NHS Choices

'A stressful job really can kill you – by raising your cholesterol,' reports the Mail Online website. This headline is based on Spanish research that looked at the relationship between job stress and lipid (fat) levels in the blood of more than 90,000 people.

The research found that people who reported difficulties coping with their job had higher levels of what has been dubbed "bad cholesterol" (LDL cholesterol) and lower levels of "good cholesterol" (HDL cholesterol). High levels of LDL cholesterol can clog up the arteries, increasing an individual's risk of developing cardiovascular diseases such as coronary heart disease.

A significant strength of this study is its size – an impressive 90,000 people participated. But the study did not look at diet, which can also affect cholesterol levels. It could well be the case that people in stressful jobs tend to have unhealthy diets and it is this, rather than stress itself, that is to blame for their higher "bad" cholesterol rates.

While increased LDL levels are a risk factor for cardiovascular diseases, this study did not explore the effect this would have on people's long-term health. The Mail Online's claim that a stressful job will kill you is therefore not supported by this study.

 

Where did the story come from?

The study was carried out by researchers from Ibermutuamur – a mutual insurance company dealing with work-related accidents and occupational illnesses – and two universities in Spain. There were no external sources of funding for the study.

It was published in the peer-reviewed Scandinavian Journal of Public Health.

The Mail Online's headline over-interprets the research, as the study did not assess whether people in stressful jobs were more likely to die. The body of the story was reasonably accurate, but it did not highlight that this type of study cannot prove that one factor is definitely causing another.

 

What kind of research was this?

This was a cross-sectional study that explored whether there is a link between job stress and abnormal levels of fats (lipids) in the blood.

Some studies have found a link between job stress and an increased risk of coronary disease. There are various theories about how this link might come about – for example, by stress increasing the likelihood of unhealthy habits such as smoking.

Some studies have also suggested that stress could directly influence levels of lipids in the blood by possibly adversely affecting the body's metabolism. However, these studies have been small and in selected populations, and have had mixed results.

In the current study, researchers wanted to assess stress and lipid levels in a large representative sample of workers. As this study is cross-sectional, both stress and lipid levels were assessed at the same time. This means the study cannot establish whether participants' lipid levels were directly influenced by their stress levels.

 

What did the research involve?

The study involved workers covered by the Ibermutuamur insurance company who had yearly medical check-ups. More than 430,000 participants were recruited between 2005 and 2007, and a study questionnaire was sent out to more than 100,000 randomly selected individuals. Completed questionnaires were returned by 91,593 of these people.

The questionnaire included the question, "During the last year, have you frequently felt that you cannot cope with your usual job?". Participants who answered "yes" were considered to have job stress.

The questionnaire also included 11 questions relating to anxiety and depression symptoms, such as "Have you felt keyed up, on edge?" and "Have you had difficulty relaxing?".

The researchers took fasting blood samples from participants and measured levels of total cholesterol, HDL cholesterol (so-called "good" cholesterol), and levels of a type of lipid called triglycerides. The levels of so-called "bad" cholesterol were calculated based on these measurements.

Participants were classed as having abnormal lipid levels based on pre-specified levels if they reported taking lipid-lowering medication or had been diagnosed as having abnormal lipid levels.

The researchers then looked at whether abnormal lipid levels are linked to job stress. They took into account the following confounders:

• age
• gender
• smoking
• basic measures of alcohol consumption and physical leisure activity
• obesity 
• type of job ("blue collar" or "white collar")

 

What were the basic results?

Job stress was reported by 8.7% of participants. Participants reporting job stress also had higher levels of anxiety and depression symptoms.

After the researchers took into account factors that could affect the results and adjusted them accordingly, people who reported job stress were found to have 10% higher odds of having abnormal lipid levels (odds ratio [OR] 1.1, 95% confidence interval [CI] 1.04 to 1.17).

They also had increased odds of:

• high levels of "bad" cholesterol (LDL)
• low levels of "good" cholesterol (HDL)
• a high total cholesterol to "good" cholesterol ratio
• a high "bad" cholesterol to "good" cholesterol ratio
   

How did the researchers interpret the results?

The researchers concluded that their results support an association between job stress and abnormal lipid levels in the blood.

 

Conclusion

This study has found an association between job stress and abnormal lipid levels in the blood. Its strengths include the large number of workers assessed (more than 40,000) and the use of the same methods to assess all of the participants.

However, the fact that both job stress and lipid levels were assessed at the same time means it is not possible to say for certain whether job stress might have directly caused changes in blood lipid levels.

There are also other limitations and points to note:

• The study did not assess diet. People with job stress may have less healthy diets, which could account for the differences seen in the blood lipid levels, rather than these differences being a direct impact of job stress.
• Job stress was assessed by a single question, which may not fully capture all aspects of job stress. Also, different people may consider different things stressful, and the question did not disentangle the exact stressful workplace situations and an individual's ability to cope with them.
• Workers who were off sick would not have had the routine medical check-up. This means the sample may have missed some people with more serious health problems with stress.
• The authors acknowledge that the effect of job stress seen is relatively small – a 10% increase in the odds of having abnormal lipid levels.

Overall, it is not clear from this study whether stress is a direct cause of the increased lipid levels seen. Studies looking at whether interventions to reduce work stress can reduce lipid levels in the blood would provide an indication if this is in fact the case.

Despite these limitations, there is a wide range of good quality evidence that workplace stress can have a harmful effect on your physical and mental health.

While some people may thrive on pressure, persistent high levels of stress are likely to be harmful.

Read more about what you can do to reduce your levels of workplace stress.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

A stressful job really CAN kill you - by raising your cholesterol. Mail Online, May 17 2013

Links To Science

Catalina-Romero C, Calvo E, Sánchez-Chaparro MA, et al. The relationship between job stress and dyslipidemia. The Scandinavian Journal of Public Health. Published online January 2 2013 

”Sunshine vitamin 'may treat asthma'”, BBC News informs us, as a new lab-based study suggests vitamin D could help control symptoms of severe asthma.

Asthma is caused by inflammation of the airways, related to malfunctioning of the body’s immune system. In theory, the immune system mistakes harmless substances, such as dust mites, as a threat and triggers inflammation of the lungs and airways (which causes the symptoms of asthma).

The study in question looked at IL-17A, which is one of the molecules thought to be associated with the malfunctioning immune response seen in asthma. Researchers examined whether vitamin D had an effect on the levels of the molecule produced by white blood cells in a laboratory experiment.

Researchers found that vitamin D reduced the levels of IL-17A produced by cells from people with asthma. This included cells from people who had previously failed to respond to the treatment of choice for severe asthma – oral corticosteroids – often referred to as steroids.

While this study suggests that vitamin D can have an effect on IL-17A levels in the laboratory, it is certainly too early to hail vitamin D as a potential “cure” for asthma. A positive effect on cells in the lab does not guarantee vitamin D supplements will improve symptoms for people with asthma. Clinical trials in people with asthma are ongoing to test whether this will be the case.

 

Where did the story come from?

The study was carried out by researchers from King’s College London; Queen Mary, University of London, and the Homerton University NHS Foundation Trust. It was funded by Asthma UK and the National Institute for Health Research, and some researchers received Medical Research Council Funding. The study was published in the peer-reviewed Journal of Allergy and Clinical Immunology.

This study was reported by the BBC, Daily Mail, and the Daily Express. The BBC correctly points out that treating asthma patients with vitamin D “has not yet been tested”. The main text of the Mail’s coverage is generally accurate, although their headline suggests that “Vitamin D ‘helps beat the symptoms of asthma’”, when this was not assessed by the study. The Express’s coverage over-interprets the results by suggesting that “Soaking up sun could be a cure for asthma” or could be “the best way of treating asthma”.

 

What kind of research was this?

This was a laboratory study looking at the effect of vitamin D on one type of white blood cell (T helper cells called TH17 cells) from people with asthma.

One type of T helper cell called TH2 is known to be involved in inflammation of the airways in asthma. However, some evidence suggests that other T cells may also play a role.

TH17 cells are involved in defending the body against bacterial and fungal infections. There is some evidence that these cells may be involved in severe asthma. Also, one of the inflammatory substances produced by these cells, called IL-17A, may exacerbate asthma and reduce patients’ ability to respond to standard treatment for severe asthma – oral corticosteroids (steroids).

Previously, studies had shown that vitamin D could influence the T cells from patients with severe asthma, and also affect TH17 cells. The researchers in the current study wanted to see if vitamin D affected IL-17A production by TH17 cells collected from asthma patients. They also wanted to see whether this effect was different in people who were resistant to steroid treatments.

 

What did the research involve?

The researchers took blood from 10 healthy adults and 28 patients with moderate to severe asthma and extracted white blood cells, including T cells. The patients had to have had diagnosed asthma for at least six months. Of the patients, 18 had asthma that did not respond as well to oral steroid treatment (steroid resistant asthma), and 10 had asthma that responded to steroids.

The researchers grew the white blood cells in the laboratory, either with or without vitamin D and the steroid dexamethasone, and looked at how much IL-17A was being produced. They assessed whether this varied between people with and without asthma, or in people with steroid resistant asthma.

 

What were the basic results?

White blood cells from people with asthma produced higher levels of IL-17A than those from non-asthmatic patients. Furthermore, white blood cells from people with steroid resistant asthma produced the highest levels of IL-17A.

Treating the white blood cells with vitamin D reduced the production of IL-17A. This reduction occurred in cells from people with steroid-resistant asthma and steroid-sensitive asthma, and was not affected by adding the steroid dexamethasone.

 

How did the researchers interpret the results?

The researchers concluded that their results support the hypothesis that vitamin D could improve disease control in people with asthma by reducing IL-17A levels, regardless of whether the person’s asthma is steroid-resistant.

 

Conclusion

The current laboratory study suggests that vitamin D can reduce white blood cell production of an inflammatory molecule implicated in asthma.

These results were obtained from cells in the laboratory, and further research will be needed to determine whether this effect will also be seen if people with asthma are given vitamin D.

While the results perhaps give a reason to investigate vitamin D further, not all treatments showing initially positive results in laboratory studies go on to have a positive effect on real-world clinical outcomes.

The good news is, as the Daily Mail reports, the results of this study are being followed up with a randomised controlled trial in participants with steroid resistant asthma.

Randomised controlled trials are the best way of testing if treatments are effective. This trial, and others, will tell us if vitamin D works as a treatment for asthma and if so, who it might be effective at treating. 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Sunshine vitamin 'may treat asthma'. BBC News, May 20 2013

Vitamin D 'helps beat symptoms of asthma’. Daily Mail, May 20 2013

Soaking up sun could be a cure for asthma. Daily Express, May 20 2013

Links To Science

Nanzer AM, Chambers ES, Ryanna K, et al. Enhanced production of IL-17A in patients with severe asthma is inhibited by 1α,25-dihydroxyvitamin D3 in a glucocorticoid-independent fashion. The Journal of Allergy and Clinical Immunology.

 

 

"Children are picking up the caring roles the state has abandoned," The Guardian says, while The Independent says that 180,000 children work as unpaid carers.

These new figures come from the Office for National Statistics, which has pulled together data on unpaid care in England and Wales from the 2011 census.

The census (which has been carried out every 10 years since the middle of the nineteenth century) reveals an increase in the proportion of the population who are providing unpaid care.

This has risen from 11.5% in 2001 to 11.9% in 2011 in women, and from 8.8% to 9% in men. There tend to be more female carers than male, with the highest burden of care falling on the 50-64 age group for both sexes.

A related report produced by the charity The Children’s Society – based on the same data – has highlighted the issue of children acting as unpaid carers.

The charity's report describes how the census data estimated that there are around 160,000 unpaid young carers in England. It goes on to explain that this is likely to be an underestimate.

 

What does the ONS find about the gender of carers?

Just over half (58%) of the 5.41 million people providing some level of unpaid care in England are female and 42% are male. This higher proportion of female carers is consistent across all regions. Female carers are representative of 11.9% of the total female population of England and Wales, and male carers are representative of 9% of the male population. Ten years ago these figures were 11.5% and 8.8%.

The level of care provided was most often between one and 19 hours a week. However, 2.9% of the female population and 2% of the male population provided 50 or more hours of care a week. In 2011 in England, 9.5% of the male working population and 13.3% of the female working population were also providing some level of unpaid care. In England, 1.2% of the female population and 1% of the male population were in full-time employment at the same time as providing 50 or more hours of unpaid care. If you are a working carer, read the NHS Choices advice on combining caring with working or studying.

Links To The Headlines

180,000 children work as unpaid carers for relatives. The Independent, May 16 2013

Carers putting their own health at risk, census shows. The Daily Telegraph, May 16 2013

Children are picking up the caring roles the state has abandoned. The Guardian, May 16 2013

Young carers: Quarter of a million children provide care for others. BBC News, May 16 2013

“IVF advance triples couples' chances of having a baby”, The Daily Telegraph reports.

The innovation in question is actually based on an old imaging technique called time-lapse photography, where a camera is set to record a series of images at regular intervals. This technology is now available for monitoring the development of IVF embryos before they are transferred into the womb.

The researchers in this study developed a way of using the information collected to identify which embryos had a low or high chance of having an abnormal number of chromosomes (called aneuploidy). Aneuploidy can reduce the chances of embryos successfully implanting and resulting in a healthy live birth.

In this study, the researchers looked back at time-lapse imaging for embryos from 69 couples who had IVF. They wanted to know if their technique correctly identified embryos which were more likely to result in a pregnancy or live birth.

The time-lapse cameras allowed the researchers to potentially ‘screen’ embryos for risk of aneuploidy. From this, they would then be able to choose the low risk embryos for implantation.

The researchers found that 73% of the embryos their assessment would have classed as low risk resulted in a pregnancy at five to six weeks, and 61% resulted in a live birth. These rates were higher compared to the overall rate for all embryos (at any risk level), where the pregnancy rate was 42% and the live birth rate was 39%. However, it is important to restate that the new system was not used to intervene, so the results are based purely on observation.

While the results are promising, the technique is still in its early stages. Further research is needed to more widely test the technique and directly compare its results to standard methods.

 

Where did the story come from?

The study was carried out by researchers from CARE Fertility, an independent provider of fertility treatment and related services in the UK and Ireland. No sources of financial support were reported and the authors reported that they had no financial or commercial conflicts of interest.

The study was published in the peer-reviewed medical journal, Reproductive Biomedicine Online.

The study was well reported in the media, with BBC News coverage including an informative video to explain the technique.

However, potentially confusing figures are reported in other parts of the media.

The Times reported that the new technique “could give a 78% chance of success” while the Daily Mail reports that “Early trials show 78% of women having the test will have a healthy baby”.

The Guardian’s reporting suggests that “Doctors in Nottingham who devised the procedure say it could raise live birthrates at their clinic to 78%...” and this may be where this figure has come from.

However, this 78% figure does not come from the research paper itself, which reports that 61% of the low risk embryos successfully resulted in a live birth – not 78%.

 

What kind of research was this?

This study looked at whether the novel technique based on time-lapse images of IVF embryos might help select the embryos most likely to successfully produce a baby.

Until now, the researchers say that the vital decision about which IVF embryo should be selected and transferred into the mother’s womb is mainly based on between two and six observations of the developing embryo under the microscope.

To observe the embryo’s development, doctors have had to remove the culture dish containing the embryos from the very controlled environment of the incubator and place them under a microscope in the ambient air of the laboratory. This is usually only performed once a day to minimise disturbance to the embryo.

The authors of the study report that a major reason for IVF failure and miscarriage is that the implanted embryo has an abnormal number of chromosomes (aneuploidy). To accurately detect any chromosomal abnormality requires an invasive biopsy of the developing embryo, followed by genetic testing.

Currently it is not possible to reliably identify those embryos with an increased chance of aneuploidy with the normal microscopic observations of the embryo.

The current study tested a way of identifying the embryos at low risk of having abnormal numbers of chromosomal, using time-lapse imaging of the embryo. A relatively new system now allows doctors to obtain a stream of thousands of microscopic images of developing embryos (time-lapse images), without having to remove embryos from the incubator.

Using this system, the researchers previously found that embryos with an abnormal number of chromosomes take a different length of time to reach certain developmental stages than normal embryos. Based on this, they developed a method to identify those embryos at low, medium, and high risk of having an abnormal number of chromosomes.

In their current study, the researchers looked back at the results of IVF procedures where the embryos had been assessed using time-lapse imaging. They wanted to see if their method could identify those embryos which were more likely to go on to successfully implant, develop and be born.

It is important to note that the study did not actually use the method to select embryos for implantation – it only looked at what might have happened if the method had been used.

This is an appropriate first step for this type of research and, if the results are promising, the method would need to go on to be tested “for real” to select embryos, to see if it performed better than standard methods.

 

What did the research involve?

This study looked at the treatment outcomes for 88 embryos from 69 couples who attended the CARE Fertility clinic in Manchester between April 2011 and December 2012, and who had a known outcome from their IVF.

This meant that they knew if transfer of the embryo(s) had resulted in:

• failed implantation – where the woman had a negative pregnancy test
• clinical pregnancy – defined as the presence of a developing embryo with a heart beat at between six and eight weeks of pregnancy
• a live birth – identified through the mother completing a clinic delivery outcome form, which according to regulations is reported to the UK Human Fertilisation and Embryology Authority

The researchers excluded cases where two embryos were implanted but did not both have the same outcome, as they would not be able to tell which embryo had which outcome.

The egg cells collected from the women had been fertilised using intra-cytoplasmic sperm injection (ICSI), where a single sperm is injected directly into the egg. The fertilised eggs were then placed into the time-lapse incubator for culturing and imaging for five to six days.

The inbuilt microscope took images of the fertilised egg cell every 20 minutes. The image-analysis software recorded the precise timing of developmental events as they occurred. The embryos had been selected using standard existing methods before being transferred into the womb (that is, not using the new risk assessment method).

The researchers used this previously collected data model to assess the embryos, and grade whether the embryos were at low, medium or high risk of having an abnormal number of chromosomes. They then looked at what proportion of each of these three groups of embryos had achieved clinical pregnancy and live birth, and if this differed between the groups.

 

What were the basic results?

The researchers found that of the 88 embryos they assessed, 33 were at low risk for having an abnormal number of chromosomes, 51 at medium risk, and four at high risk.

Overall, 42% of the embryos successfully implanted and had a fetal heart beat at five to six weeks.

Among the low risk embryos, almost three-quarters (73%) successfully implanted and had a fetal heart beat at five to six weeks, compared to a quarter (25.5%) of medium risk embryos and no high risk embryos.

This meant that the 73% figure for low risk embryos is a relative increase of 74% compared with the rate for all embryos (42%) – what the media has translated as a ‘74% chance of successful pregnancy’.

The researchers had data on whether or not women had a live birth for 46 of the embryos (18 low risk, 26 medium risk, two high risk). The rest of the pregnancies had not reached term during the study period.

Overall, 39% of the embryo transfers resulted in a live birth. Among the low risk embryos, 61% resulted in a live birth. Among medium risk embryos, 19% resulted in live birth. None of the high risk embryos resulted in a live birth.

Therefore, the 61% figure for low risk embryos is a relative risk increase of 56% compared with the rate for all embryos (39%) – this is where media reports of the ‘increasing live birth rates to above 50%’ come from.

 

How did the researchers interpret the results?

The researchers say that their risk classification model using time-lapse imaging introduces a non-invasive way of selecting the embryos that are at a low risk of having an abnormal number of chromosomes. They say that this can result in higher likelihood of successful pregnancy and live birth.

 

Conclusion

This study reports on a new technique using ‘time-lapse imaging’ to non-invasively identify the IVF embryos least likely to have abnormal numbers of chromosomes.

An embryo having an abnormal number of chromosomes is one of the reasons IVF can be unsuccessful.

By looking back at the results of previous IVF procedures, the study showed that embryos identified as being low risk using the new method were the most likely to result in a live birth.

To date, IVF techniques rely on removing the embryo from the incubator about once daily over the course of five to six days to view its development under the microscope. As such, current methods only allow for a few static images which cannot give a reliable indication of whether an embryo has chromosome abnormalities, and also disturb the developing embryo. To select the best embryo for implantation, biopsies of the embryo have to be taken to examine the genes. The new technique potentially offers a non-invasive way to assess the risk of chromosome abnormality using detailed time-lapse images.

The results of this study are promising, but there are some limitations:

• It only assessed the outcomes for only 69 couples who received care at one fertility service. Larger numbers of embryos would ideally need to be assessed to confirm the results. Ideally, prospective studies comparing this new technique with standard techniques would also be carried out.
• The researchers note that their methods and results may not be directly transferable to other laboratories or other types of patient populations. 

The technique, while potentially promising, is still in an early stage of development. 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

IVF could be revolutionised by new technique, says clinic. The Guardian, May 17 2013

'Most exciting breakthrough in IVF treatment in 30 years' could triple number of births. The Independent, May 17 2013

IVF advance triples couples' chances of having a baby. The Daily Telegraph, May 17 2013

IVF test that 'trebles the chance of a baby': Photo method helps doctors implant best embryo. Daily Mail, May 17 2013

IVF 'may be boosted by time-lapse embryo imaging'. BBC News, May 17 2013

New IVF Technique Could Triple Number Of Births. Sky News, May 17 2013

IVF time lapse photographing technique breakthrough could help avoid miscarriages and triple number of births. Daily Mirror, May 17 2013

New IVF technique using time-lapse photos to increase number of healthy births. Metro, May 17 2013

Links To Science

Campbell A, Fishel S, Bowman N, et al. Retrospective analysis of outcomes after IVF using an aneuploidy risk model derived from time-lapse imaging without PGS. Reproductive BioMedicine Online. Published online May 13 2013

 

“Study shows girls with absent fathers more likely to develop depression," the Mail Online has revealed.

It reports on a large UK study that found that girls whose biological fathers were absent during the first five years of their childhood had an increased risk of symptoms of depression. No increase in risk was found for girls whose fathers were absent later in childhood, and no increase in risk was found for boys with absent fathers.

Researchers collected information regarding the physical absence of the biological father during childhood, as well as information on depression symptoms when the child was 14. They assessed whether there was any association between these factors.

During their analysis, the researchers took into account several factors that may influence the link, such as family characteristics. However, despite the researchers' efforts to take these variables into account, the reasons why a father may be absent from the family home can be incredibly complicated. This means we can’t be sure whether other factors have produced the association between absent fathers and depression in girls.

 

Where did the story come from?

The study was carried out by researchers from the University of Bristol and was funded by the UK Medical Research Council, the Wellcome Trust and the University of Bristol.

The study was published in the peer-reviewed journal Psychological Medicine.

Media coverage of this research was broadly accurate, though neither ITV nor Mail Online outlined any of the study’s limitations.

 

What kind of research was this?

This was an analysis of data from a prospective cohort study called the Avon Longitudinal Study of Parents and Children. This is a study that has been ongoing since the 1990s that assesses influences on the health and development of children.

The researchers were interested in the potential link between the absence of the biological father in early childhood and the risk of mental health problems. They were specifically interested in symptoms of depression that were not necessarily severe enough to be considered clinical depression.

As a prospective cohort study, this research is less likely to be affected by certain types of bias, especially recall bias. It was important that the researchers collected data on the effect of family factors on the children’s mental health at the time, rather than at a later date, to help ensure the information was accurate. Prospective studies allow for this.

 

What did the research involve?

The researchers measured two main factors:

• absence of the biological father during childhood
• experience of depressive symptoms during the teenage years

To measure parental absence, the researchers used questionnaires, filled out by the children’s mothers regularly throughout the children’s lives. These questionnaires asked whether the ‘present live-in father-figure is the natural father of the child and, if not, how old the child was when the natural father stopped living with the family’. This information was used to divide the children into three groups:

• biological father present
• biological father not present during the first five years of life (during early childhood)
• biological father not present from age 5 to 10 (during middle childhood)

To assess the teenagers’ experiences of depressive symptoms, the researchers asked the study participants to complete a 13-item questionnaire when they were approximately 14 years old. This asked about the presence of certain symptoms over the previous two weeks. The questionnaire is reported to be a reliable and valid measure of depression in children. Children scoring 11 or higher on this questionnaire were considered to have high levels of depressive symptoms. This is not the same as being diagnosed with depression, however.

The researchers then analysed the data, comparing the risk of having high levels of depressive symptoms among children whose biological father left during early or middle childhood to the risk in children whose fathers were still living with them. These analyses were adjusted for several factors (confounders) that could be linked to both the absence of the father and depressive symptoms, including:

• socioeconomic status (including home or car ownership, major financial problems, family size and parents’ jobs)
• mother’s characteristics (including having a child before the age of 20, experiencing depression during pregnancy), and
• any parental conflict between the mother and her current partner

Separate analyses were carried out for boys and girls, to determine whether the child’s gender had any impact on the relationship between father’s absence and depressive risk.

 

What were the basic results?

There were approximately 14,500 children in the original cohort study, approximately 11,000 of whom had data available on the presence or absence of their biological father. Among these children, approximately 6,000 had available data regarding depressive symptoms at age 14.

Overall, girls reported higher levels of depressive symptoms than boys, regardless of whether their father lived with them or not – a trend that has also been found in previous studies.

Girls

The study included:

• 374 girls whose father left during early childhood, 87 (23.3%) of whom had high depressive symptoms at age 14
• 193 girls whose father left during middle childhood, 27 (14.0%) of whom had high depressive symptoms at age 14
• 2,295 girls whose father was present throughout childhood, 332 (14.5%) of whom had high depressive symptoms at age 14

Boys

The study included:

• 357 boys whose father left during early childhood, 30 (8.4%) of whom had high depressive symptoms at age 14
• 185 boys whose father left during middle childhood, 17 (9.2%) of whom had high depressive symptoms at age 14
• 2,227 boys whose father was present throughout childhood, 166 (7.4%) of whom had high depressive symptoms at age 14

When assessing the association between the absence of the father in early childhood and teenage depressive symptoms, researchers found that:

• Girls with absent fathers during early childhood had a 53% greater chance of experiencing high levels of depressive symptoms compared with girls with fathers present during this time (odds ratio  [OR] 1.53, 95% confidence interval [CI] 1.07 to 2.21).
• Boys with absent fathers were no more likely to report high levels of depressive symptoms at age 14 than boys whose fathers were present during early childhood (OR 1.08, 95% CI 0.65 to 1.79).

There was no significant association between middle childhood father absence and teenage depressive symptoms.

 

How did the researchers interpret the results?

The researchers concluded that “father absence in early childhood increases risk for adolescent depressive symptoms, particularly in girls”.

 

Conclusion

This large prospective cohort study suggests that there is a link between a father’s absence during the first few years of life and a girl’s risk of experiencing depressive symptoms.

This study has several strengths, including its large sample size, its long-term follow-up and prospective collection of data for the analyses. It also attempted to consider confounding variables during the analysis and was based in the UK, which helps to ensure that the results are applicable here.

There are some limitations, however, that should be taken into account, including the following.

• Only a third of the original cohort was analysed due to missing data on key factors. It is unclear to what extent those included differed from the entire population-based cohort. The researchers report that drop-outs were more likely among participants in lower socioeconomic groups. This factor is linked to both parental absence and depressive symptoms, so it could reduce the validity of the results and how much we can infer from them.
• The adjusted analyses further reduced the available sample size due to missing data on confounding factors, and the researchers suggest that this may have resulted in loss of statistical power to detect an effect.
• Several potential confounders were not included in the analysis, and could have influenced the results. The study authors report some of these potential confounders (quality of parent-child relationship, the father’s involvement in the child’s life regardless of whether he lived in the same house).
• The questionnaire used to assess depressive symptoms is not a measure of clinical depression. A high score on this questionnaire does not indicate that the child has or will develop a diagnosable depressive disorder.

Overall, this study suggests that early childhood family environments may play an important role in the mental health of children. At this stage we don’t know what accounts for the study’s results, and the researchers say that this should inspire future research into the possible biological and psychological mechanisms underpinning this relationship.

Depression is one of the most common mental health conditions, yet there is very little good quality evidence about how to prevent people developing depression. Research that gives us insight into the factors that increase children’s likelihood of developing depression would be invaluable.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

A quarter of young girls with absent fathers 'grow into depressed teenagers': Researchers say boys cope better with parental separation. Mail Online, May 15 2013

Study shows girls with absent fathers more likely to develop depression. ITV News, May 15 2013

Links To Science

Culpin I, Heron J, Araya R, et al. Father absence and depressive symptoms in adolescence: findings from a UK cohort. Psychological Medicine. Published online May 14 2013

"Human embryonic stem cells created from adult tissue for first time," The Guardian reports, while the Daily Mail's front page leads with the somewhat fanciful warning that new research raises the "spectre of cloned babies".

These headlines are based on newly published research into the use of a technique known as somatic cell nuclear transfer (SCNT) as part of embryonic stem cell research. It should be noted that no babies were born as a result of this research, and the researchers had no intention of producing a live cloned human being.

SCNT involves taking donated egg cells from women and removing their genetic material. These are then fused with human cells – in this case skin cells – and the fused cell begins behaving in a similar way to an embryo by producing human stem cells.

This research is the first time the technique has been successful using human cells.

When these stem cells were tested, researchers found that the cells were able to develop into other types of cells in a manner similar to that seen in stem cells derived directly from embryos.

The researchers say that this could have exciting implications. The technique could potentially be used to take skin cells from a patient to create "personalised" stem cells. The resulting stem cells could then possibly be used to repair damaged tissue, or even treat genetic conditions.

However, there remain ethical concerns over the implications of using SCNT to develop stem cells. These concerns, as well as scientific and financial considerations, will need to be taken into account as this field continues to develop.

  

Where did the story come from?

The study was carried out by researchers from Oregon Health and Science University (OHSU) and Boston University School of Medicine in the US, as well as Mahidol University in Thailand. It was funded by OHSU, the Leducq Foundation and the US National Institutes of Health, and was published in the peer-reviewed journal, Cell.

Media coverage of this study was as varied as people's feelings are about stem cell research. It ran from the medically hopeful headline of The Independent ("Human cloning breakthrough raises hopes for treatment of Parkinson's and heart disease"), to a straight-to-the-facts headline from The Guardian ("Human embryonic stem cell created from adult tissue for first time"), to fear and controversy from the Daily Mail ("New spectre of cloned babies: Scientists create embryos in lab that 'could grow to full term'").

Despite its headline and further warnings of "designer babies", the Daily Mail does provide a quite useful figure outlining the process the scientists used in the research.

 

What kind of research was this?

This was a laboratory study that aimed to produce embryonic stem cells from adult skin cells. Embryonic stem cells are unique in that they are able to develop (or differentiate) into other types of cells. Because of this, it is thought that they could play a critical role in the treatment of a wide variety of diseases.

Researchers have been looking into ways of using a patient's own cells to create embryonic stem cells, as this would ensure that the genetic material in any cells used therapeutically would match the patient's DNA. In theory, this should prevent the body from rejecting the cell.

The researchers report that previous attempts to produce embryonic stem cells using this technique have failed, as the cells stopped dividing before they reached an advanced enough stage. During their experiments, researchers identified two reasons for this inability to sufficiently grow the cells and developed techniques to overcome these limiting factors.

Laboratory studies are necessary for developing techniques and procedures that may one day lead to new medical therapies.

This study will no doubt be very exciting for researchers working with stem cells, but we're still a long way from the findings of this study being translated into new treatments for conditions such as Parkinson's disease or heart disease.

 

What did the research involve?

The researchers used a technique called somatic cell nuclear transfer (SCNT) to transfer genetic material from adult human skin cells into a human egg cell in order to produce embryonic stem cells. SCNT has been used to clone animals before, and is thought to have potential applications in the study and treatment of human diseases.

SCNT involved taking the nucleus (the part of a cell containing most of the genetic information) from a person's skin cells, inserting its cells into a donor's unfertilised egg cell that had its nucleus removed. The skin cell nucleus was then fused with the donor egg cell. Once this happened, the person's genetic material was in a vehicle that was theoretically able to divide.

Researchers then optimised methods to prompt the egg cell to start and continue to divide using electricity and chemical compounds, including caffeine.

Once this cell division yielded approximately 150 cells – a stage called a blastocyst – researchers were able to isolate the embryonic stem cells. The researchers then tested these stem cells to see if their genetic material retained any traces of the genetic material from donor egg cell's nucleus. They also tested whether or not the embryonic stem cells were able to develop into other types of cells.

 

What were the basic results?

The researchers were able to use SCNT to generate human embryonic stem cells. These cells were found to match the nuclear genetic material of the person's skin cells, and did not contain any trace of the donor egg's nuclear genetic material.

The embryonic stem cells were able to develop into several different types of cells, including heart cells. They were also found to express genes similar to those expressed by embryonic stem cell lines derived following IVF procedures, which the researchers referred to as "genuine" embryonic stem cells.

 

How did the researchers interpret the results?

The researchers say that this study represents the first successful attempt at generating human embryonic stem cells following somatic cell nuclear transfer.

They say that the observed ability for these embryonic stem cells to develop into heart cells demonstrates their potential use in regenerative medicine.

 

Conclusion

This research represents the first time that human embryonic stem cells have been developed using the "cloning technique" known as somatic cell nuclear transfer (SCNT).

It is important to note that this study did not attempt to clone a human being by creating a baby in a lab. It is unclear at this point whether the cells in this study would continue to stably divide in a manner sufficient for an embryo to develop to full-term.

While this study is certainly a breakthrough for researchers in the field, its findings are unlikely to translate quickly into regenerative medicine or other medical therapies.

There are some scientific limitations to the approach, including the fact that only a fraction of the fused cells were able to divide sufficiently to reach the blastocyst stage and, of those that did, not all were able to generate stable embryonic stem cell lines.

It is also worth considering that donated egg cells from women are required before SCNT can be carried out, potentially limiting the ability of scientists to generate stem cells on an "industrial" basis.

SCNT does not represent the only approach to embryonic stem cell development. Researchers around the world continue to investigate several methods for developing and using stem cells. It is not immediately clear how the current research will fit into this field, or whether it will trigger a major shift in stem cell research.

In addition to these scientific hurdles, there are ethical and financial considerations that will likely need to be addressed.

Despite these issues, this research does represent a breakthrough in the use of SCNT in the stem cell research field and has implications for disease research.

What the study emphatically does not represent is an impending expansion into cloning babies.

 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Human embryonic stem cells created from adult tissue for first time. The Guardian, May 15 2013

Embryonic stem cells: Advance in medical human cloning. BBC News, May 15 2013

New spectre of cloned babies: Scientists create embryos in lab that 'could grow to full term'. Daily Mail, May 15 2013

Cloning breakthrough by US scientists. The Daily Telegraph, May 15 2013

Stem Cells Made From Cloned Human Embryos. Sky News, May 15 2013

Cloned babies fear as stem cells are created from skin. Daily Express, May 16 2013

Links To Science

Tachibana M, Amato P, Sparman M, et al. Human Embryonic Stem Cells Derived by Somatic Cell Nuclear Transfer. Cell. Published online May 15 2013

“Double drug hope for brittle bone sufferers”, reports the Daily Mail.

This headline follows a small but well-designed trial of treatments for postmenopausal osteoporosis. As women go through the menopause, levels of the hormone oestrogen begin to fall. This drop in oestrogen can lead to a thinning and weakening of the bones, increasing the risk of broken bones (fractures).

While current treatments can help prevent further weakening of the bones, they are not particularly effective at restoring bone strength – known as bone mineral density (BMD). In this study, researchers found that using a combination of teriparatide (Forsteo) and denosumab (Prolia) led to a significant improvement in BMD, when compared to using either medicine on its own.

While this research is encouraging, there are still questions that need answering. For instance, it isn’t clear whether this combination treatment is effective at preventing fractures (more participants would be required) or safe past 12 months (the length of this study).

Similarly, the research was mainly in white, city-dwelling postmenopausal women, so the effectiveness may differ in women from different places and ethnic backgrounds. Similarly, it is not clear whether it would benefit men with osteoporosis (which is less common, but still accounts for roughly 20% of cases).

Aside from these limitations, this research is a positive step forward in the search for new treatment options for osteoporosis. The encouraging results are likely to lead to further, larger studies.

 

Where did the story come from?

The study was carried out by researchers from at the Massachusetts General Hospital, Boston (US) and was funded by the National Center for Research Resources as well as the pharmaceutical manufactures Amgen and Eli Lilly.

Amgen manufactures denosumab and Eli Lilly manufactures teriparatide.

However, the publication states that the funders of the study had no role in study design, data collection, data analysis, data interpretation, or the writing of the report.

The corresponding author had full access to all the data in the study and had final responsibility for the decision to submit for publication.

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

The media reporting generally described the research findings accurately although discussion about the limitations of the research was minimal.

 

What kind of research was this?

This research used a randomised control trial (RCT) to test whether combining two approved osteoporosis medicines (teriparatide and denosumab) would improve bone mineral density in postmenopausal women.

Osteoporosis is a condition that affects the bones, causing them to become weak and fragile and more likely to break (fracture). These fractures most commonly occur in the spine, wrist and hips, but can affect other bones such as the arm or pelvis. Approximately 3 million people in the UK are thought to have osteoporosis. Although commonly associated with postmenopausal women, osteoporosis can also affect men, younger women and children.

The two drugs, teriparatide and denosumab, are already used individually to treat osteoporosis but they work in slightly different ways. So the researchers wanted to test whether there was any added benefit of using the two drugs together.

Despite drugs being available for osteoporosis, the researchers’ say no currently approved treatment actually restores normal bone density in most patients with osteoporosis – they merely halt the decline. And options for those with severe osteoporosis are limited; the resulting risk of fracture, aside from affecting people’s quality of life, puts a considerable strain on the NHS. It is estimated that there are around a quarter of a million fractures each year in the UK. This means there is a continual need for new or improved treatments.

An RCT is one of the most reliable ways of testing whether a new drug, or in this case combination of drugs, is effective.

 

What did the research involve?

Between September 2009 and January 2011 the researchers enrolled 100 postmenopausal women (aged 45 years or older, with at least 36 months since last period) with osteoporosis who were at high risk of bone fracture. Women were enrolled through a mailing advertisement and on referral to Massachusetts General Hospital in Boston (US).

Bone mineral density is measured by ‘T-score’ and is simply the number of units, known as standard deviations, above or below the expected average for a healthy 30-year-old adult of the same sex and ethnicity as the patient. Only about 2.5% of women would have a T-score less than -2.0, for example.

The researchers defined high fracture risk as either:

• T-score –2.5 or less at the spine, hip, or femoral neck
• T-score –2.0 or less with at least one risk factor; fracture after age 50 years, parental hip fracture after age 50 years, previous overactive thyroid, inability to get up from a chair with arms raised, or current smoking
• T-score –1.0 or less already with history of a fracture from osteoporosis

Women were split into three equal groups to receive 20 microgram teriparatide daily, or 60 milligram denosumab every six months, or both.

Bone mineral density was measured at 0, 3, 6, and 12 months. This included measuring bone density at the lumbar spine, hip bone and neck of the femur using low-dose x-rays and bone biomarkers. Calcium intake (which can influence bone strength) was also recorded at the start of the study through a food frequency questionnaire.

Women who completed at least one study visit after baseline were assessed in a modified intention-to-treat analysis. Physicians interpreting bone mineral density assessments and the laboratory staff doing bone-marker assays were unaware of patients’ treatment groups.

The analysis compared changes in bone density from baseline (the start of the study) to the different time points (3, 6, and 12 months) for each of the different locations (spine, hip bone, and neck of femur).

 

What were the basic results?

Of the 100 eligible women, 94 completed the 12 month study. At 12 months, the main findings were that:

• Lumbar spine bone density had increased significantly more in the combination group (9.1%, standard deviation (SD) 3.9) than in the teriparatide (6.2%, SD 4.6) or denosumab (5.5%, SD 3.3) groups.
• Femoral-neck bone density also increased more in the combination group (4.2%, SD 3.0) than in the teriparatide (0.8%, SD 4.1) and denosumab (2.1%, SD 3.8) groups.
• Total hip bone density also increased more in the combination group (4.9%, SD 2.9; teriparatide, 0.7% SD 2.7; denosumab 2.5%, SD 2.6).

All these results were statistically significant.

 

How did the researchers interpret the results?

The researchers concluded that, “combined teriparatide and denosumab increased bone mineral density more than either agent alone and more than has been reported with approved therapies.” Furthermore, “combination treatment might, therefore, be useful to treat patients at high risk of fracture.”

 

Conclusion

This small but well-conducted RCT showed that combining licensed osteoporosis medicines teriparatide and denosumab may increase bone density more than either medicine used on their own, in postmenopausal women at high risk of bone fracture.

The researchers highlighted that their results were not consistent with previous trials looking at combination therapies for osteoporosis, which found no benefit of combining them.

However, previous research did not use the same combination of medicines in the same dose as the present trial. It could be the case that the dosages used in previous research were not given at the optimal level.

And while the study showed statistically significant differences in bone density at 12 months, this does not necessarily mean the treatment lead to a reduced rate of fractures – which is the ultimate aim of treating osteoporosis. Larger, longer-term studies are required to see what impact this combination treatment has on fracture risk, as well as assessing how safe and effective both drugs are in the longer-term.

This is particularly relevant because teriparatide is only licensed to be used for a maximum of 24 months (a point the Daily Mail usefully highlighted). It remains to be seen what would happen when this combination of therapies were stopped – would the benefits be reversed, and would it be safe to continue using the medicine longer than recommended?

These issues would need to be thoroughly addressed before this potentially useful combination could feasibly be routinely used in the NHS.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on twitter.

Links To The Headlines

The double drug hope for brittle bone sufferers. Daily Mail, May 15 2013

Links To Science

Tsai JN, Uihlein AV, Lee H, et al. Teriparatide and denosumab, alone or combined, in women with postmenopausal osteoporosis: the DATA study randomised trial. The Lancet. Published online May 15 2013

 

"Depressed people are out of sync with the rest of the world because their body clocks are broken," reports the Mail Online website, while The Independent claims that depressed people live in a "different time zone".

The story comes from a study that looked at the activity of genes thought to be involved in regulating the body's internal clock – the innate sense that most people have of the changes over a 24-hour day to night cycle (circadian rhythms).

Researchers did a detailed study of gene expression, the effect that certain proteins contained inside individual genes have on genetic activities inside the body.

The study involved examining brain tissue taken from people who donated their brains to science after their deaths. Of the sample, 55 people had no history of psychiatric illness, while 34 patients had a history of severe depression (major depressive disorder, or MDD).

Researchers found that the gene activity associated with regulating circadian rhythms was much weaker, and often disrupted, in the brains of patients who had MDD.

These results possibly present, as philosophers put it, a "causality dilemma" (a chicken and egg problem) – does depression lead to a disrupted body clock, or does a disrupted body clock make people vulnerable to depression?

It is too early to say what help these findings may be in the understanding and treatment of MDD.

 

Where did the story come from?

The study was carried out by researchers from the University of Michigan, the University of California, Weill Cornell Medical College, Stanford University and the HudsonAlpha Institute for Biotechnology, and was supported by the Pritzker Neuropsychiatric Disorders Research Fund.

It was published in the peer-reviewed Proceedings of the National Academy of Sciences.

Both the Mail Online and The Independent covered the research uncritically. Given the specialised nature of this research, it's not surprising that both of the news stories appeared to be strongly based on an accompanying press release and were not a critical appraisal of the study itself.

 

What kind of research was this?

This was laboratory research using donated post-mortem brains. In it, researchers analysed in detail the gene expression of certain genes thought to be associated with circadian rhythm regulation at the time of death.

The authors point out that a common symptom of major depressive disorder is the disruption of circadian patterns, which can trigger symptoms of insomnia as well as excessive daytime sleepiness and fatigue (feeling tired all the time). However, to date there is no direct evidence of "circadian clock dysregulation" in the brains of patients with major depressive disorder.

 

What did the research involve?

Researchers used human brain tissue taken from a US donor programme with the consent of next of kin. They also took information from medical records, medical examiners and interviews with relatives to record the donors' previous physical health, medication use, psychiatric problems, substance use and details of death.

This was done in order to assess whether donors had a major depressive disorder, a severe form of depression that has a significant impact on day-to-day living.

They also assessed whether physiological stress at the time of death would have had an effect on gene expression, and took account of this potential confounding factor.

Researchers analysed the brain tissue of 55 donors with no history of psychiatric or neurological illness and 34 patients with major depressive disorder. Using specialist techniques called DNA microarray, they measured the expression of genes thought to be associated with regulating circadian rhythms in different areas of the brain.

They used the control group to build a detailed picture of circadian gene expression in brain tissue and compared the results with those found in the brains of people with MDD. They also used the rise and fall of the top 100 "cyclic" genes in 60 of the donors to predict the time of death in all the others, both cases and controls. 

 

What were the basic results?

In the brain tissue from donors without major depressive disorder, they found that the activity of "circadian" genes at certain times of the day and night was consistent with data derived from other diurnal (day-active) mammals. More than 100 genes showed "consistent cyclic patterns" over six brain regions.

However, in the brains of patients with MDD gene expression of cyclic patterns was far weaker and more disrupted, with the patients' day pattern of gene activity often resembling a night pattern.

They found that predictions of time of death were more accurate among controls than for those with MDD.

 

How did the researchers interpret the results?

The researchers say the results provide convincing evidence that there is a "rhythmic rise and fall" in the activity of hundreds of genes in the human brain associated with regulating the day/night cycle. There is also evidence that the activity of genes associated with circadian rhythms is abnormal in people with MDD.

The study identifies hundreds of genes in the human brain that are likely to be involved in the sleep/wake cycle. The researchers conclude that daily rhythms in these genes are "profoundly dysregulated" in MDD. They say the results pave the way for the identification of new biomarkers and treatments for mood disorders.

 

Conclusion

This study is of interest, but at the moment it has little bearing on our understanding and treatment of depression. It could lead to new insights and treatments in the future, but there is no guarantee that this will be the case.

Also, as the authors point out, gene activity can result from many factors, including disease and drug history. In particular, it should be pointed out that:

• the researchers relied on only 55 patients to build a "normal" picture of genetic expression associated with the sleep/wake cycle
• it is not clear whether those in the MDD group had all been formally diagnosed with MDD or how long they had had depression, and it is possible there were errors in the classification of patients either with or without MDD

In conclusion, it is too early to say whether this study's findings might help in the understanding and treatment of major depressive disorders.

 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

New forensic technique for estimating time of death by checking internal clock of the human brain. The Independent, May 13 2013

Out of sync with the world: Depressed people suffer with 'broken body clocks'. Mail Online, May 14 2013

 

Links To Science

Zi JZ, Bunney BG, Meng F, et al. Circadian patterns of gene expression in the human brain and disruption in major depressive disorder. PNAS. Published online May 13 2013

Does the 'five-second rule' really work?

We’ve all done it – dropped some food on the floor, picked it up, given it a quick wipe and put it in our mouth.

The theory is that if food dropped on the floor is picked up quickly enough, it’s safe to eat.

While some people are firm believers, others use the rule to convince themselves that it's ok to eat a fallen morsel.

'No matter if it’s at home on the carpet, the kitchen floor or in the street...if you drop it, chuck it.'

Dr Ronald Cutler

Some call it the ‘five-second rule’ others know it as the ‘three-second rule’. Whichever you're familiar with, it certainly isn’t based on science says Dr Ronald Cutler, a microbiologist from Queen Mary, University of London.

To prove what he said Dr Cutler subjected the five-second rule to the rigours of scientific testing.

His trial involved dropping pieces of pizza, apple and buttered toast on different surfaces and analysing them to see what types of germs they collected.

The pizza was dropped on a kitchen floor, the apple was dropped in the street and the buttered side of the toast was dropped on carpet – all for five seconds.

Food poisoning

The idea that dirt is 'good' and hygiene somehow 'unnatural' has been popularised in the media.

For those who believe that a little dirt never hurt anyone, here’s a sobering statistic – each year in the UK around a million people suffer a food-related illness. 

Of these, about 20,000 people require hospital treatment and up to 500 may die as a result.

Many of these cases could have been avoided through basic hygiene such as hand-washing, and preparing and cooking food properly.

Back in the lab, Dr Cutler analysed the food samples and found that they were all covered in germs compared with control samples that had not been dropped.

“The pizza was covered in bacteria, some of them faecal bacteria,” says Dr Cutler, of Queen Mary, University of London. Faecal bacteria are bacteria found in poo. “I certainly wouldn’t eat it,” he adds.

“The fresh apple slice, which had no real sticky surface, still picked up lots of bacteria – I wouldn’t eat that," Dr Cutler continues. 

The toast fared worse. “The butter helped pick up lots of bacteria and I certainly wouldn’t eat that either.”

Dr Cutler also tested a food sample that had been on the floor for less than a second and found it too was contaminated.

“Whether it’s been on the floor for five, three or zero seconds, food still picks up bacteria,” he says.

“No matter if it’s at home on the carpet, the kitchen floor or in the street, my advice is if you drop it, chuck it.”

Dr Cutler’s simple test is backed up by several studies performed in recent years proving that the five-second rule is a complete myth.

Get 10 tips to prevent food poisoning.

'Technology, food additives and air pollution are causing people to develop dementia earlier than ever,' reports the Mail Online website. But this is a claim with little to no evidence to support it.

The study the Mail reports on looked at death rates in 10 developed countries, including the UK and the US. The researchers specifically focused on what they termed "neurological deaths". These are deaths arising from conditions that affect the brain and nervous system, such as motor neurone disease and dementia.

This study found that the overall death rate has fallen over the past 30 years. But levels of neurological deaths have risen significantly when comparing data from 2008-10 to comparative data from 1979-81.

It is not clear why there has been such a rise in the number of deaths from neurological disorders. The researchers speculate that the fact that people are living longer, there have been major improvements in diagnostic techniques, and significant changes in lifestyle and the environment – such as the increased use of food additives, more pollution, and new technologies such as wi-fi and mobile phones – could all contribute to the rising numbers.

It is the claim about modern technology that captured the Mail's imagination the most. But the key word here is "speculate": more research is needed to see whether factors such as "technology, food additives and air pollution" could be held responsible for the rise in neurological deaths.

 

Where did the story come from?

The study was carried out by researchers from Bournemouth University and Southampton University. There was no funding to declare. It was published in the peer-reviewed journal, Public Health.

This story was covered poorly by the Mail Online website. Speculation about the possible causes of the increase in deaths from neurological diseases was reported as fact.

 

What kind of research was this?

This was an observational study that aimed to see how total deaths (mortality) and deaths specifically from neurological causes in older adults (aged 55 to 74 years) varied between the periods 1979-81 and 2008-10 in 10 major developed countries (Australia, Canada, France, Germany, Italy, Japan, Netherlands, Spain, the UK and the US).

This type of study can tell us how death rates and deaths from neurological causes vary over time, but it cannot tell us why these rates vary.

In order to investigate whether any of the factors suggested by the Mail Online – such as electronic devices, food additives and air pollution – play a role, ideally a randomised controlled trial, or more likely a cohort study, would have to be performed.

Even these types of studies could be difficult to carry out. Given that certain technologies such as mobile phones are now a global phenomena, it would be hard to isolate a mobile-free control group.

 

What did the research involve?

The researchers compared World Health Organization (WHO) data on total mortality and deaths due to neurological causes in people aged between 55 and 74 years old for the period 1979-81 with data from 2008-10 (or for the latest years available) in 10 major developed countries.

Neurological deaths were analysed as a whole, or divided into "nervous disease deaths" and "Alzheimer's and other dementia deaths". Nervous disease deaths included deaths from various conditions where there was inflammation or degeneration of the nervous system, including multiple sclerosis, motor neurone disease and Parkinson's disease.

 

What were the basic results?

The researchers found that total mortality for people aged between 55 and 74 years old fell substantially in every country over the 30-year period. On average, there was a fall of 45% from 25,620 deaths per million men in 1979-81, to 14,158 deaths per million men in 2008-10. For women, there was a decrease of 54% from 13,591 deaths per million in 1971-81 compared with 6,195 deaths per million in 2008-10.

In contrast, in people aged between 55 and 74 years old deaths from neurological causes rose by at least 10% in men in seven countries, and in women in eight countries. Total neurological deaths for both women and men rose significantly in Australia, Canada, Germany, Italy, Spain, the UK and the US.

Total neurological deaths increased significantly only in women in the Netherlands. On average, there were 275 deaths per million due to neurological causes in men in 1979-81. This rose to 332 deaths per million in 2008-10, an increase of 21%. In women, there were 101 deaths per million due to neurological causes on average in 1971-81, rising to 260 deaths per million in 2008-10, an increase of 29%.

When deaths from nervous diseases and Alzheimer's and other dementias were considered separately:

• In men, deaths from nervous diseases rose from 144 deaths per million in 1979-81 to 203 deaths per million in 2008-10 on average across the 10 countries surveyed.
• Seven countries had at least 10% increases in death rates from nervous diseases in men. Rates fell by at least 10% in the other three countries.
• In women, deaths from nervous diseases rose from 104 deaths per million to 137 deaths per million on average. Six countries had at least 10% increases in the rate of death from nervous diseases in women. Rates fell by at least 10% in two other countries.
• In men, deaths from Alzheimer's and other dementias rose slightly from 128 deaths per million in 1979-81 to 130 deaths per million in 2008-10 on average. Death rates from Alzheimer's and other dementias rose by at least 10% in men in five countries, and fell by at least 10% in three countries.
• In women, deaths from Alzheimer's and other dementias rose from 86 deaths per million to 123 deaths per million on average.
• Death rates from Alzheimer's and other dementias rose by at least 10% in women in seven countries, and fell by at least 10% in two countries.

 

How did the researchers interpret the results?

The researchers conclude that in contrast to major reductions in general mortality, mortality due to neurological deaths has increased in the majority of the countries analysed. They state that, "These results pose a major public health problem".

The researchers go on to discuss potential explanations for the increase in neurological deaths seen, including:

• the fact that people are living longer, making it more likely that they will develop and possibly die from some of the diseases considered to be diseases of older people
• improved diagnostic techniques, allowing more diagnoses of neurological diseases to be made
• lifestyle or environmental factors, which may increase the risk of developing some of these diseases

 

Conclusion

This research has found that the death rate in people aged between 55 and 74 years old has fallen over the past 30 years in 10 developed countries (Australia, Canada, France, Germany, Italy, Japan, Netherlands, Spain, the UK and the USA). However, during this period deaths from neurological disorders such as Alzheimer's and other dementias (such as vascular dementia), Parkinson's disease and multiple sclerosis have increased on average.

The reasons for this increase in neurological deaths can only be speculated about. The researchers suggest that the fact that people are living longer, improvements in diagnostic techniques, and changes in lifestyle and the environment could contribute to the increase.

However, although this type of study can tell us how death rates and deaths from neurological causes are varying over time, it cannot tell us why these rates might be varying. More research is required to see whether factors such as "technology, food additives and air pollution" really are responsible for the increase in death rates due to neurological disorders.

 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Technology, food additives and air pollution are causing people to develop dementia earlier than ever, says leading scientist. Mail Online, May 13 2013

Links To Science

Pritchard C, Mayers A, Baldwin D. Changing patterns of neurological mortality in the 10 major developed countries – 1979-2010. Public Health. Published online April 19 2013

Writing in the New York Times, actress Angelina Jolie has announced that she has recently undergone a double mastectomy (where both breasts are surgically removed) followed by breast reconstruction surgery.

She writes that this is because genetic testing revealed she had a 87% chance of developing breast cancer in later life, as well as a 50% risk of ovarian cancer. This means she took a decision to have ‘preventative surgery’.

Jolie explained: "I decided to be proactive and to minimise the risk as much I could. I made a decision to have a preventive double mastectomy.

"Cancer is still a word that strikes fear into people’s hearts, producing a deep sense of powerlessness. But today it is possible to find out through a blood test whether you are highly susceptible to breast and ovarian cancer, and then take action."

 

What genes contribute to breast cancer risk?

A number of genes, associated with breast cancer, have been identified. People often talk about 'having' these genes, which include BRCA1, BRCA2, TP53 or PTEN. In fact, every women has these genes, but if a fault (mutation) develops in one of the genes then it can increase the risk of a women developing breast cancer.

It is estimated that around 1 in 500 women have a high-risk mutation in one of the genes associated with breast cancer.

 

What is the risk if you have a faulty breast cancer gene?

If you have a faulty gene, it doesn't mean you'll definitely develop breast cancer, but you are at a higher risk.

Having a fault in one of the breast cancer genes raises the risk of developing breast cancer to between 50% and 85%. In other words, out of every 100 women with a faulty gene, between 50 and 85 of them will develop breast cancer in their lifetime.

 

Are all women routinely tested for faulty genes?

No. Testing, provided by the NHS, is usually only offered to women thought to be at high risk of having a faulty gene. These include:

• women with a strong family history of breast cancer where a living family member with breast or ovarian cancer is available for testing
• women with a family history of several relatives developing early-onset breast cancer (cancer that develops before the age of 50), as this is often associated with having a faulty gene

Gene testing is also available from private clinics. The tests can be expensive, with available prices quoted on the internet ranging from around £2,000 to £3,000. The Pink Lotus Breast Center, where Angelina Jolie had her treatment, states that it screens for BRCA gene mutations in women without cancer who:

• have two or more family members with breast cancer, one under the age of 50
• have a previously identified BRCA mutation in the family at any age
• are of Ashkenazi Jewish descent with a family history of breast or ovarian cancer

 

Will I need a mastectomy if I am found to have a faulty gene?

No. There are a range of treatment options available to you.

Firstly, there is the option of what is known as active monitoring. This is where you receive annual screening in the form of mammograms or MRI scans (or sometimes both) to monitor the state of your breast tissue.

Changes in your lifestyle can also reduce your individual breast cancer risk. These include eating a healthy diet, taking plenty of exercise and maintaining a healthy diet.

There is also the option of waiting to see if breast cancer develops, and if it does it can be treated using conventional methods as with other breast cancers. Breast cancer cure rates are good and continue to improve. The chance of making a full recovery, especially if the cancer is detected early, are relatively high.

Ultimately, there is no right or wrong answer about what you should do. Your care team can provide advice that will allow you to make an informed decision about your treatment. But the decision is only one you can make.

 

What happens if I decide to have a preventative mastectomy?

As much breast tissue as possible is removed through a single cut horizontally or diagonally across the chest under general anaesthetic. It’s a physically and emotionally draining operation. Expect some pain and fatigue afterwards and to spend one or two nights in hospital. It generally takes three to six weeks to recover fully.

 

What is breast reconstruction?

Basically, new breasts are formed from skin and muscle from your back, stomach or buttocks, or by using implants. It’s often possible to have reconstruction straight away – in the same operation as the mastectomy – though you can have it done later. Angelina Jolie had her breasts reconstructed with implants nine weeks after her double mastectomy. If your nipples have to be removed during the mastectomy, then they can be reconstructed with skin from another part of your body, and the areola created by tattooing.

 

Will the new breasts look and feel the same as before?

Reconstructed breasts won’t feel the same to you as your real ones did – the nerves have been cut, so they’ll always be numb, and there will be noticeable scars, but women generally report being happy with the cosmetic outcome. 

Edited by NHS Choices. Follow Behind the Headlines on twitter.

Links To The Headlines

My Medical Choice. New York Times, May 14 2013

‘Research has found emotional eaters tend to eat more when happy’, reports the Mail Online website.

The news is based on a small study looking at whether experimentally altering mood has an effect on the amount of calories a person eats.

The researchers examined the effects on what they describe as ‘emotional eaters’ – people who reported using food as a coping mechanism for emotions.

A group of 86 students, who said they were either emotional or non-emotional eaters, were shown TV and movie clips to evoke either a positive, negative or neutral mood. The researchers then assessed how much the students ate when provided with bowls of crisps and chocolate, as well as assessing their change in mood.

Emotional eaters who were shown the positive mood-inducing scenes significantly increased their food intake compared to emotional eaters shown the neutral mood-inducing scenes. However, the negative mood-inducing scenes had no effect on food intake of emotional or non-emotional students.

The common assumption is that emotional eaters eat more when in a negative mood, but this study provides very limited evidence to suggest that this may not always be the case.

However, because this experiment was based in a laboratory and researchers did not measure how hungry people were, even this finding should be viewed with caution. As ever, more and better research is needed if people with eating disorders or weight problems are to be helped effectively.

Where did the story come from?

The study was carried out by researchers from Maastricht University in The Netherlands and was funded by the Netherlands Organisation for Scientific Research. It was published in the peer-reviewed journal, Appetite.

The story was picked up by the Mail Online website and it was covered appropriately, although the limitations of the study could have been described in more detail.

What kind of research was this?

This was a laboratory study looking at the effect of experimentally influencing mood changes in a group of students reported to be emotional or non-emotional eaters, and then looking at the effect on their food and calorie intake.

The researchers say emotional eaters are thought to increase their food intake in response to negative emotions, but little is known about the effect of positive emotions on their food intake. Meanwhile, non-emotional eaters are not believed to change their intake levels in response to emotions, and they might even restrict food intake in response.

The main limitation of this research is that a study of a small, select population sample under experimental conditions can only provide very limited indications about the possible influence emotions may have upon the eating patterns of different people in daily life.

For example, if you thought that researchers could be measuring how much you were eating it could make you, perhaps unconsciously, reluctant to eat as much as you normally would. Alternatively, being in this type of study could make you nervous, leading you to eat more than you normally would.

 

What did the research involve?

The researchers recruited 86 psychology students in their second year at Maastricht University in the Netherlands who received credit points for their participation. The students were predominantly female (75%) and had an average age of 21.6 years (range 19 to 43).

The students answered a series of questionnaires to assess their mental health and eating behaviours. Emotional eating was assessed using a questionnaire called the Dutch Eating Behaviour Questionnaire (DEBQ). Students were asked, ‘Do you have a desire to eat when you’re feeling lonely?’ and provided answers on a five-point Likert scale that ranged from ‘never’ to ‘very often’.

The researchers then carried out a series of experiments in a laboratory setting that aimed to change the student’s mood. Students were randomly allocated to view clips from television or films that aimed to evoke either a positive, negative or neutral mood:

• 28 students were shown two clips to evoke a positive mood. Firstly, they were shown a scene from the television series Mr Bean (which showed Mr Bean struggling to copy answers from his neighbour during an exam). The second clip was taken from the movie ‘When Harry Met Sally’ which showed the famous scene where Meg Ryan’s character simulates an orgasm in front of other diners in a restaurant.
• 28 students were shown one negative clip from the film ‘The Green Mile’, which showed an innocent man being executed.
• 30 students were shown part of a documentary about fishing to evoke a neutral mood.

The students were told to give in to the emotions the clips evoked, and were presented with bowls containing 191g of chocolate (white, milk and dark, equivalent to 1,000 kcal), 225g of salted crisps (1,229 kcal) and 225g of ketchup crisps (1,217 kcal). The bowls were weighed before and after the experiment to determine the amount of food eaten and calorie intake. 

The students were asked to assess their mood using a visual analogue scale (this is essentially a straight line – where the far left of the line represents poor mood and the far right represents very good mood) at five points during the experiment:

• before the experiment began
• immediately after watching the television or movie scenes
• 5 minutes after the experiment
• 10 minutes after the experiment
• 15 minutes after the experiment

The students were told when entering the laboratory that they were taking part in an experiment on the effect of movie clips on taste perception.

The researchers analysed their results using validated methods and adjusted the results for gender, body mass index (BMI), external eating and dietary restraint as assessed by the DEBQ, and negative mood as assessed by the Positive and Negative Affect Schedule (PANAS).

 

What were the basic results?

Overall, there was no significant difference between emotional eaters eating more than non-emotional eaters who were shown positive, negative or neutral clips.

When looking specifically at only the emotional eaters:

• those shown the positive mood-inducing scenes significantly increased their intake of food compared to those shown the neutral mood-inducing scenes
• there was no difference in food intake between students shown negative mood-inducing scenes and those shown neutral or positive mood-inducing scenes

 

How did the researchers interpret the results?

The researchers concluded that self-reported emotional eaters respond in a different way to emotions than non-emotional eaters. They say that emotional eaters ate more in a positive mood compared to a neutral mood, whereas non-emotional eaters ate about the same amount in both conditions.

In discussing the results, the researchers say the findings could be of value for the treatment of obesity.

 

Conclusion

Overall, this small study provides very limited evidence to suggest emotional eaters eat more when feeling in a positive mood. There are several limitations to this study, some of which are noted by the researchers. These include the facts that:

• the laboratory setting may not be an appropriate setting to test emotional eating with different mood feelings. It is possible that students felt uncomfortable in this setting and limited their food intake as they were being watched
• the students were told they were partaking in an experiment of taste perceptions, so may have been inclined to eat more than they normally would have because of what they were told the study was looking at
• no hunger measurements were taken during the study and how hungry each student was could have greatly affected the results
• there was no group included in the study that did not eat, so it is not possible to say from the findings that the changes in mood were due to food intake
• all of the participants were students, so findings may not be the same as if the same experiments were carried out in different groups who report being emotional eaters

To draw firmer conclusions about the effects of mood on emotional eating, larger studies of different groups are required that carry out experiments in more natural environments. 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Forget comfort eating - could happiness be the reason you're piling on the pounds? Mail Online, May 13 2013

Links To Science

Bongers P, Jansen A, Havvermans R, et al. Happy eating: The underestimated role of overeating in a positive mood. Appetite. Published online April 10 2013

 

‘WHO warns that a deadly novel coronavirus could be passed from person to person’, The Independent reports.

The news – featured in much of the media – is based on the latest ‘state of play’ advice from the World Health Organization (WHO) on the novel coronavirus (nCV).

nCV, which is genetically similar to the SARS virus, was first reported in the autumn of 2012 and appears to have originated in the Middle East.

Initial symptoms of nCV are similar to a severe case of the flu and include:

• fever
• cough
• shortness of breath
• breathing difficulties

Unlike flu, nCV is thought to have a high risk of causing serious, life-threatening, complications such as pneumonia and kidney failure.

 

What have the WHO said about nCV?

The WHO has confirmed that as of May 12 2013 there have been 34 confirmed cases – the majority of which occurred in Saudi Arabia.

The current thinking is that the virus mainly affects people who are already ill and have a weakened immune system.

 

How does nCV compare to SARS?

Despite nCV being similar to SARS (both come from the coronavirus ‘family’ of viruses) there are important differences between the two.

The bad news is that nCV appears to be much more deadly than SARS. Of the 34 people who have contracted it, 18 have died. Resulting in a death rate (or in medical terms, a case fatality rate) of around 52%.

The good news is that nCV seems to be far less contagious than SARS.

From the available evidence, it seems that nCV can only spread from person to person if prolonged close physical contact takes place. In other words, you may catch it if you share a home with an infected person, but not if you share a bus or an airplane.

While remaining vigilant to any potential threat, the WHO does not consider nCV to pose the same kind of potential threat as SARS or swine flu.

 

What is being done to counter the threat of nCV?

Global research efforts into nCV are being lead by the Kingdom of Saudi Arabia. It is currently in the process of establishing surveillance systems to track any further spread of infection.

Saudi health officials are also trying to establish the source of the virus and how it spreads.

 

Is there any treatment for nCV?

A recent study found that two anti-viral drugs, ribavirin and interferon-alpha 2b, can help slow the replication of the virus in human cells. This may potentially help reduce the risk of complications such as kidney failure.

However, there is currently no effective vaccine for nCV.

 

Is there any threat to people in the UK?

Based on the current evidence, the threat to people living in the UK is thought to be minimal.

One issue of concern is that visitors to Saudi Arabia during the Hajj in October could contract the infection.

This risk should be reduced if you take some common-sense precautions, such as:

• washing your hands frequently
• cover your mouth and nose when you sneeze or cough
• avoid sharing food, drink and utensils
• regularly clean surfaces with disinfectant

Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

New coronavirus can spread between humans, says WHO official. The Guardian, May 13 2013

WHO says new coronavirus may be passed person to person. BBC News. May 12 2013

WHO warns that deadly novel coronavirus could be passed from person to person. The Independent, May 13 2013

Coronavirus: Infection 'Spreads Between People'. Sky News, May 13 2013

Second French coronavirus case. ITV News, May 13 2013 

'Redheads are at increased risk of skin cancer even if they don't spend time in the sun,' is the headline on the Mail Online website.

The story refers to a discussion piece in a journal that outlines theories about the results of some animal experiments. This research involved mice genetically engineered to have red fur and predisposed to develop melanoma.

Although exposure to ultraviolet (UV) light is known to be a major risk factor for melanomas, the researchers found that genetically engineered mice with red fur still had a high risk of developing melanomas even without UV exposure.

The article discusses potential explanations for why this could be the case, and these theories now need to be tested to see if they are correct.

It is not yet clear how well these animal studies represent what happens in people with red hair. It would be very difficult to test this directly, as keeping people completely away from sunlight would be impractical and potentially unethical.

UV light exposure is known to increase the risk of melanoma in redheads and non-redheads alike. It is important that people with red hair should continue to use sensible precautions to avoid excessive UV exposure and sunburn, despite this news.

 

Where did the story come from?

The article was written by researchers from the Cutaneous Biology Research Center at Massachusetts General Hospital in the US.

No sources of funding for the article were reported. It was published as an "Ideas and Speculations" article in the journal BioEssays. These pieces are described as "creative thinking and predictions on open questions and recent developments in biology".

It is not clear whether the article is peer-reviewed.

The news is based on an article by researchers that presents possible explanations for their previous finding that genetically engineered mice with red fur and a predisposition to melanoma develop this cancer even without UV exposure.

Some of the Mail Online reporting suggests that the findings of this research are more conclusive than is possible to say at this stage: "Scientists have discovered that the production of red hair pigment causes an increased risk of melanoma".

However, the BioEssays article was only presenting possible explanations for observations from animal experiments. It was not claiming to have definitive proof that these findings apply to humans.

 

What kind of article was this?

This was an article discussing the potential link between the red pigment in red hair and skin cancer.

People with red hair and fair skin are known to be at greater risk of getting melanoma, the least common but most serious form of skin cancer, which is responsible for around two thousand deaths a year in the UK.

In general, it is thought that redheads' pale skin makes them more susceptible to UV damage from the sun's rays.

However, the authors of the article say that a recent study from their lab suggests that the pigment that causes hair to turn red (pheomelanin) could itself be linked to the increased risk of cancer, even without UV exposure.

In their article, the authors discuss two possible ways in which the red pigment in red hair might increase the risk of cancer. These preliminary ideas – or hypotheses – are based on previous research and a general understanding of human and cancer biology.

A hypothesis is a possible explanation of why something that researchers have observed might happen. Researchers design experiments to test whether their hypothesis is correct. This process is fundamental to the scientific method.

 

What did the article say?

The researchers first describe how the red colour in red hair is made, and discuss the results of their recent study before going on to present their hypotheses.

Specific cells in the skin called melanocytes make two kinds of pigment – a brown pigment called eumelanin and a red-orange pigment called pheomelanin. A biochemical process within cells determines how much of each pigment is made.

This process involves a protein called MC1R, which influences the switch between the production of these pigments based on the strength of the signal it sends to the cell and whether the cell has enough of the amino acid cysteine.

In redheads, variations in the gene for the MC1R protein means that it sends weak signals. This means that the cells' stores of cysteine are usually enough for it to favour producing the red/orange pigment pheomelanin.

The researchers recently carried out a study where they introduced a genetic mutation commonly found in melanoma cells into the melanocytes of mice. When they also introduced a genetic mutation into these mice that inactivated the MC1R protein, the mice had red fur and developed melanoma, even without UV exposure. If they introduced another genetic mutation that stopped pigment being made altogether, the mice were albino but they did not develop melanoma.

This led the researchers to suspect that the red pigment pheomelanin could be itself increasing the risk of melanoma. Their research also found that the mice with red fur had more damage to their skin cell DNA caused by very reactive chemicals called free radicals. Free radicals can cause damage to cells at a molecular level.

The researchers do not yet know how the red pigment might be linked with the free radical DNA damage that can increase the risk of melanoma. However, they have presented two hypotheses:

The first hypothesis

The researchers' first hypothesis was that the red pigment itself might generate more free radicals, and that these cause DNA damage that could lead to melanoma. They say that the red pigment is already known to make free radicals when it is exposed to UVA light, but it may be able to do this without UVA light. These free radicals could potentially:

• damage DNA directly
• damage its building blocks, or
• use up the cell's stores of antioxidants, making it more vulnerable to damage by other free radicals

The researchers also discuss in detail the biochemical ways in which the red pigment might generate free radicals.

The second hypothesis

The second hypothesis was that the process of making the red pigment might use up the cell's stores of antioxidants, rather than the red pigment itself. This might make the cells more vulnerable to damage by other free radicals.

They say that the amino acid cysteine used in making the red pigment is also found in the most important antioxidant in the cell, glutathione. If cysteine is used to make the red pigment, this might reduce the cell's ability to make this antioxidant.

The researchers report that red-haired wild boars have been found to have less glutathione in their muscles. However, they acknowledge that it is not possible to say from this whether there is less glutathione due to free radicals from the red pigment itself or the making of the red pigment.

 

What were the researchers' conclusions?

The researchers presented two hypotheses that could explain how the red skin and hair pigment pheomelanin could increase the risk of the skin cancer melanoma.

They say that their two proposed methods could both be occurring, and that more research could help identify how redheads can reduce their risk of melanoma.

 

Conclusion

The researchers' article discusses potential ways in which the red pigment found in the cells of people with red hair might increase the risk of melanoma, the most serious form of skin cancer. It is not a standard report of a research study, but the authors put forward potential explanations for their previous research findings. These now need to be tested to see if they are correct.

The researchers' previous research found that mice genetically engineered to be predisposed to melanoma and red fur developed melanomas even without UV exposure. It is not clear to what extent these genetically engineered mice represent what happens in humans.

It would be very challenging to test this – keeping people completely away from UV light would not be feasible or ethical, as we need some sun exposure to make vitamin D, which is needed to make and maintain strong bones. For this reason, research in mice can be very helpful.

It is important that redheads do not take this news as a reason not to protect themselves from the effects of the sun. We already know that UV light exposure increases the risk of melanoma in people regardless of hair colour. People with red hair should continue to use sensible precautions to avoid excessive UV exposure and sunburn.

Read more about reducing your melanoma risk. 

 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Redheads are at increased risk of skin cancer even if they don't spend time in the sun. Mail Online, May 10 2013

Links To Science

Morgan AM, Lo J, Fisher DE. How does pheomelanin synthesis contribute to melanomagenesis? BioEssays. Published online May 7 2013

Teaching your child good eating skills

Children with special needs can take longer to learn how to eat independently. Read these top tips for mealtimes.

'Learning how to eat neatly is crucial to helping our children to integrate'

 

Deborah French

Eating a meal can be particularly challenging for children who have disabilities. A lack of fine motor skills (like finding it hard to hold a fork), sensory restrictions (like being paralysed or unable to see) and co-ordination difficulties are some of the many reasons that may delay the learning process. This can be frustrating for you and your child.

Author Deborah French has four children, two of whom have special needs. Her eldest daughter, Amariah, has Down syndrome and her son, Henry, has autism spectrum disorder. "Socialising with others generally includes eating together," she says. "So learning how to eat neatly is crucial to helping our children to integrate."

Deborah, who also runs cookery classes for children with special needs, came to realise that nagging her children about their table manners wasn't working. Instead, she developed practical solutions to help them learn, with rapid results. 

Deborah's top tips for happy mealtimes
1.  Be patient

"When stress or frustration controls your reactions while trying to teach your child, they will reflect your mood and act accordingly. They will fear your reaction to their mistakes and as a result will not be able to give their best efforts. Give instructions calmly, with positive reinforcement."

2.  Invest in a funky child-sized apron

"As your child gets older, even though it may still be necessary for them to wear a bib to protect their clothing, this can also be demoralising and embarrassing in front of other family members or peers. An apron is more discreet and will help eliminate any negative feelings your child may harbour before mealtime has even begun."

3.  Encourage your child to help lay the table

"Irrespective of the nature of your child's disability, take the time to involve them in preparing the table for dinner. Even watching you collect cutlery, cups and napkins helps your child to feel they have participated. During this process talk your child through what you are doing and why. For example: 'We use a fork to pick up pieces of food on our plate instead of our fingers. That way the fork gets dirty and not our fingers'."

4.  Use heavy cutlery and solid crockery

"As parents, we instinctively opt for plastic or disposable utensils to avoid breakage and to make cleaning up easier. But for a child who has either low or high muscle tone or difficulty with their fine motor skills, a plastic fork simply feels like air. These children need to be able to feel the cutlery they are holding. The same is true for plastic plates and cups, which are unstable and easily knocked over. Solid cutlery and crockery will make it easier to teach your child how to eat."

Find out about other eating equipment that can help.

5.  Take the time to eat with your child

"If you eat your evening meal later than your child, compromise by ensuring that during your child's mealtime, you too are seated at the table. Even if you enjoy your coffee or a smaller version of what your child is eating, they will be encouraged by your presence. You can then talk about your food and how you eat with your cutlery. Take note of how quickly your child imitates your actions."

6.  Keep a standalone mirror and wet cloth handy

"The most effective way of teaching self-awareness to a child is to let them view themselves. Even as adults, how often after enjoying a meal with friends have we been unaware that a chunk of food, usually green in colour, has become wedged between our front teeth?

"Apply this theory when helping your child to understand food residue on their face after eating. Before they leave the table, place the mirror in front of them and encourage them to look at their reflection and clean themselves using the wet cloth."

7. Encourage your child to clear their place

"Again, irrespective of your child's disability, teach them how to participate in the cleaning up process after eating according to their ability. This may involve them handing their plate to you or taking it to the side to be washed; alternatively wiping their place clean as best they can. Any level of participation helps to develop their self-awareness and obligations at mealtimes.

"It's important to remember that everyone likes to feel valued and needed. When you give your child responsibilities, they feel important to you and the family. This in turn boosts their self-confidence and speeds up the learning process."

Read our interview with Deborah about parenting children with special needs.

Specialist eating and drinking equipment

To help your child learn good eating skills, you may find that specialist eating or drinking equipment will make a real difference. The Caroline Walker Trust, a food charity, recommends a number of helpful aids to eating that parents of children with learning disabilities may find useful for their child.

These include:

• Different shaped cups, with one or two handles, of different weights, materials, transparencies and designs. The cups should be designed not to shatter or break if they are bitten.
• A transparent cup can be helpful when helping someone to drink, because you can see how much liquid they're taking.
• Cutlery of differing shapes, sizes, depths and materials. Again, the cutlery shouldn't shatter if it is bitten. Solid plastic cutlery or plastic-coated metal might be better for people who have a bite reflex when cutlery is placed in their mouth. Shorter-handled cutlery is easier to manage and handgrips or irregularly shaped handles may help someone in using a utensil.
• Plates and bowls that do not slip, have higher sides to prevent spillage, or are angled to make access to food easier.
• Insulated crockery that keeps food hot if mealtimes are lengthy.
• Non-slip mats that support crockery.
• Straws, which can help those with a weaker suck and can have different widths.
• Feeding systems that deliver food to the diner's mouth through, for example, a rotating plate and a mechanical or electronically controlled spoon. Some systems are powered, others are hand- or foot-operated.

For more information and details of suppliers, read this factsheet from Disabled Living Foundation.

The Daily Mail claims a study has found a ‘Vampire treatment that rejuvenates ageing hearts’.

But before you go to grab your cloak and false pointy teeth, the research it reports on was actually in mice.

The study looked at possible ways to treat age-related cardiac hypertrophy – when the muscles of the heart become thickened, leading to a corresponding decrease in functioning ability.

Researchers joined the blood circulation of pairs of young and old mice. And one month later they looked at the resulting effects on the animal’s heart muscle.

They found that old mice who shared blood with young mice had reduced levels of cardiac hypertrophy compared to similar mice not treated with ‘young blood’.

The researchers suggest that this could be due to a chemical called growth differentiation factor 11 (GDF-11), which is high in the blood of young mice, and could help repair tissue damage.

An obvious limitation of the study is that results in mice do not always apply to humans. In humans, heart failure is where the heart cannot pump enough blood to meet the body’s needs, and this can have many different causes.

Thickening of the heart muscle is just one type of heart failure, which can be caused by high blood pressure, but can also be an inherited condition.

It is difficult to know to what extent the same growth factor could be responsible for heart muscle thickening in people with this type of heart failure. Also, its relevance – if any – to other types of heart failure (for example due to muscle damage following heart attack, due to an abnormal heart rhythm, or due to heart valve disease) is even less clear.

The findings are of scientific interest but are not going to miraculously reverse the entire disease process of heart failure in humans.

 

Where did the story come from?

The study was carried out by researchers from the Harvard Stem Institute and other research institutes in the US, and was funded by the American Heart Association, Glenn Foundation and National Institute of Health.

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

The Mail over-interprets the findings from this animal research. It is also unclear where the sub-headline ‘could be ready for use in clinical trials within 4 years’ has come from.

 

What kind of research was this?

The researchers say that loss of normal heart function leading to heart failure is one of the most debilitating diseases of ageing.

In particular, they discuss the type of heart failure that is often caused by high blood pressure, where the heart muscle becomes thickened and stiff (cardiac hypertrophy) so the heart chambers cannot dilate so well and fill with blood. This is known as ‘diastolic’ heart failure, as it relates to a problem when the heart is trying to refill with blood (diastolic), rather than contract (systolic).

The researchers suggest that animal studies have previously shown that chemicals circulating in the body of a young animal have been shown to restore function to the skeletal muscle of an old animal.

This process was done by what is called ‘parabiosis’ where two animals are surgically joined and so share their blood circulation.

The current animal study aimed to use a parabiosis model to try and reverse the thickening of heart muscle.

 

What did the research involve?

For their experiments the researchers used old mice (aged about two years) and young mice (aged two months). They used parabiosis to surgically join the blood circulation of pairs of old and young mice.

After they had been joined for one month, the researchers analysed samples from the heart muscle of the mouse pairs.

For comparison they also looked at the effect of shared blood circulation between young-young and old-old mice pairs.

They also compared with a ‘sham’ parabiosis where they surgically joined the tissue of pairs of young and old mice (at the knee joint), but without sharing their circulation.

To look into what could be the cause of any observed effects upon heart muscle, they also intensively monitored the blood pressure of mice while they were joined, and looking at levels of different chemicals in the blood of young and old mice.

 

What were the basic results?

The researchers found that the effect of surgically combining the circulation of the young and old mice pairs was clearly visible. The hearts of old mice that had their circulation joined to a young mouse looked much smaller and were less heavy than those of old mice who had been joined to old mice.

When they looked at the heart muscle cells under the microscope they found that the cells of old mice joined to young mice had a significantly smaller cross-sectional area than those of old mice joined to old mice, or those in the ‘sham’ parabiosis condition where their circulation hadn’t been joined to the young mice.

The effect of parabiosis on heart muscle cells was similar in both male and female old mice.

Meanwhile, the heart muscle cells of the young mice were no different in any of their three combinations (young-young, young-old or sham parabiosis).

They also carried out a number of experiments into what could be having the observed effects.

They ruled out that the smaller heart muscle cells of the old mice could have been caused by a reduction in their blood pressure. This was because all of the joined mice actually showed increases in their blood pressure compared to before they were joined. 

They also considered the possibility that the changes could be due to behavioural change from the physical constraint of being joined to another mouse, rather than any effect of the shared blood.

However, if this was the case then it would be expected the heart muscles of old mice in the sham parabiosis would also have decreased in size, and they had not.

Overall, the researchers considered the effects could be due to some chemical in the shared circulation. Separately analysing the blood from young and old mice they found that several components of their blood are different. In particular, levels of a molecule called growth differentiation factor 11 (GDF-11) are found to be lower in the blood of older mice.

When they went on to treat the heart muscle cells from rats with GDF-11 in the laboratory, they found that GDF-11 prevents the thickening of the heart cells. In a further experiment involving older female mice, the hearts of a group injected with GDF-11 were significantly lighter and the cells were significantly smaller than those of a group injected with a placebo.

 

How did the researchers interpret the results?

The researchers’ animal experiments suggest that the thickening of heart muscle can be influenced at least in part by certain chemicals circulating in the blood. They suggest that GDF-11 could reverse thickening of heart muscle, and so conclude that ‘at least one component of age-related diastolic heart failure is hormonal in nature and reversible’.

 

Conclusion

This study finds that sharing the circulation of young and old mice appears to reverse the age-related thickening of heart muscle cells in the older animal, and it seems this could be due to a certain growth factor in the blood of the young animal. The findings will be of scientific interest, and further our understanding of the processes of heart ageing in animals.

However, the findings have very limited direct relevance to humans, and do not suggest a new treatment for heart failure.

It is also certainly unknown at this point whether increasing levels of this factor in the blood of people with this type of heart failure would somehow reverse the entire disease process. Its relevance to other types of heart failure not associated with thickened heart muscle is even less clear.

Even if further research were to demonstrate that this growth factor could have a potential role in heart failure treatments in humans; joining the circulation of young people with those with heart failure in the manner used in this study is clearly not a possibility.

If the chemical were to be extracted from donor blood, or synthetically produced, there would still be many safety issues to considered, even if the treatment were found to have an effect.

Overall the research does not suggest a new treatment for heart failure in humans, though it may represent the first step towards a possible treatment at some point at the future.

However, due to the uncertainties discussed above it is impossible to estimate the likelihood of this prediction becoming fact.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

The vampire treatment that 'rejuvenates' ageing hearts: Dose of young blood can reverse life-threatening thickening of organ. Daily Mail, May 10 2013

Links To Science

Loffredo FS, Steinhauser ML, Jay SM, et al. Growth Differentiation Factor 11 Is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy. Cell. Published online May 9 2013

‘Children's exposure to traffic pollution could…lead to diabetes' BBC News explains, reporting on a German study.

The study included around 400 children aged 10. Researchers looked at measures of air pollution and proximity to the nearest road at the address each child had lived as a baby.

They also measured each child’s blood sugar and insulin levels.

The second measurement allowed them to calculate each child’s level of insulin resistance – to what extent the cells of the body fail to respond to the hormone insulin (which the body uses to convert blood sugar into energy).

Once insulin resistance reaches a certain level, the symptoms of type 2 diabetes can develop.

The researchers found an association between exposure to air pollution and increased levels of insulin resistance.

However, an association is not the same as proof of a direct causal effect. Living near a busy road would usually imply that a child lives in an urban environment. So there could be a range of environmental factors, other than air pollution, affecting levels of insulin resistance (as well as a wide-range of other possible individual genetic and health-related factors).

The study also does not tell us whether any insulin resistance measured in the child actually had any clinical significance and would lead to a child developing diabetes in later life.

Due to these limitations, further studies in other population samples would be useful.

 

Where did the story come from?

The study was carried out by researchers from German Center for Diabetes Research and other institutions in Germany, and was funded by German Federal Ministry of Education and Research, and The European Community’s Seventh Framework Programme.

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

The quality of the reporting on the study in the UK media is mixed. The BBC News headline gives an accurate representation of the current study as it includes the all-important word ‘may’. However, the Mail Online’s headline linking air pollution to a child’s risk of developing diabetes may be misleading.

This study has many limitations, not least, that increased levels of insulin resistance in childhood, while a risk factor, is not a guarantee that a child will grow up to develop type 2 diabetes.

Also, the association between childhood and diabetes may confuse some readers into thinking that the study was looking at type 1 diabetes – the form of the condition that normally begins in childhood and where the body’s own immune system destroys the insulin-producing cells, so the person is not able to produce any insulin at all.

 

What kind of research was this?

This was a cohort study looking at whether there was an association between air pollution and insulin resistance.

The researchers say that previous research has shown that traffic and air pollution may increase the risk of diseases affecting the lungs and cardiovascular system.

This is speculated to be due to exposure to pollution that may trigger oxidative stress (a disruption in the body’s ability to repair cellular damage). Pollution could also lead to low levels of inflammation in certain cells of the immune system and those lining the blood vessels.

Animal studies have also suggested that pollution may make cells of the body more resistant to the action of insulin – the hormone released from the pancreas that helps the body to make use of the glucose in the blood.

The researchers say that no study has yet looked at whether traffic-related air pollution can lead to insulin resistance in school-aged children. This German cohort study aimed to look at the relationship between particulate matter in the air and proximity to the nearest road at the child’s birth address, and the child’s insulin resistance when they reached the age of 10.

The limitations of such a study include it being difficult to conclude that the air pollution at the birth address has directly caused the child’s insulin resistance at age 10.

There may be many other genetic, environmental and health-related factors involved.

The study also does not tell us whether any insulin resistance measured in the child has any clinical significance, and whether it is related to later development of type 2 diabetes in adult life.

 

What did the research involve?

The researchers included sub-groups of 10-year-old children taking part in two separate birth cohorts in Munich, South Germany and Wesel, West Germany:

• The German Infant Study enrolled almost 6,000 healthy newborns and was a trial looking at the effect of a hypoallergenic infant formulae on a child’s risk of allergy (in addition to looking at other environmental and genetic influences).
• The Lifestyle-Related Factors study included just over 3,000 healthy newborns and was an observational study looking at the effect of lifestyle factors on the child’s immune system and risk of allergies.

The present study included 397 children randomly sampled from these two cohorts (though 82% came from the Munich cohort) who had blood samples taken for insulin and glucose measurement at age 10, and who had information available for air pollution exposure at the time they were born.

To measure pollution exposure at the birth address, the researchers used models to estimate levels of:

• nitrogen dioxide (N02)
• particulate matter of less than 2.5 micrometres in diameter
• particulate matter of less than 10 micrometres in diameter

Particulate matter is the term for a mixture of solid particles and liquid droplets found in the air.

Measurements were taken at selected monitoring sites on three occasions over 14 consecutive days, and in different seasons.

When conducting their analyses, factors taken into account at each monitoring site were location, surrounding land use, population density and traffic patterns.

Other factors taken into account that could have an influence on the results (confounders) related to the individual child included:

• parental education (used as an indicator of socioeconomic status)
• exposure to second-hand smoke
• height and weight at age 10
• whether they had started to go through puberty

 

What were the basic results?

There were no differences between children in the two cohorts, except that those from Wesel were more likely to have been exposed to second-hand smoke and to be of lower socioeconomic status. Pollutant levels were also higher in Wesel than Munich.

After adjustment for all potential study-centre and child-related confounding factors, each two-point standard deviation increase in nitrogen dioxide levels was associated with a 15.8% increase in insulin resistance (95% confidence interval (CI) 3.8 to 29.1).

Each two-point standard deviation increase in particulate matter of less than 10 micrometres in diameter, was associated with a 17.5% increase in insulin resistance (95% CI 1.9 to 35.6). There was no significant association with particulate matter of less than 2.5 micrometres in diameter.

Distance to the nearest road, as would be expected, was significantly associated with pollutant levels (shorter distance equalled higher levels of nitrogen dioxide and particulate matter). Shorter distance to the road was also associated with increased insulin resistance (each 500 metre decrease in distance to road increased insulin resistance by 6.7%, 95% CI 0.3 to 13.5).

The researchers found that the link between pollution levels and insulin resistance was stronger in children who had not moved from their birth address by age 10.

 

How did the researchers interpret the results?

The researchers conclude that traffic-related air pollution may increase the risk of insulin resistance in children. They say that the associations observed may have important public health implications despite the small effect seen.

 

Conclusion

This German study looked at the relationship between air pollution and proximity to the nearest road at the child’s birth address, and the child’s insulin resistance when they were aged 10. Though links were found between increasing levels of nitrogen dioxide and levels of particles less than 10 micrometres in diameter and increasing insulin levels at age 10, there are important limitations to bear in mind:

• Though the researchers have attempted to adjust for many potential confounders, it is difficult to conclude that the air pollution at the birth address has directly caused the child’s insulin resistance at age 10, when there may be many other genetic, environmental and health-related factors involved.
• The confidence intervals around the increase in insulin resistance with each incremental increase in pollutant levels are very wide. For example, each increase in particles of less than 10 micrometres was associated with a 17.5% increase in insulin resistance, but the actual increase could lie anywhere between 1.9% and 35.6%. This means we can have less confidence in the reliability of these estimates.
• The study does not tell us whether any insulin resistance measured in the child has any clinical significance, and whether it will be related to higher risk of developing type 2 diabetes in adult life.
• Also, as mentioned above, the news headlines should not be wrongly interpreted to mean that a child has increased risk of developing type 1 diabetes – the type that readers may associate with start in childhood.  
• Lastly, the results are based on only a relatively small sample of children from two regions in Germany. Studies of much larger samples from different countries would give more weight to any observations.

Overall, this study cannot prove that air pollution increases a child’s risk of developing diabetes, only that there may be an association with insulin resistance.

As it is unlikely that we are going to live in a world free from air pollution anytime soon, the most effective way of reducing your child’s diabetes risk is to encourage them to take plenty of exercise and eat a healthy diet. These types of good habits in childhood often carry on into adulthood meaning that your child is more likely to maintain a healthy weight – a proven method of reducing type 2 diabetes risk.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Diabetes: dirty air 'may raise' insulin resistance risk. BBC News, May 10 2013

Why living near a busy road could be dangerous for your child's health: Traffic pollution linked to diabetes risk in children. Mail Online, May 10 2013

Air pollution could raise diabetes risk. The Daily Telegraph, May 10 2013

Links To Science

Thiering E, Cyrys J, Kratzsch J, et al.  Long-term exposure to traffic-related air pollution and insulin resistance in children: results from the GINIplus and LISAplus birth cohorts (PDF, 278KB). Published online May 9 2013

Older people with a history of smoking heavily should be offered annual low-dose CT scans to screen for lung cancer according to new US guidelines reported by the Reuters news agency.

These guidelines recommend that annual CT (computerised tomography) scans should be offered to current or former smokers aged 55-74 who have smoked 20 cigarettes a day for 30 years or more. However, screening should only be offered in facilities that can provide high standards of clinical care, the guidelines say.

Screening means testing everyone in a particular population for early stages of a disease before they have any symptoms. In the UK, screening is already in place for some cancers, such as bowel and breast cancer, but lung cancer is not currently screened for.

Mass-population screening, such as that carried out for bowel and breast cancer, is unfeasible for lung cancer because of the cost. One study has estimated that to save one lung cancer death would cost around $250,000. However, focusing resources on high-risk groups, as recommended in the US guidelines, is a more cost-efficient approach.

Heavy smokers are particularly at risk of developing lung cancer because cigarettes contain a number of cancer-causing substances (carcinogens).

Screening could be of particular use in heavy smokers because the symptoms of lung cancer often do not develop until the cancer is at an advanced stage. This makes treatment of the condition challenging.

The US guidelines point to research that suggests that these recommendations could cut rates of lung cancer deaths in smokers or ex-smokers by around 20%.

Who produced the guidelines?

The guidelines on screening have been produced by the American College of Chest Physicians.

They form part of comprehensive guidance for US doctors on the diagnosis and management of lung cancer.

 

What are the pros and cons of CT screening for lung cancer?

An obvious pro of CT screening for lung cancer is that it could cut lung cancer deaths. Lung cancer is one of the leading preventable causes of death in the UK and around the world.

However, no screening technique is without risk.

One risk, often overlooked, is the danger of false positives. This is where the screening test detects a sign that turns out to be harmless. In cases of lung cancer this would usually be when a lesion (abnormality in tissue) is detected, but the lesion turns out to be non-cancerous (benign).

In the general population, the rates of false positives for screening could be unacceptably high. For example, the authors say that more than 90% of nodules found by CT in the studies they looked at turned out to be benign.

This figure drops dramatically for high-risk groups, such as smokers, but one study quoted in the guidelines estimated that the false positive rate in high-risk groups could still be around one in four.

While CT scans themselves have a very low risk of causing complications, other more invasive procedures used to confirm or discount a diagnosis of lung cancer do not.

Screening could subject people to unnecessary tests that turn out to cause them harm, and there is still the possibility of false negatives. No matter how good a test is, it is likely that some cancers will be missed, leading to false reassurance.

There is also risk from radiation exposure. Although one low-dose CT scan involves only a small amount of radiation, if further imaging is required it can rapidly drive up the radiation dose patients receive.

 

What evidence did the guidelines look at?

The guidelines looked at evidence on the effectiveness of different methods of screening for lung cancer. These were:

• chest X-ray
• examining mucus from the airways for abnormal cells (sputum cytology)
• low-dose CT screening

The guidelines’ authors conducted a systematic review of randomised controlled trials (RCTs) and observational studies looking at the effectiveness of the different methods of screening. Most of the studies focused on middle-aged or older people with a history of smoking and, therefore, at high risk of lung cancer. In particular, they examined the death rates from lung cancer among people at high risk who were screened by low-dose CT, X-ray or sputum analysis.

The review also looked at the potential downsides of screening, including:

• the death rates, or complications resulting from further investigations of any suspected cancers, in people who had been screened
• the death rates from radiation exposure of people who had low-dose CT screening
• the rate of surgery for benign disease

 

What were the results?

The main finding came from one large RCT (the National Lung Screening Trial), involving more than 53,000 participants who had three annual rounds of screening. This trial showed a 20% reduction in the rate of death from lung cancer in people who were screened with low-dose CT, compared with those screened using a chest X-ray (relative risk 0.80, 95% confidence interval 0.73 to 0.93).

This trial also found that low-dose CT posed “few harms” when carried out in the context of a structured programme of care. The risk of death or major complications from further investigations into harmless conditions was between 4.1 and 4.5 per 10,000.

Other research found that using chest X-rays or sputum analysis did not reduce lung cancer deaths.

 

What recommendations on screening did the guidelines make?

The guidelines recommend that:

• Smokers and former smokers aged 55-74 who have smoked for 30 pack-years or more and who either continue to smoke or have quit within the past 15 years should be offered annual screening with low-dose CT.
• This should only be done in settings that can deliver the same standard of care provided to participants in the big lung cancer screening trial.
• CT screening should not be offered to people who do not meet the above criteria, say the guidelines. For example, if they are younger or older or have smoked less, since benefits outside the high-risk group are uncertain.
• Screening for lung cancer using X-rays or sputum analysis is not recommended.

 

Links To The Headlines

Older, heavy smokers should get CT scan for lung cancer, doctors group advises. Reuters, May 2013

Links To Science

Detterbeck FC, Mazzone PJ, Naidich DP, et al. Screening for Lung Cancer: Diagnosis and Management of Lung Cancer, 3rd ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. Published online May 2013

"Middle class professionals… are the country’s biggest problem drinkers," is the stark and somewhat misleading claim in The Daily Telegraph, with similar claims appearing across the UK media.

The story is based on a study looking at just 49 ‘white collar’ people’s attitudes towards alcohol consumption. The study involved interviewing five small groups in a ‘focus group’ setting.

Researchers found that among these small groups:

• problem drinking was something that was seen to happen to other people – such as teenagers in city centres or binge drinkers in pubs
• if regular alcohol consumption did not significantly disrupt day-to-day functioning (such as in work or parenting skills) or lower social standards, then it was acceptable and harm-free
• regular ‘controlled’ drinking at home (for example as a way to relax), was also acceptable and harm-free 

It is important to note the study was very small and these findings may not be applicable to other countries or cultures. However, the attitudes reported suggest that key messages of some public health campaigns about reducing harm from alcohol are going unheard or being ignored.

It is not just binge drinking that can damage your body; regularly drinking above the recommended limits – whatever the social context – can also be harmful.

 

Where did the story come from?

The study was carried out by researchers from Newcastle University and the University of Sunderland, UK and was funded by the Public Health NHS Directorate Stockton-on-Tees.

It was published in the peer-reviewed journal, BMC Public Health and made freely available to read on an open-access basis.

The story was picked up widely in the media. While the findings of the study were reported accurately, the tone of some of the reporting was slightly confusing.

It appears that some of the media fail to understand the nature and implication of this method of qualitative research. Such studies can provide useful insights into people’s attitudes and behaviours; however, they cannot provide hard statistical evidence. So headlines such as the Daily Express’s “Middle class ‘drink more than teens’” are misleading, as are sweeping statements like the Telegraph’s “Middle class professionals who drink at home are the country’s biggest problem drinkers”.

 

What kind of research was this?

This was a qualitative study looking at the drinking habits of a small number of adult ‘white collar workers’ in the UK. The study explored their views on alcohol use, how public health messages about alcohol are perceived, and the role alcohol plays in the workers' personal and professional lives.

The researchers say that little is known about white collar workers’ views on drinking alcohol.

Qualitative research uses individual in-depth interviews, focus groups or questionnaires to collect, analyse and interpret data on people’s behaviours and the reasons behind them. Typically, the number of participants is relatively small, but the transcripts from interviews and focus groups provide a large amount of data. Such studies report on meanings, concepts, definitions, metaphors, characteristics, symbols, and descriptions. As such, their conclusions can be more subjective than quantitative research, as questions are often exploratory and open-ended.

 

What did the research involve?

The researchers carried out interviews with 49 volunteers (17 male, 32 female) from five workplaces in the UK. The participants were aged between 21 and 55 years and were all working full time (at least 35 hours per week). To be included, participants had to be working in managerial, supervisory, clerical or other professional roles, referred to by the researchers as ‘white collar workers’.

Group interviews (focus groups) were carried out by the researchers at each of the five workplaces during lunch breaks. The five focus groups were made up of workers from:

• local government offices (focus groups one and two)
• a private sector chemical storage company (focus group three)
• a prison (focus group four)
• a tax office (focus group five)

The group interviews lasted between 45 and 75 minutes and were led by two researchers. The researchers used open-ended questions loosely based around four main themes related to drinking alcohol:

• lifestyle behaviours
• drinking at home
• variations in drinking during the week
• the effect of drinking on work

The researchers say areas of agreement and disagreement were explored with the participants, and that questions were continually adapted depending on the flow of conversation. The participants were informed that the purpose of the research was not to find out the quantity or frequency of alcohol consumption of the volunteers. The volunteers were given a £5 voucher and lunch for their time.

The researchers then used a particular technique called ‘constant comparison’ to analyse their results and grouped findings into themes relating to views of alcohol.

 

What were the basic results?

After analysing the focus group findings, the researchers reported three main themes.

Unacceptable or problem drinking

Unacceptable or problem drinking was perceived by the volunteers as being associated with long-term, heavy or binge drinking of ‘others’. The researchers reported that the participants highlighted ‘others’ as including young people, people with complex needs, and other stereotypes. The perception of excessive drinking was associated with looks and behaviour, rather than how much they have drunk. Personal drinking was viewed as a controlled choice rather than something they ‘need to do’.

Drinking at home

Drinking at home was considered normal, convenient and a socially acceptable form of relaxation from the responsibilities of work or parenting. Volunteers reported less drinking at ‘leisure premises’ such as a bar or pub, and driving was identified as the greatest factor influencing drinking behaviours. Drinking alcohol was considered part of everyday life and not something that interferes with other parts of life or causes harm.

Effect of drinking on functioning

Ability to function at work and act responsibly were key indicators of whether drinking was within acceptable limits. So, if a person was able to maintain employment in skilled jobs, they were therefore perceived to be drinking in a way that was not considered harmful. Despite awareness of guidelines for drinking, little notice was taken by participants and there was confusion about what a ‘unit’ was, the researchers report. Public health messages were also considered to have little or no personal relevance.

The researchers say that discussions indicated that the volunteers' reported alcohol use exceeded recommended guidelines for both the amount and how often drinking occurred. Interestingly, when the ill effects of alcohol were discussed, they were reported as only in relation to coping with a hangover and the loss of valuable time while feeling unwell. More subtle, insidious adverse effects such as gradual loss of liver function did not appear to occur to the volunteers.

Finally, lunchtime drinking at work was considered a 'thing of the past' and very much taboo.

 

How did the researchers interpret the results?

The researchers say that this study helps reveal the meanings attached to alcohol use by white collar workers and identifies resistance to public health messages. They say, "these findings suggest that current public health interventions have not been effective in engaging this group who are likely to drink at unhealthy levels but be highly resistant to reducing their alcohol consumption – especially as they do not consider their use to be problematic unless it impairs their capacity to fulfil responsibilities or function at work".

They conclude by saying, "future public health messages around alcohol should be less focused upon the crime and personal safety implications of irresponsible drinking and be more sensitive to the lifestyles and long-term health of the populations they target".

They add that further research is needed to identify which factors (other than driving) would engage white collar workers to change their views and drinking behaviours.

 

Conclusion

Overall, this research provides some early findings of so-called ‘white collar’ workers' views of drinking behaviours in the UK.

Although the study was very small, with only 49 volunteers' views analysed, it is useful in determining emerging themes, and the researchers do state that there was relative consistency across the five groups. The researchers also note that ‘strong personalities’ within the group may have influenced how the other participants responded.

Research among larger groups of white collar workers is needed to draw firmer conclusions about the drinking culture in the UK. It is worth noting that these findings may not be applicable to other countries or cultures. Ethnicity, cultural identity and religious beliefs of the participants were not reported, which may have influenced how participants responded to the questions.

One important final message to stress – and one that seems to have not been grasped by the volunteers in the study – is that it is not where you drink, why you drink, or who you drink with that matters. It is how much you drink.

Regularly exceeding the recommended daily amounts for alcohol can harm your health, regardless of whether it is with three litres of strong white cider on a park bench, or a bottle of Californian merlot in front of a DVD box set. 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Middle class wine drinkers 'think they know better than health experts'. The Daily Telegraph, May 8 2013

Middle classes are 'ignoring the dangers of using casual drinking to combat stress'. Daily Mail, May 9 2013

Alcohol abuse: Concern over middle-aged middle classes using booze to relieve stress. Daily Mirror, May 8 2013

Middle class ‘drink more than teens’. Daily Express, May 9 2013

Links To Science

Ling J, Smith KE, Wilson GB, et al. The ‘other’ in patterns of drinking: A qualitative study of attitudes towards alcohol use among professional, managerial and clerical workers. BMC Public Health. Published online October 23 2012

 

The need to improve the safety of medical devices such as hip and breast implants made the headlines today. The Daily Telegraph reports that experts are calling for an end to the "secrecy" surrounding how they are regulated.

The story is based on an opinion piece published in the British Medical Journal, which calls for European data on medical devices, including their safety and any adverse effects, to be made available to the public.

A second, related, article makes the point that the regulation of medical implants, and the collection and publication of related data on patient safety, fails to match that of medications.

Collecting and publishing high quality data could help prevent widespread problems with medical implants, such as those seen with Poly Implant Prothèse (PIP) breast implants.

The PIP scandal caused global concern after it was discovered that French-made breast implants contained industrial rather than medical grade silicone.

Concerns have also been raised about metal-on-metal hip replacements wearing down sooner than had been expected, potentially causing damage to surrounding tissue.

The authors argue that EU proposals for new legislation to regulate medical devices, which are currently being debated, should include their proposals to develop systems for collecting evidence.

 

What is the problem?

The article has been written by experts from the interventional procedures advisory committee of the National Institute for Health and Care Excellence (NICE). This body looks at the evidence on medical implants and devices, as well as surgical procedures, to see if they are safe, clinically effective and provide good value for money.

The experts point out that some medical devices and surgical procedures are introduced and used by health professionals with little evidence about their safety from clinical trials or observational data. 

The term “medical devices” covers a huge range of materials, from very basic supplies, such as bandages, to extremely complex equipment, such as life-support machines.

The report says that the regulations concerning the evidence required on both efficacy and safety of new devices are less stringent than those for medicines. In many cases, data on safety and the possibility of adverse events is not routinely collected.

In addition, many medical devices are produced by small specialist firms that lack the funding and experience to conduct adequate research.

Within Europe, regulations require manufacturers to obtain a CE mark of quality for a new device. However, for the CE mark to be given, the amount of evidence needed on safety is usually small.

In contrast, the amount of evidence on patient safety needed before a new drug can legally be brought to market is huge.

The report also says that there are no legal frameworks governing the introduction of new medical or surgical procedures – whether or not they involve a new device – and the evidence on safety and effectiveness is usually poor. The reasons why the evidence is poor include lack of commercial sponsorship and the difficulties of setting up research trials.

All these factors mean that when a device or procedure starts to be used on patients, there is limited data on both its efficacy and short-term safety. “Adoption of the new procedure or device is typically driven by marketing and the enthusiasm of clinicians, rather than by evidence,” say the authors.

There is also no organised system of collecting data on devices and procedures once they are in use.

 

What recommendations does the analysis make?

The report proposes several solutions to the problem of inadequate data collection on the safety and efficacy of medical devices and procedures. These include:

• Device tracking. An efficient device-tracking mechanism (like a barcode) would make it easier to inform patients and recall devices where necessary and improve monitoring and data collection.
• Use of registers. Countries and health systems should be encouraged to use existing procedure registers (such as NICE guidance in the UK) and set up new ones where needed. The UK’s National Joint Registry is one example.
• Data linkage. New registers should be linked to routinely collected health services data, national mortality statistics and other sources of relevant information.
• Bypassing patient consent. Getting patients’ consent to use their data in registers has failed in the past. The authors suggest that where data collection is in the public interest, patient consent should not be required.
• International collaboration. Sharing data between countries may help.
• Post-market surveillance. Data collected by device manufacturers could provide useful information about the use of products worldwide.
• Adopting a framework for collecting evidence on new procedures. The authors say there is now a well recognised framework for generating evidence on any new procedure, from its first use into the long-term.

 

What happens next?

Some headway has recently been made into improving the safety of devices, says the report. It points out that the European Commission has adopted proposals for two new regulations on medical and surgical devices to improve patients’ safety. If they are agreed these regulations will apply from 2017.

However, the authors point out that proposed changes to legislation, both in Europe and elsewhere, do not include suggestions to improve the collection of data.

An accompanying commentary by a research group at Herdecke University in Germany argues that Europe needs “a central, transparent and evidence-based regulation process for devices”.

They have submitted a petition to the European Commission, European Parliament and European Council arguing for the regulation process to be centralised with independent assessment “by a new public body similar to the European Medicines Agency”.

They also recommend that post-marketing surveillance should be legally compulsory “to ensure that benefits and harms of the device in real world settings are similar to those shown in clinical trials”.

Finally, the German researchers call for transparency of the assessment process and results.

They believe that all available data on medical devices “should be publicly accessible and should include all relevant information concerning assessment, including data on safety, performance, and incidents”.

However, as the authors of this report point out, the outcome of discussion with the relevant authorities is “difficult to predict”. 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Experts call for transparency over medical devices. The Daily Telegraph, May 8 2013

Links To Science

Campbell C, Stainthorpe AC, Longson CM. How can we get high quality routine data to monitor the safety of devices and procedures? BMJ. Published online May 7 2013