placebo pill.

After half an hour they were given descriptions of seven cognitive tasks and asked to rate their desirability. The tasks were described as puzzles, but frustratingly no detailed information was provided on the type of tasks described to the undergraduates.

The researchers then selected two tasks rated positively by each participant, who then chose which task he or she would perform later. After another half hour they were instructed to rate the tasks again and try to ignore their earlier evaluations, as they were told by the researchers that preferences can change over time.

In the second experiment, researchers recruited 95 undergraduates (just over half were women with an average age of 20) who met the same criteria as in the first experiment. They were randomised to be given either 1g of paracetamol or a placebo pill.

They were also handed a mug with the university logo. Participants were randomised again so that half were told the mug was theirs to keep, while the other half were told it was the property of the laboratory.

They were all instructed to examine the mug for 30 seconds. They were not told about the mug's true value. After 30 minutes they were instructed that they could sell the mug and were asked to list the selling price.

 

What were the basic results?

In the first experiment, participants rated their rejected task with fewer positive attributes to try to reduce any mental discomfort. However, people who took paracetamol were less negative about the rejected task compared with those taking placebo, suggesting they experienced less pain in decision making.

In the second experiment, among participants who had been told the mug was theirs, those who took paracetamol set lower selling prices than those who took the placebo drug.

People who took paracetamol and were told the mug was theirs also set lower prices than the other group, who were told the mug was not theirs.

Among all those who took a placebo, mug prices were not significantly higher among those told the mug was theirs than those told it was university property.

 

How did the researchers interpret the results?

The researchers say their experiments showed that paracetamol reduced the pain of decision making. They say that in the first experiment, paracetamol reduced participants' need to reduce discomfort by adopting a more negative attitude towards the rejected task.

In the second experiment, in which they were asked to set the price of a mug, participants who took paracetamol set lower selling prices, presumably because they experienced lower levels of loss aversion.

"Making decisions can be painful, but a physical painkiller can take the pain away," the researchers concluded.

 

Conclusion

This experimental study involved giving people paracetamol or a placebo, then asking them to take part in two very specific decision-making scenarios to test the psychological states of cognitive dissonance and loss aversion.

The results of the first experiment suggested people who took paracetamol were less negative about the rejected task than those who took a placebo, suggesting they experienced less cognitive dissonance.

The results of the second experiment found those who took paracetamol set lower selling prices than those taking a placebo, presumably because they experienced lower levels of loss aversion.

However, the researchers' hypothesis that paracetamol can help with the mental discomfort associated with decision making remains just that – a hypothesis.

There are many limitations to this study, including its small specific sample of healthy young adults, and these are highly experimental scenarios that do not necessarily relate to real-life situations.

The results also do not give a clear and consistent pattern. For example, people who took a placebo in the second experiment didn't rate the value of the mug differently regardless of whether they were told it was theirs or not, suggesting they were not experiencing loss aversion in any case.

Our capacity to make difficult decisions is a complex area that involves many factors, and the idea that any uncertainty or conflict around a decision would be removed just by taking a painkiller is surely dubious.

In any case, even if the pain of decision making was reduced, it does not seem to necessarily follow that we would subsequently then make the "right" decision.

The suggestion that we should be encouraged to slip a pill every time we face a painful decision is certainly not advisable. Paracetamol is a medical drug that is only designed to treat physical pain and reduce fever.

It is safe to use at recommended doses and for the proper reasons, but sustained regular use is not recommended – even a small overdose can cause potentially fatal liver damage.

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

Links To The Headlines

Acetaminophen could also help to ease our anxieties: Pills could reduce the anguish of situations that cause psychological pain. Mail Online, October 29 2014

Links To Science

DeWall CN, Chester DS, White DS. Can acetaminophen reduce the pain of decision-making? Journal of Experimental Social Psychology. Published online September 22 2014

Categories: Medical News

Details of autism genes uncovered in global study

Medical News - Thu, 10/30/2014 - 14:30

“A massive international study has started to unpick the ‘fine details’ of why some people develop autism,” BBC News reports.

A team of international researchers looked for variations in the DNA sequences of the genes in 3,871 people with autistic spectrum disorder (ASD) and 9,937 unaffected family members or unrelated controls.

The researchers identified 107 genes containing variations associated with ASD. In more than 5% of the people with ASD, these genes had new (not inherited) mutations that led to genes either not working at all, or working less well.

The genes encoded proteins involved in synaptic formation, the (expression) activity of other genes, and proteins involved in modifying the packaging of DNA inside cells.

Synapses are junctions where signals are passed from one nerve cell to another, and are found in the brain and nervous system. They are thought to be essential in underpinning consciousness, thinking and behaviour.

This study sheds more light on ASD, but does not necessarily mean that screening for the condition is closer.

Deciding whether screening is a good option involves considering a wide range of issues in addition to determining how well people with ASD can be identified, including an assessment of the options open to someone identified as having or being at risk of ASD.

For example, if screening was going to be offered during pregnancy, would it be ethical to terminate a viable pregnancy on the grounds that the child would develop ASD? Many people with ASD live fulfilling and rewarding lives.

 

Where did the story come from?

The study was carried out by an international team of researchers and was funded by the US National Institutes of Health and other sources.

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

The news stories differed in terms of the number of genes reportedly associated with ASD; these figures differed depending on what they took to be statistically significant. For the record, there was strong evidence for 22 genes and weaker evidence for another 107 genes.

Despite headlines suggesting that autism screening is closer, this is debatable. ASD is a highly complex condition and we still don’t fully understand what causes it.

While mutations in many genes have been found to be associated with the disorder, environmental factors may also play a role.

None of the UK media considered whether screening for ASD would actually be desirable. As there is currently no cure for ASD, screening could offer the option of terminating a pregnancy (or rejecting an embryo for an IVF procedure).

However, a case could be made that screening, either during pregnancy or once the child was born, would allow parents to be given information about what to expect, and treatment could be started soon after birth.

 

What kind of research was this?

This was a case-control study that compared the sequence of genes in people with ASD (the cases) and controls, who were either family members or unrelated people. Any changes that were only found in people with ASD, or in more people with autism than without, could be contributing to the condition. They also looked at whether these variations had been inherited by the person with ASD from one of their parents, or if they were “new” variations that had happened in their very early development.

This is the ideal study design to identify variants that are associated with ASD. It is a complex disease, with many genes potentially associated with it – each contributing a small amount to a person’s risk. Environmental factors may also play a role. Different people with ASD may have different combinations of genetic risk factors, and some people without the condition may have some of these genetic risk factors. This complexity makes it very difficult to say for certain that all of the genetic variations identified definitely contribute to the condition, and to justify screening.

 

What did the research involve?

The researchers sequenced all of the parts of genes that contained instructions for making proteins (called “the exome”), and that lay on any chromosomes other than the X and Y chromosome (called the “autosomes”).

They did this in 3,871 people with ASD and 9,937 controls, and compared them to look for variations associated with ASD. The researchers noted that this is the largest sample ever studied in this way.

The researchers used new statistical methods to look for variations associated with ASD. Because of the large number of genes being looked at, and the multiple comparisons involved, there is a risk that some of the statistically significant associations found will be false (for example a significant association is seen when none exists). One way of overcoming this problem is to adjust the thresholds for what is considered a statistically significant result – called controlling the “false discovery rate”. For example, setting a false discovery rate of 0.05 means that 5% of significant associations would be expected to be false. The researchers looked at which genes were associated with ASD using different false discovery rates.

The researchers also looked at what the genes with variations did in the body, to understand how they might be contributing to causing ASD.

 

What were the basic results?

The researchers identified 22 autosomal genes that were associated with ASD when they set the cut-off so that at least 95% of associations are expected to be true (false discovery rate <0.05).

33 autosomal genes were associated with ASD when the cut-off was set so that at least 90% of associations seen are expected to be true (false discovery rate <0.1). Of these 33 genes, 15 were considered to already have good evidence of being associated with ASD, 11 had some previous evidence of association but not as strong, and seven had never been reported as being associated with autism before.

When the cut-off was set so that at least 70% of associations seen are expected to be true (false discovery rate <0.30), 107 autosomal genes were associated with ASD. More than 5% of the people with ASD had new (not inherited) mutations in these genes that either stop the gene from working entirely, or make it work less well.

This study would not have identified all genes associated with ASD risk, and the researchers estimated that, based on their results, there could be 1,150 genes contributing to autism risk.

The genes associated with ASD contained instructions for making proteins involved in various processes, including:

  • making the junctions between nerve cells (synapses)
  • changing how active other genes are
  • modifying the packaging of DNA inside cells

 

How did the researchers interpret the results?

The researchers conclude that people with ASD have more loss-of-function mutations than would be expected in the population as a whole, and that these mutations are concentrated in a “handful” of genes.

They say that their findings suggest that genes involved in synapses (nerve junctions), transcription (gene activity) and DNA packaging are involved in ASD.

 

Conclusion

This large study compared the sequence of the genes in 3,871 people with ASD with 9,937 unaffected family members or unrelated controls.

Overall, 107 autosomal genes were found to be associated with ASD, with about 30% of these expected to not to be associated with the condition. These genes had new (not inherited) mutations, resulting in less or no function in more than 5% of the people with ASD. The researchers also estimated that over 1,000 genes could be contributing to autism risk. This gives some idea of how complex the genetics of autism appear to be – not all people with the condition will carry the same genetic risk factors, and some people without the condition will carry some of these genetic risk factors.

The researchers looked at what processes the genes they identified are involved in. The genes encoded proteins involved in synaptic (nerve junction) formation, the (expression) activity of other genes, and proteins involved modifying the packaging of DNA inside cells. This gives researchers more of an idea of what might be going wrong within the cells of people with ASD.

ASD is a complex condition, and mutations in many genes have been found to be associated with the disorder – with many more yet to be found. This study sheds more light on the condition, but we still have a lot to learn. This means that using this type of genetic information to screen for this condition is unlikely to happen in the foreseeable future.

There is also the possibility that learning more about the genetics of ASD could lead to new treatments.

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

Links To The Headlines

Study points to new genetic risks for autism. BBC News, October 30 2014

Autism screening closer as 100 genes linked to disorder are identified. The Daily Telegraph, October 29 2014

Autism breakthrough as researchers find over 100 new genes linked to the social disorder. Mail Online, October 29 2014

Links To Science

De Rubeis S, He X, Goldberg AP, et al. Synaptic, transcriptional and chromatin genes disrupted in autism. Nature. Published online October 29 2014

Categories: Medical News

Milk may be linked to bone fractures and early death

Medical News - Wed, 10/29/2014 - 15:15

"Drinking more than three glasses of milk a day may not protect bones against breaking – and may even lead to higher rates of death," the Mail Online reports.

Do not be alarmed – your milkman is no Hallowe'en death-bringer. In fact, there are many reasons to treat this news – and the research behind it – with some caution.

The research comprised an analysis of two large Swedish cohort studies, in which a group of men and a group of women were given food questionnaires and then followed up for an average of 20 years. Researchers looked at whether how much milk they drank was linked to fractures or death during follow-up.

In women, drinking any more than 200g of milk daily (less than one glass) was linked to increased risk of dying during follow-up. This increased risk ranged from 21% for one to two glasses to an increased risk of 93% for three or more.

More than one glass a day was also linked to an increased risk of fractures in women. There wasn't such a clear link with either early death or fractures in men.

However, people involved in the study may not have been able to reliably estimate their volume of milk intake per day, and there may have been various unmeasured factors influencing the outcomes.

This was also a Swedish population, who may have distinct health and lifestyle factors or environmental influences, which means the results are not applicable to other populations.

For example, milk in Sweden is fortified with vitamin A (unlike the UK), and high levels of vitamin A intake have been linked to an increased risk of fracture.

These findings are undoubtedly worthy of further research, but people should not feel the need to drink less milk based on this study alone.

 

Where did the story come from?

The study was carried out by researchers from Uppsala University and the Karolinska Institutet in Sweden.

It was funded by the Swedish Research Council, and one of the researchers was reported to be an employee of the Swedish National Food Agency.

The study was published in the peer-reviewed British Medical Journal. This article is open access, meaning it can be accessed and read for free online.

The majority of the UK's media headlines are needlessly alarmist, although the actual reporting of the study tended to be more restrained. Many of the sources include quotes from independent experts, who discuss the limitations of the study and highlight the fact Swedish milk is fortified with vitamin A.

 

What kind of research was this?

This was an examination of the findings of two Swedish cohort studies – one in men and one in women – which aimed to investigate whether drinking more milk is linked to outcomes of fracture or mortality (death) from any cause.

The researchers say it is well known that a diet rich in dairy, containing high amounts of essential nutrients such as calcium and vitamin D, is considered to reduce the risk of osteoporotic fractures.

However, they say there may be undesirable effects because milk contains D-galactose, a type of sugar (although it tastes much less sweet than other types of sugar).

Experimental evidence in animals has suggested D-galactose is associated with ageing, with observations including oxidative stress (where damage occurs at the molecular level) to tissues, and changes to gene activity and the immune system.

The researchers say an injected dose of 100mg/kg of D-galactose has been shown to accelerate biological signs of ageing in mice, which is equivalent to 6 to 10g in humans, or the amount found in one to two glasses of milk.

The researchers therefore wanted to test their theory that a high consumption of milk may increase oxidative stress and inflammation in humans, and so increase the risk of mortality and fracture.

Cohort studies are a good way of looking at whether particular exposures are associated with disease outcomes. However, they cannot prove cause and effect.

In this study, important limitations include that the food questionnaire may not give a reliable indication of milk intake or of lifetime patterns.

Also, there may be a variety of other health and lifestyle factors (confounders) that are influencing any association between milk intake and fractures or mortality, which the study has not been able to take into account.

 

What did the research involve?

This study used data from two community-based Swedish cohorts:

  • The Swedish Mammography Cohort, which recruited more than 90,000 middle-aged to elderly women from two Swedish counties from 1987-90. Food frequency questionnaires were given to the women at enrolment and again in 1997. The current study included 61,433 women who completed both of these questionnaires.
  • The Cohort of Swedish Men, which recruited more than 100,000 middle-aged to elderly men from two counties in Sweden in 1997. The men were given a single food frequency questionnaire at enrolment, and this study is representative of 45,339 men who completed this questionnaire.

In both studies, the food frequency surveys questioned up to 96 foods and drinks consumed over the past year, including how many servings of the item per day or per week.

Dairy items included milk, fermented milk, yoghurt and cheese, with instructions that one serving of milk equalled one 200ml glass.

The researchers say milk intake was specified according to fat content, and they summed intake into a single measure representing total milk intake on a continuous scale.

Looking at outcomes, the researchers examined those recorded between enrolment for the two studies and the end of December 2010. All participants were linked to the Swedish Cause of Death Registry, so the researchers could identify any deaths related to all causes, cardiovascular diseases or cancers.

Fractures were identified by linking all participants to the Swedish National Patient Registry and by looking for any hospital admissions or outpatient visits with diagnostic codes related to fracture.

Regarding adjustment for confounders, the researchers adjusted their analyses for many factors, including age, body mass index (BMI), total energy intake, healthy dietary pattern, calcium and vitamin D supplementation, and physical activity levels.

The researchers assessed the risk of mortality or fracture according to categories of milk intake (less than 200g per day, 200-399g per day, 400-599g per day, and 600g per day or more) and for each additional 200g of milk per day corresponding to each additional glass of milk. They also looked at the effects of other dairy items, such as cheese and fermented milk products.

 

What were the basic results?

The women's cohort consumed, on average, 240g milk per day, and the men 290g – around one to two glasses day. The researchers observed a general trend that increased milk intake was associated with increased energy intake overall and increased intake of most other nutrients, while alcohol intake tended to decrease.

Deaths

During an average 22 years of follow-up, 15,541 women died (25% of the cohort), with a third of these deaths as a result of cardiovascular disease and a fifth related to cancer.

The men were followed for an average of 13 years, during which time 10,112 died (22% of the cohort), with just under half of these deaths as a result of cardiovascular disease and just over a quarter caused by cancer.

In the women's cohort, compared with drinking less than one glass of milk a day (less than 200g/day), each increasing category of intake was associated with a 21% increased risk of death from any cause for one to two glasses, and 93% increased risk for three or more glasses.

Any intake above one glass a day was associated with an increased risk of cardiovascular death, but an increased risk of cancer death was only seen with intakes above two glasses a day.

In the men's cohort, the link with all-cause death was less strong. Intakes above two glasses of milk per day were associated with a 5-10% increased risk of death from any cause, but the links were only of borderline statistical significance, meaning these may be chance findings.

Looking at cause of death for men, there was a just significant increased risk of cardiovascular death above two glasses a day, but no significant link with cancer deaths.

Fractures

In the women's cohort, 17,252 had a fracture (28%) during follow-up, while in the men's cohort, 5,379 had a fracture (12%).

In women, each increasing category of milk intake above less than one glass a day was associated with an increased risk of fracture of 7% for one to two glasses, and 16% for two or more. Risk of hip fracture specifically also increased with each intake above less than one glass.

In men, there was no significant link between milk intake and any fracture, or hip fracture specifically.

Other milk products

No increased risk was found with increased intake of other dairy products, such as cheese or fermented milk – in fact, the opposite was seen.

Higher intakes of other dairy products were associated with a lower risk of mortality and fractures in women. Risk reductions in men were more modest or were non-existent.

 

How did the researchers interpret the results?

The researchers concluded that, "High milk intake was associated with higher mortality in one cohort of women and in another cohort of men, and with higher fracture incidence in women."

However, they give due caution that, "Given the observational study design with the inherent possibility of residual confounding and reverse causation, a cautious interpretation of the results is recommended. The findings merit independent replication before they can be used for dietary recommendations."

 

Conclusion

This Swedish study found women who drink more than 200g (less than one glass) of milk a day have an increased risk of death and fractures. In men, the link between milk and risk of death or fractures was less strong.

There was no link between milk intake and fractures, and the risk increases for death above two glasses a day were small and of borderline statistical significance.

The study has various strengths, including its large population size of both men and women, and long-term follow-up. Also, the Swedish registries used to identify causes of death and hospital attendances for fracture are likely to be accurate and reliable.

However, there are important limitations to bear in mind when interpreting meaning from this study, as follows:

  • The study cannot prove direct cause and effect between milk and these outcomes. Although the researchers have tried to take account of various health and lifestyle factors, the study may not have been able to fully account for the influence of these factors (for example, former or current smoking categories were considered, but within these there is going to be a wide range of frequency and duration). There may also be other unmeasured factors influencing the association.
  • There may also be the possibility for reverse causation. For example, postmenopasual women who were at risk of, or had been diagnosed with, osteoporosis could have been at an increased risk of having a fracture and may have been increasing their milk intake to try to boost their calcium levels.
  • It may be hard to reliably estimate milk intake, particularly if you consider that people do not necessarily consume measured glasses of milk per day. Milk is added to drinks or cereal, or is used in cooking. Overall, this could make it difficult to give a reliable indication of milk intake. It is also hard to know whether these food frequency questionnaires represent a lifelong pattern.
  • Also, the study relates to a specific population of Swedish middle-aged to elderly men and women. This population may have particular health, lifestyle and environmental influences, meaning their results are not generalisable to all other populations. For example, Swedish milk is fortified with vitamin A, so results may not apply to the UK, where we do not have fortified milk as standard.

The reverse pattern – decreased risk of death and fractures in women with higher intakes of other dairy products such as cheese and yoghurt – further highlights the uncertain picture painted by these results.

The researchers clearly acknowledge the potential limitations of their research, saying that, "Given the inherent possibility of confounding and reverse causation, a cautious interpretation of the results is recommended."

The findings are undoubtedly worthy of further research, but people should not be overly concerned or feel the need to alter their milk intake as a result of this single study.

A balanced lifestyle is most important for health, including taking regular exercise, not drinking too much alcohol, avoiding smoking and having a healthy, balanced diet – milk contains many important nutrients and can be part of this. 

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

Links To The Headlines

Dangers of more than 3 glasses of milk a day: High intake may not protect against broken bones and could actually increase chance of death. Mail Online, October 28 2014

Three glasses of milk a day can lead to early death, warn scientists. The Daily Telegraph, October 28 2014

High milk diet 'may not cut risk of bone fractures'. BBC News, October 29 2014

Milk might not be as good for us as we thought, study suggests. The Independent, October 28 2014

Three glasses of milk a day linked to earlier death. Daily Express, October 29 2014

Links To Science

Michaëlsson K, Wolk A, Langenskiöld S, et al. Milk intake and risk of mortality and fractures in women and men: cohort studies. British Medical Journal. Published online October 28 2014

Categories: Medical News

Could sex with 21 women 'cut prostate risk'?

Medical News - Wed, 10/29/2014 - 13:30

"Sleeping with more than 20 women protects men against prostate cancer, academics find," The Daily Telegraph reports.

The study in question included more than 1,500 men diagnosed with prostate cancer and a matched group of men without prostate cancer from the general population. Researchers then interviewed the men about their sexual activity.

The study concluded that having more than 20 female partners over a man’s lifetime was associated with a decreased risk of prostate cancer, while having several male partners seemed to increase the risk.

However, studies like this one cannot prove that having several female partners reduces the risk of prostate cancer, or that having more male partners increases risk.

If having multiple female partners reduced prostate cancer risk, it would be expected that the more partners you had, the lower your risk would be. However, this study did not find such a relationship between the number of female partners and associated risk. The protective effect was only seen in men in the upper category of having 21 or more female partners, and strangely, no other category.

The findings do not give a clear or coherent picture, and there may be many other factors influencing the relationship.

The most important thing to remember – regardless of number, or gender, of partners – is to practice safe sex with a condom to reduce the risk of sexually transmitted infections (STIs).

 

Where did the story come from?

The study was carried out by researchers from the Université du Québec, the University of Montreal and the University of Montreal Hospital Research Centre. It was funded by the Canadian Cancer Society, the Cancer Research Society, the Fonds de la recherche du Québec-Santé (FRQS), the FRQS-RRSE, and the Ministére du Développement économique, de l’Innovation et de l’Exportation du Québec.

The study was published in the peer-reviewed medical journal Cancer Epidemiology.

The media coverage of this story was almost universally poor, with news articles reporting non-significant findings or omitting the fact that some associations were only found in a sub-type of prostate cancer, or omitting the comparator.

For example, The Independent, the Mail Online and the Telegraph report that men who slept with more than 20 women were 19% less likely to develop an aggressive type of cancer than those who had only one female sexual partner, whereas this association was actually not statistically significant.

They go on to say that having more than 20 male partners doubled the risk of prostate cancer. In the Mail and Telegraph, this is compared to men who had never slept with a man. This is again incorrect. Having more than 20 male partners compared to having one was associated with an increased risk of less-aggressive prostate cancer, but it was not significantly associated with prostate cancer risk overall or risk of aggressive prostate cancer. Having more than 20 male partners compared to only having female partners was not significantly associated with any type of prostate cancer.

It would appear that most media outlets simply took the accompanying press release at face value, without actually bothering to read the study or subject it to any kind of critical analysis – a practice that is sadly all too common these days.

 

What kind of research was this?

This was a case-control study comparing sexual activity and STIs in men diagnosed with prostate cancer (the cases) and men matched by age from the electoral registry (the controls). 

Case-control studies like this one cannot prove that the number of sexual partners, or their gender, is directly associated with risk of prostate cancer. There may be many factors (confounders) influencing the relationships observed in this study.

 

What did the research involve?

The researchers compared 1,590 men diagnosed with prostate cancer in a Montreal hospital between 2005 and 2009 (the cases) and 1,618 randomly selected age-matched men from the electoral list (the controls).

The men were interviewed to obtain information on sociodemographic factors (for example, highest level of education, family income, marital status), lifestyle (including sexual activity and STIs), medical and environmental factors.

Men were asked whether they had ever had sexual intercourse, the age they first had sexual intercourse, the number of female partners they had and the number of male partners they had.

Men were also asked to describe their sexual orientation in terms of the following categories:

  • heterosexual
  • bisexual, with a preference for women
  • bisexual, with a preference for men
  • bisexual, with no preference for women or men
  • homosexual

Men were also asked whether they had ever had the following STIs:

The researchers looked to see if there was an association between sexual activity and STIs and developing prostate cancer. The researchers also divided prostate cancer into aggressive (Gleason score =>7) and less-aggressive (Gleason score <7) forms of prostate cancer to see if there were different associations. (See Diagnosing prostate cancer for more information about Gleason scores)

The researchers adjusted their analyses for age, whether the men were of European, Black, Asian or other ancestry, family history of prostate cancer, and prostate cancer screening history.

 

What were the basic results?

Men with prostate cancer, compared to controls, were more likely to be Canadian-born and to be of European or Black ancestries, and less often of Asian ancestry. Twice as many men with prostate cancer had a first-degree relative (for example, brother or father) with prostate cancer than controls. Almost all men with prostate cancer reported being screened for prostate cancer within two years before being diagnosed with prostate cancer, whereas 76% of controls reported being screened in the preceding two years. Cases and controls had similar family income, marital status, smoking history and alcohol use.

Never having sexual intercourse was not associated with a difference in risk of prostate cancer overall. The age men first had intercourse was also not associated with a difference in risk of prostate cancer.

Compared with having one female sexual partner, having more than 20 female sexual partners was associated with a decreased risk of prostate cancer (odds ratio [OR] 0.72, 95% confidence interval [CI] 0.56 to 0.94). Men who have sex with men were included in this analysis.

Compared with having one male sexual partner, having more male sexual partners did not alter the risk of prostate cancer.

There was no association found between individual types of STIs, or with all STIs combined, and prostate cancer. However, the researchers state that this might have been because few men had an STI.

When aggressive and less-aggressive prostate cancer were analysed separately, the researchers observed no associations with aggressive prostate cancer. Never having sex, having had two to three male partners compared to never having had one, and having two to three or 21 male partners or more compared to having had one were associated with increased risk of less-aggressive prostate cancer; having more than 20 partners of either gender or more than 20 female partners compared to having one was associated with reduced risk of less-aggressive prostate cancer.

 

How did the researchers interpret the results?

The researchers conclude that “our findings are in support of a role for the number of sexual partners in prostate cancer development.”

 

Conclusion

This case-control study has suggested that having several female partners over a man’s lifetime is associated with a protective effect against prostate cancer, whereas having several male partners increased the risk.

However, case-control studies like this one cannot prove that having several female partners reduces the risk of prostate cancer, or that having more male partners increases risk. When it comes to complex issues such as lifestyle, sexuality and cancer outcomes, there could be a wide range of contributing factors.

If having multiple female partners reduced prostate cancer risk, it would be expected that the more partners you had the lower your risk would be. However, this study did not find such a relationship between number of female partners and associated risk. The protective effect was confined to men in the upper category of having more than 20 female partners.

You would reasonably expect to see a kind of dose-dependent relationship, so, for example, having 15 or 16 partners would also have a protective effect. No such relationship was seen, raising the possibility that the “21 or more” outcome was a statistical fluke; a confidence interval of 0.56 to 0.94 is of borderline statistical significance.

Similarly, the results are confusing for men who had male partners. Having two to three, or more than 20, male partners increased risk of less-aggressive prostate cancer compared to one male partner. However, between four and 20 was not associated with increased risk.

It seems possible that the associations seen in this study were the result of performing multiple comparisons. That is, where performing an increasing number of comparisons increases the chances that you will find some significant associations, even if there is not truly a significant link. If there were truly significant links, you would expect to see more consistent trends.

If these are real links, there could still be other factors that are influencing the relationship. It is difficult to know whether face-to-face interviews of sexual activity will have given reliable results, and also possible that a man’s knowledge of his cancer status could have influenced his recall.

Further work is required to determine whether having multiple female partners really is associated with a reduced risk of prostate cancer, and to see whether the gender of partners really makes a difference.

The most important thing to remember – regardless of the number or gender of partners – is to practice safe sex with a condom to reduce the risk of STIs.

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

Links To The Headlines

Sex with 21 women lowers risk of prostate cancer, academics find. The Daily Telegraph, October 28 2014

Sex with more than 20 women reduces risk of prostate cancer, according to study. The Independent, October 28 2014

Men who sleep with multiple women REDUCE their risk of prostate cancer. Mail Online, October 28 2014

Is sleeping around good for you? Sex with more than 20 women could 'lower prostate cancer risk'. Daily Mirror, October 28 2014

Links To Science

Spence AR, Rousseau M, Parent M. Sexual partners, sexually transmitted infections, and prostate cancer risk. Cancer Epidemiology. Published online September 29 2014

Categories: Medical News

Agave syrup no better than placebo cough remedy

Medical News - Tue, 10/28/2014 - 15:00

“Placebo cough treatment benefits children and their parents, study suggests,” The Daily Telegraph reports.

A US study found that children’s reported cough symptoms improved even though they were just given a dummy treatment (placebo).

The study compared the effectiveness of agave nectar (a sweet syrup similar to honey, from the agave plant), placebo (flavoured coloured water) or no treatment for night-time cough in 119 children aged between two and 47 months old. Parents were given surveys to record cough symptoms over two days.

Agave nectar and placebo both provided more relief from cough symptoms than no treatment, but there was no difference in relief between agave nectar and placebo.

It is possible that as parents were assessing their children’s symptoms, this could be an example of the placebo effect. That is, parents who thought they were giving their child some syrup, rather than giving nothing, felt that it helped their child’s symptoms. The placebo effect, where people get better because they expect to get better, may sound unlikely, but it has been well documented for decades.

It is also possible that giving something to swallow – either syrup or plain water – is better than nothing when trying to ease a child’s cough.

The best thing that you can do to help a young child with a cough or cold is to make sure that they stay well hydrated with plenty of warm drinks. Honey shouldn't be given to babies under the age of one, due to the risk of infant botulism.

 

Where did the story come from?

The study was carried out by researchers from Penn State College of Medicine, Pennsylvania, and was funded by an unrestricted grant to the Penn State College of Medicine by Zarbee’s Inc, which makes a number of products, including cough syrups. One of the study’s authors has worked as a paid consultant for Zarbee’s Inc, which represents a potential conflict of interest. However, seeing as the main result of the study was that placebos were as effective as agave syrup in treating coughs, it would appear that the study was free of any commercial interference or influence.

The study was published in the peer-reviewed medical journal JAMA Pediatrics. This article was open access, so can be read for free online.

The research was well covered by The Daily Telegraph, though it should be noted that the research article is published in JAMA Pediatrics rather than JAMA Neurology, as the paper wrongly stated.

While the focus of the news - and indeed the title of the research paper - suggest that scientists were looking at whether placebos work for cough mixture, by definition placebos don’t work (except via the placebo effect). In fact, the researchers were testing whether a new formulation of agave syrup could improve cough symptoms. It didn’t improve symptoms any more than placebo.

 

What kind of research was this?

This was a randomised controlled trial (RCT) that aimed to compare the effectiveness of novel pasteurised agave nectar, compared to placebo or no treatment, on nocturnal cough and sleep difficulty associated with acute cough in infants and toddlers.

Agave nectar is a syrup similar to honey that is produced in Central and South America. Unlike honey, it hasn’t been associated with botulism.

An RCT is the ideal way to compare the effectiveness of different treatments.

 

What did the research involve?

The researchers studied 119 children aged between two and 47 months old, who had a cough for seven days or less and visited their GP. Children had a non-specific cough, meaning it was not thought to be due to any particular disease or condition and most likely due to a viral infection. These types of infections are common in young children, as their immune systems are underdeveloped.

They could have other symptoms of a temperature, runny nose or congestion, but were excluded from the study if they had symptoms suggesting more serious conditions, such as asthma or pneumonia.

Children were also ineligible if they had used any medication or honey to treat their cough within six hours of bedtime on the evening before or on the day of enrolment.

Parents were asked to complete a questionnaire about their child’s symptoms the night before. They were asked to rate between one (not at all) to seven (very often/severe):

  • how often did your child cough last night?
  • how severe was your child’s cough last night?
  • how bothersome was your child’s cough last night?
  • how severe was your child’s stuffy nose last night?
  • how severe was your child’s runny nose last night?
  • how much did last night’s cough affect your child’s ability to sleep?
  • how much did your child’s cough affect your own ability to sleep last night?

The parents of the studied children reported at least “moderately often” or “moderately severe” (a score of four or more) on at least two of three questions related to cough frequency, cough effect on child sleep and cough effect on parent sleep.

The children were randomised to:

  • grape-flavoured pasteurised agave nectar (from Zarbee’s Inc, which funded the study)
  • coloured grape-flavoured water (placebo)
  • no treatment

The children received one of these options 30 minutes before bedtime.

Within 30 minutes of waking, the parents again completed the same questionnaire about their child’s symptoms.

The researchers compared the change in symptoms between nights for the three different groups.

 

What were the basic results?

Within each study group, symptoms significantly improved from baseline.

When treatment-night effects of agave nectar, placebo and no treatment were compared, agave syrup and placebo were both superior to no treatment for all symptoms apart from how bothersome the cough was.

However, there were no significant differences in any outcome when agave syrup was compared to placebo.

 

How did the researchers interpret the results?

The researchers concluded that “in a comparison of agave nectar, placebo and no treatment, a placebo effect was demonstrated, with no additional benefit offered by agave nectar. Health care professionals should consider the potential benefits and costs when recommending a treatment with only a placebo effect for infants and toddlers with non-specific acute cough.”

 

Conclusion

This RCT compared the efficacy of agave nectar, placebo or no treatment for night-time cough in children aged between two and 47 months old.

Agave nectar and placebo both provided more relief from cough symptoms than no treatment, but there was no difference in relief between agave nectar and placebo.

It's possible that as parents were assessing their children’s symptoms, this study could be an example of the placebo effect. That is, parents who thought that they were giving their child some syrup, rather than giving nothing, felt that it helped their child’s symptoms. Equally, it is possible that giving something to swallow – either syrup or plain water – is better than nothing at helping to ease a child’s cough.

All children included in this study had a cough for less than a week and other cold-like symptoms, such as runny nose or congestion. This is likely due to a viral infection and requires no specific treatment. There is no good evidence that over-the-counter cough medicines actually work against an acute cough. The Medicines Regulatory Agency in the UK currently advises that over-the-counter cough and cold medicines shouldn’t be given to children under six years. Honey also shouldn’t be given to children aged under one.

The best thing you can do to help a young child with a cough or cold is to make sure that they stay well hydrated with plenty of warm drinks.

The study does highlight the remarkable impact the placebo effect can have in certain cases. There are libraries full of evidence showing how symptoms can dramatically improve for a range of conditions, even though a patient was given a sugar pill or a salt water injection. This may suggest that the mind can have a considerable effect on the symptoms of the body in some cases.

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

Links To The Headlines

Placebo cough treatment benefits children and their parents, study suggests. The Daily Telegraph, October 27 2014

Links To Science

Paul IM, Beiler JS, Vallati JR, et al. Placebo Effect in the Treatment of Acute Cough in Infants and Toddlers - A Randomized Clinical Trial. JAMA Pediatrics. Published online October 27 2014

Categories: Medical News