"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

'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 as I could. I made a decision to have a preventative 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. However, having this high risk mutation does not mean that a woman will definitely develop 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 is a range of treatment options available to you.

First, 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 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 compared with other forms of cancer.

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 one only 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). However, public health officials in the UK have stated that there is no evidence of 'sustained' transmission (ie. no-one who has been infected by another person, has gone one to infect more people).

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%. However, it is not clear whether there are cases of mild illness that have not been reported or confirmed. This means the real case mortality rate is far lower.

And 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 aeroplane.

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

For more information, read the Public Health England advice on the novel coronavirus.

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