Medical News

Social care reforms announced

Medical News - Tue, 01/19/2038 - 06:14

Most of the UK media is covering the announcement made in Parliament by Jeremy Hunt, Secretary of State for Health, about proposed changes to social care.

The two confirmed points to have garnered the most media attention in the run-up to the announcement are:

  • a ‘cost cap’ of £75,000 worth of care costs – after this point the state would step in to meet these care costs
  • raising the current means-testing threshold for people to be eligible for state-funded social care from £23,520 to £123,000

The government expects these changes will lead to fewer people having to sell their homes in order to pay for their long-term care needs.

Speaking in Parliament, Mr Hunt said that the current system was ‘desperately unfair’ as many older people face ‘limitless, often ruinous’ costs. The minister stated that he wants the country to be ‘one of the best places in the world to grow old’.


What is social care?

The term social care covers a range of services provided to help vulnerable people improve their quality of life and assist them with their day-to-day living.

People often requiring social care include:

  • people with chronic (long-term) diseases
  • people with disability
  • the elderly – particularly those with age-related conditions, such as dementia

Social care services can include:

  • healthcare
  • equipment
  • help in your home or in a care home
  • community support and activities
  • day centres


How does the current adult social care system work?

Currently, state funding for social care is based on two criteria:

  • means – people with assets of more than £23,520 do not qualify for funding
  • needs – most local authorities will only fund care for people assessed to have substantial or critical needs

The majority of people currently requiring social care pay for it privately. These are known as ‘self-funders’.


What prompted these reforms to adult social care?

Put simply, on average, the UK population is getting older.

When the welfare state was created in the early 20th century, it was not expected that people would someday routinely live into their 70s, 80s, and even 90s.

The increase in life expectancy is a good thing, however, it brings a new set of challenges.

While people are living longer, they are also spending more of their lives in ill health. Older people are more likely to have potentially complex care needs that can be expensive to manage.

Many people are currently ineligible for state-funded social care under the existing laws. To meet the costs of these care needs, these ‘self-funders’ have, in many cases, had to sell or remortgage their home, or sell other assets to pay for the costs of their care.

Without reforms, experts agree that the cost of social care for both the state (through taxes) and to ‘self-funders’ is likely to become increasingly problematic.

To try and find the best way to resolve some of the difficulties of fairly funding adult social care, the Department of Health set up a commission. This independent commission reported its findings to ministers in July 2011. The government considered these findings in its white paper on care and support published in July 2012, and in the drafting of the proposed new legislation.


What happens next?

The government has introduced a Social Care Bill which will need to be passed by the Houses of Parliament.

If the bill is successfully passed it is expected the amendments will come into force by 2017.


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

Links To The Headlines

Social care: Jeremy Hunt hails 'fully-funded solution'. BBC News, February 11 2013

Social care reforms: Almost 2 million pensioners will be denied state help. The Daily Telegraph, February 11 2013

Social care reform: how your family may be affected. The Daily Telegraph, February 11 2013

Dilnot 'regrets' decision to set social care cap at £75,000. The Guardian, February 11 2013

Hunt statement on adult social care cap: Politics live blog. The Guardian, February 11 2013

Categories: Medical News

Having a spine similar to a chimp could lead to back pain

Medical News - 10 hours 3 min ago

"People with lower back problems are more likely to have a spine similar in shape to the chimpanzee," BBC News reports. Research suggests that humans with similar shaped vertebrae to chimps are more vulnerable to developing a slipped disc.

Back pain is a common problem that affects most people at some point in their life and is one of the leading causes of what is known as a slipped disc – when one of the discs that sit between the bones of the spine (the vertebrae) is damaged and presses on the nerves.

But our knuckle-walking ape cousins don’t suffer nearly as much. One explanation is that our back problems are due to the extra stress placed on our backs from standing upright.

Scientists studying the vertebrae of chimpanzees, medieval humans and orangutans found humans with disc-related back problems had spines more similar in shape to chimpanzees.

Back problems in this study were defined as the presence of a lesion called a Schmorl's node; they are most often seen in people who have a slipped disc and can be a general sign of degeneration in the spine, though their significance is not completely understood. The participants, however, were long dead, so we don’t actually know if they had back pain.

The researchers think this knowledge could be used to identify people who are more likely to have back problems, based on the shape of their spines. This is plausible, but not yet a reality.

Where did the story come from?

The study was carried out by researchers from Universities in Canada, Scotland, Germany and Iceland. It was funded by the Social Sciences and Humanities Research Council, Canada Research Chairs Program, Canada Foundation for Innovation, British Columbia Knowledge Development Fund, MITACS, and Simon Fraser University.

The study was published in the peer-reviewed science journal BMC Evolutionary Biology. This is an open-access journal, so the study is free to read online.

Generally, the UK media reported the story accurately, avoiding the common pitfall of saying, or implying, that humans have evolved from chimps. This is not the case. We both have a common ancestor, so are cousins, albeit cousins who shared a grandparent 5-10 million years ago.

Many articles suggested that the finding may help identify people at a higher risk of back pain, such as athletes. However, any implications from this study are not completely clear, and we don’t yet know how useful this knowledge would be in practice.


What kind of research was this?

This was an evolutionary study looking at the spines of human and non-human primates to see how differences might relate to back problems.

Back pain is a common problem that affects most people at some point in their life. However, our ape cousins don’t suffer nearly as much. One explanation is that our back problems are due to the extra stress placed on our backs from standing upright. Non-human apes don’t walk upright nearly as much as humans.

Our ape ancestors' vertebral shape would not have been adapted for walking upright. Because of this, the research team predicted that people whose vertebrae were at the more ancestral end of the range of shape variation can be expected to suffer disproportionately more from load-related spinal disease.


What did the research involve?

The last thoracic (upper back) and first lumbar (lower back) vertebrae from 71 humans, 36 chimpanzees and 15 orangutans were scanned using computers and compared in detail for subtle differences in their shape and position of bony landmarks.

The human vertebrae were from skeletons dug up from the medieval and post-medieval period, while chimpanzee and orangutan vertebrae were a mix of wild and zoo animals from US Natural History museums.

Of the human vertebrae, about half had Schmorl’s nodes, and half did not. The spine is made up of stacks of bone (vertebrae) and discs (cartilage), making the spine both strong and moveable. The nodes are small bulges of the cartilage disc into the adjacent bony vertebrae.

They are most often seen in people who have a slipped disc and may be a general sign of degeneration and inflammation in the spine.

However, the nodes' significance in slipped discs and back pain is not completely understood. For example, some people who have them have pain, while others do not. For the purposes of this research, vertebrae with the Schmorl’s nodes were referred to as “diseased” and those without referred to as “healthy”. None of the non-human ape vertebra were classed as diseased.

They fed all the information into a statistical model to predict spine health for human and non-human apes.


What were the basic results?

The predictive model was able to show there were differences in the vertebrae in healthy humans, chimpanzees and orangutans. Crucially, it found no difference between diseased human vertebrae and chimpanzees.

This suggested that humans with Schmorl’s nodes are closer in shape to chimpanzee vertebrae than healthy human vertebrae.


How did the researchers interpret the results?

The research team concluded: "The results support the hypothesis that intervertebral disc herniation [a "slipped disc"] preferentially affects individuals with vertebrae that are towards the ancestral end of the range of shape variation within H. sapiens [modern humans] and therefore are less well adapted for bipedalism [walking upright on two legs]. This finding not only has clinical implications, but also illustrates the benefits of bringing the tools of evolutionary biology to bear on problems in medicine and public health."



This evolutionary research used a small sample of vertebrae from humans, chimpanzees and orangutans to show that people with a disc bulge had spines more similar in shape to chimpanzees than healthy humans. The research team took this as a sign that people with vertebrae shape more similar to chimpanzees may be more likely to have disc-related back problems because they are less well adapted, evolutionary speaking, to walking upright.

The main limitation of the study is the use of Schmorl’s nodes to label spines as "diseased" vs. "healthy", and to assume the presence of the nodes was a sign of back pain. Obviously, the skeletons could not be asked whether they experienced back pain. The significance of Schmorl’s nodes is still not completely understood. Not everyone with them has back pain, so the results are less widely applicable than they may appear.

The study also used a relatively small number of vertebrae to reach its conclusions. The reliability of the findings would be improved if they were replicated using more vertebrae.

The implications of the study were summed up by lead scientist Dr Kimberly Plomp, in The Daily Telegraph, who said: "The findings have potential implications for clinical research, as they indicate why some individuals are more prone to back problems … This may help in preventative care by identifying individuals, such as athletes, who may be at risk of developing the condition."

This may be possible, but at this stage in the research, we can’t draw any firm conclusions.

The study isn’t applicable to all back pain, only those related to specific disc bulges. The findings are not relevant to the large number of people with general mechanical back pain, without specific cause, or to people with other disease or injury causes of back pain.

For advice on how to prevent and treat back pain, visit the NHS Choices Back Pain Guide.

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

Links To The Headlines

Lower back pain linked to chimpanzee spine shape. BBC News, April 27 2015

Back pain sufferers may have 'vertebrae like apes'. The Daily Telegraph, April 27 2015

Back pain 'linked to chimpanzee ancestors'. ITV News, April 27 2015

Links To Science

Plomp KA, Viðarsdóttir US, Weston DA, et al. The ancestral shape hypothesis: an evolutionary explanation for the occurrence of intervertebral disc herniation in humans. BMC Evolutionary Biology. Published online April 27 2015

Categories: Medical News

Parents 'may pass anxiety on to their children'

Medical News - 10 hours 3 min ago

The Mail Online has given stressed-out parents one more thing to worry about, saying: "Anxiety is 'catching' and can be passed on to children", adding that, "Attitudes of over-anxious parents can severely affect children's behaviour".

The study that prompted these headlines used an interesting "children of twins" study design intended to filter out the influence of genetics, which is known to have an effect on anxiety.

To do this, researchers studied patterns of anxiety in families of identical twins, who are genetically identical, and in families of non-identical twins.

They found there was some link between anxiety and neuroticism (a tendency to have negative thought patterns) in parents and their adolescent children.

There was no evidence that genetics was playing a significant role, but modest evidence that non-genetic factors were. This suggested that anxiety, far from being hardwired into DNA, might be passed on in other ways, such as through learned or mimicked behaviour.

In the Mail Online, journal editor Dr Robert Freedman said: "Parents who are anxious can now be counselled and educated on ways to minimise the impact of their anxiety on the child's development."

This suggestion seems a touch premature – as noted by the researchers, there is a chicken and egg situation here that has not been resolved. Do children worry because they sense their parents are worried, or do parents worry because they see their children are worried about something? 

Family life is not always easy, but one way to boost your physical and mental health is to make the time to do activities as a family

Where did the story come from?

The study was carried out by researchers from universities based in London, Sweden and the US. It was funded by the Leverhulme Trust, the US National Institute of Mental Health, and the National Institute for Health Research.

The study was published in The American Journal of Psychiatry, a peer-reviewed medical journal. It has been made available online on an open-access basis, so it is free to read or download as a PDF.

Generally, the Mail Online reported the story accurately, but hardly mentioned the study's limitations. The quote from journal editor Dr Robert Freedman saying that, "Parents who are anxious can now be counselled and educated on ways to minimise the impact of their anxiety on the child's development", seems a little premature, based on the relatively weak associations found in this research.  

What kind of research was this?

This twin study investigated the relative role of genetic factors (nature) and non-genetic factors (nurture) in the transmission of anxiety from parent to child.

Non-genetic factors might be, for example, the children observing their parents' anxious behaviours and mimicking them, or the parenting style of anxious parents.

The researchers say it is well recognised that anxiety can run in families, but the underlying processes are poorly understood. This study wanted to find out whether genetics or environment was more important in the transmission of anxiety, by observing identical twins.

This type of study is commonly used for this type of question. It does not aim to pinpoint exact genes or non-genetic factors that play a role in a trait. 

What did the research involve?

The team gathered self-reported anxiety ratings from parents and their adolescent children. They compared the results between identical twin families and non-identical twin families to see to what extent non-genetic factors were driving anxiety transmission, in contrast to genetics. 

Data came from the Twin and Offspring Study of Sweden, which has information on 387 identical (monozygotic) twin families and 489 non-identical (dizygotic) twin families. A twin family comprised a twin pair where both twins were parents, each twin's spouse, and one of each of their adolescent children.

In families where the twins were identical, the cousins would share, on average, 50% of the same DNA with their (blood) aunt or uncle. In families where the twins were not identical, the cousins would share less of their DNA, on average, with their aunt or uncle.

If cousins whose parents are identical twins are more similar to their aunt or uncle for a trait than cousins whose parents are non-identical twins, this suggests that genes are playing a role.

Only same-sex twin pairs were used. Twin offspring were selected, so cousins were the same sex as one another and did not differ in age by more than four years, so they were as similar as possible. The average age of the twin offspring was 15.7 years.

This type of study design, known as a "children of twins" study, is intended to dampen down the potential influence that family genetics could have on the outcomes being investigated.

Anxious parental personality was self-reported using a 20-item personality scale. They rated phrases such as, "I often feel uncertain when I meet people I don't know very well", and, "Sometimes my heart beats hard or irregularly for no particular reason".

Each item was ranked between 0 (not at all true) and 3 (very true), covering social and physical signs of anxiety, as well as general worry. There was a similar self-reported scale to measure neuroticism.

Offspring anxiety symptoms – social, physical and general worry – were measured in a similar way, using questions from a Child Behaviour Checklist.

Both parents and offspring rated their anxiety and neuroticism over the last six months. The researchers used computer modelling of the relationships between individuals and their traits to estimate the contribution of genetic and non-genetic factors. 

What were the basic results?

Analysis of the data suggested genetic factors were largely not driving the transmission of anxiety or neuroticism from parent to adolescent. Ratings of anxiety and neuroticism within and between twin families were only very weakly linked.

However, there was "modest evidence" that non-genetic transmission of both anxiety and neuroticism was happening. Although still a relatively weak relationship, it was statistically significant, unlike the genetic finding. 

How did the researchers interpret the results?

The research team said their results supported the theory that direct, environmentally mediated transmission of anxiety from parents to their adolescent offspring was the main driver, and not genetics.   


This study tentatively shows that environmental factors, as opposed to genetics, play a more important role in the transmission of anxiety from parents to their adolescent children.

However, it used self-reported anxiety ratings over a six-month period, so this tells us very little about any potential longer-term effects of anxiety transmission while growing up.

The correlations in the main results were quite weak. This means that not every adolescent with an anxious parent will "catch" or "take on" their parents' anxiety. This suggests that it's a more complex issue.

The results showed non-genetic (environmental) factors were more important than genetic, but precisely what these environmental factors were is not something this study can tell us.

The study used a clever and unique sample of twins and their families to drill down into the age-old debate about the influence of nature versus nurture. However, it doesn't prove that environmental factors are the main driver overall.

That notwithstanding, the authors suggest two main contrasting explanations for the results:

  • parental anxiety causes their children to be more anxious – this could happen through different learning and mirroring behaviours known to occur when children and adolescents grow and develop; for example, an adolescent witnessing repeated examples of parental anxiety may learn that the world is an unsafe place that should be feared
  • anxiety in the offspring influences the parenting they receive – the flipside is that a teenager showing anxious behaviour may cause their parents to worry; the research team add that this might in turn worsen the anxiety in the teenager, creating a negative feedback loop

This twin study doesn't bring us any closer to knowing which explanation might be true, or to what extent this can be impacted by changes in behaviour.

Despite these limitations, the hypothesis that children are sensitive to their parents' attitudes and mood seems plausible. So, learning more about how to manage your stress and feelings of anxiety could be good for both you and your children.

For more information and advice, visit the NHS Choices Moodzone.

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

Links To The Headlines

Anxiety is 'catching' and can be passed on to children, scientists warn over-protective parents. Mail Online, April 24 2015

Links To Science

Eley TC, McAdams TA, Rijsdijk FV, et al. The Intergenerational Transmission of Anxiety: A Children-of-Twins Study. The American Journal of Psychiatry. Published online April 2015

Categories: Medical News

Gene editing technique could prevent inherited diseases

Medical News - Fri, 04/24/2015 - 15:45

“Researchers in the US have raised hopes for a simple genetic therapy that could prevent devastating diseases being passed on from mothers to their children” The Guardian reports.

The diseases in question are caused by mutations in the small pieces of DNA found in the powerhouses of the cells – the mitochondria. This DNA is passed directly from mother to child.

Mitochondrial diseases can cause symptoms including muscle weakness, seizures and heart disease – and have reduced life expectancy.

One option to treat this, as we have discussed several times, is so-called “three-parent” IVF, where unhealthy mitochondria are effectively replaced by healthy mitochondria from a donor egg.

This new technique from the US may eventually offer an alternative approach.

The researchers developed a way to target and break down mutated mitochondrial DNA. They found that they could successfully use this technique in mouse eggs. Once fertilised, these eggs could go on to produce healthy and fertile mice, with little of the targeted mitochondrial DNA in their cells. The technique also seemed to work on hybrid mouse-human cells carrying human mitochondrial DNA mutations in the lab.

This new technique is of interest because if it were effective and safe in humans, it could offer a way to prevent mitochondrial diseases without the need for the donor egg. The research is at an early stage, and many questions remain that need to be answered through future studies before this technique could be considered for testing in humans.


Where did the story come from?

The study was carried out by researchers from the Salk Institute for Biological Studies and other research centres in the US, Japan, Spain and China.

The researchers were funded by the Leona M. and Harry B. Helmsley Charitable Trust, the US National Institutes of Health, National Basic Research Program of China, Chinese Academy of Sciences, National Natural Science Foundation of China, the JDM Fund, the Muscular Dystrophy Association, United Mitochondrial Disease Foundation, the Florida Department of Health and the G. Harold and Leila Y. Mathers Charitable Foundation.

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

Both the Guardian and The Independent cover this research reasonably. One quote from a study author suggests that: "the technique is simple enough to be easily implemented by IVF clinics around the world", but it is important to realise that much more research is needed to make sure the technique is effective and safe before it could be tested in humans.


What kind of research was this?

This was laboratory and animal research aiming to develop a new way of preventing transmission of mutations in the mitochondrial DNA. This research is appropriate for the early development of new techniques, which may eventually be used to treat human disease.

While most of our DNA is found in a compartment of our cells called the nucleus, there is some DNA within the cell’s many mitochondria. These are the energy producing "powerhouses" of the cells. Mutations in this DNA can cause a range of serious diseases affecting the organs that need a lot of energy – such as the brain and muscles.

We inherit our mitochondria from our mothers. Researchers have developed techniques to avoid passing these mutations on, involving transferring the DNA from the mother’s nucleus into a donor egg. Manipulation of human embryos is tightly controlled in the UK, and after much debate, the government recently agreed to make it legal to perform these "three-parent IVF" techniques to prevent mitochondrial diseases.

One concern with these techniques is that the child inherits mitochondrial DNA from a third person (the egg donor). The current research aimed to develop a different technique to avoid passing on mitochondrial mutations that does not involve a donor egg. It is specifically aimed at women who have a mixture of mitochondria in their cells – some carrying a disease-causing mutation and some not.


What did the research involve?

The researchers developed a technique to reduce the amount of mutation carrying mitochondrial DNA. This involved injecting into the cells genetic instructions for making a protein to be sent to the mitochondria and cut the mitochondrial DNA in a specific place. They first tested this technique on mouse egg cells that carried a mixture of two types of mitochondrial DNA, one of which could be cut by the protein (the "target" mitochondrial DNA) and one which could not. They then checked to see if it could reduce the amount of “target” mitochondrial DNA.

They then tested it on fertilised "mixed mitochondrial DNA" mouse egg cells to see if it had the same effect and whether it affected development of the embryo. They also implanted treated embryos into host mother mice to see if the offspring were born healthy and how much of the target mitochondrial DNA they carried.

Finally, they modified their technique slightly so they could use it against human mitochondrial DNA carrying disease-causing mutations. After testing this adapted technique in mice, they tested it on cells in the lab containing human mitochondria with mutations that caused one of two different mitochondrial diseases:

  • Leber’s hereditary optic neuropathy and dystonia (LHOND)
  • neurogenic muscle weakness, ataxia and retinitis pigmentosa (NARP)

These are both rare conditions in humans that cause symptoms affecting the muscles, movement and vision.

These hybrid cells were created by fusing mouse egg cells and human cells carrying the mitochondrial mutations.


What were the basic results?

The researchers found that their technique reduced the amount of the target type of mitochondrial DNA in the "mixed mitochondrial DNA" mouse egg cells. Their technique performed similarly in fertilised embryos from these eggs. These embryos appeared to develop normally in the lab when examined under a microscope. The technique did not appear to affect the DNA in the mice’s nuclei.

When the treated embryos were implanted into host mothers, the offspring born also had much less of the target type of mitochondrial DNA throughout their bodies. They appeared to be healthy and develop normally in the tests performed, and could themselves produce healthy offspring. These offspring had such low levels of the target type of mitochondrial DNA that it was barely detectable.

The researchers were able to adapt their technique to target human mitochondrial mutations. It reduced the amount of mitochondrial DNA containing the LHON or NARP mutations in hybrid egg cells in the lab.


How did the researchers interpret the results?

The researchers concluded that their "approaches represent a potential therapeutic avenue for preventing the transgenerational transmission of human mitochondrial diseases caused by mutations in [mitochondrial DNA]".



This early research has developed a new technique to reduce the amount of mutation-carrying DNA within mitochondria. The hope is that this technique might be used in the eggs of women carrying disease-causing mitochondrial mutations.

The government has recently given the go ahead for a technique that allows a woman who carries such a disease from passing it on to her child – making the UK the first country to do so.

This technique has raised some ethical and safety concerns, as it places the woman’s chromosomes into a donor egg with healthy mitochondria. This means that once this egg is fertilised it contains DNA from three people – the DNA in the nucleus comes from the mother and father, and the mitochondrial DNA comes from the egg donor.

This new technique is of interest because if it were effective and safe in humans, it could offer a way to prevent mitochondrial diseases without the need for the donor egg. This technique shows promise, but is still in its early stages. It has thus far only been tested in mice, and in human-mouse hybrid egg cells carrying mutated human mitochondria in the lab.

It is also specifically aimed at women who have a mixture of normal and mutated mitochondrial DNA, as it relies on the normal mitochondrial DNA being there to "take over" once the mutated DNA has been reduced. It would not work in women who have only mutated mitochondria, and there may be a certain level of normal mitochondrial DNA that needs to be present for the technique to work.

All of these issues are likely to be investigated in future studies.

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

Links To The Headlines

Hopes raised for new genetic therapy to prevent inherited diseases. The Guardian, April 23 2015

Scientists develop technique that could stop a genetic disease being passed on to future generations. The Independent, April 23 2015

Links To Science

Reddy P, Ocampo A, Suzuki K, et al. Selective Elimination of Mitochondrial Mutations in the Germline by Genome Editing. Cell. Published online April 23 2015

Categories: Medical News

Air pollution linked to silent strokes

Medical News - Fri, 04/24/2015 - 15:00

"Adults who live in towns and cities suffer ageing of the brain and increased risk of dementia and [silent] strokes because of air pollution," The Daily Telegraph reports.

A "silent stroke" (technically known as a covert brain infarct) are small areas of damage caused by lack of oxygen to the brain tissue, but are not severe enough to cause obvious symptoms. They may be a sign of blood vessel disease, which increases the risk of one type of dementia (vascular dementia).

This headline is based on a study which took brain scans of more than 900 older adults and assessed their exposure to air pollution. It found that higher levels of small particles in the air around where an individual lived were associated with a greater likelihood of them having signs of a "silent stroke" on a brain scan.

There was some evidence of association between the particles and slightly smaller brain volume, but this link did not remain once people’s health conditions were taken into account.

Limitations of the study include that the researchers could only estimate people’s air pollution exposure based on average air quality of where they lived in one year, rather than lifetime exposure. It should also be noted that the news has suggested a link to dementia, but the study did not actually assess this.

The findings need to be investigated in future studies before firm conclusions can be drawn.

If you are concerned about air pollution, then the Department for Environment, Food & Rural Affairs (DEFRA) provides alerts when pollution is known to be high or very high in a particular region.

Where did the story come from?

The study was carried out by researchers from Beth Israel Deaconess Medical Center and other centres in the US. It was funded by the US National Institutes of Health and the United States Environmental Protection Agency.

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

The Daily Telegraph headline suggests that air pollution could increase a person’s risk of dementia, but this is not what the study assessed, and none of the participants had dementia, a stroke or mini-stroke (also known as a transient ischaemic attack).

They also suggest that it is living in towns and cities that increases risk, but this was not what the study assessed. It compared people with different levels of particulate matter in the air where they lived, not whether they lived in towns and cities, and in their main analyses they did not include people living in rural areas far from major roads.

The Mail Online similarly overstates findings, by stating that "living near congested roads with high levels of air pollution can cause ‘silent strokes’". While an association was found, a direct cause and effect relationship remains unproven.


What kind of research was this?

This was a cross-sectional analysis assessing whether there was a link between air pollutant exposure and changes in the brain linked to ageing.

The authors report that long-term exposure to air pollution is associated with, for example, increased risk of stroke and cognitive impairment. However, its effects on the structure of the brain are not known. If air pollution is linked to structural brain changes, these could, in turn, contribute to the risk of stroke and cognitive problems.

This type of study can show links between two factors, but cannot prove that one caused the other. As the study was cross-sectional, it cannot establish the sequence of events and whether exposure to air pollution came before any differences or changes in brain structure. As an observational study, there may also be factors other than air pollution exposure that could be causing the differences seen. The researchers did take steps to try to reduce the impact of other factors, but they may still be having an effect.


What did the research involve?

The researchers took brain scans of 943 adults aged 60 and over. They also estimated their exposure to air pollution, based on where they lived. They then analysed whether those with more exposure to air pollution were more likely to have smaller brain volume or signs of damage.

Participants in this study were taking part in an ongoing longitudinal study in the US state of New England. Only those who had not had a stroke or mini-stroke and did not have dementia were selected to take part.

The type of effects on the brain that the researchers were looking for were referred to as "subclinical". This means that they did not cause the people to have symptoms and therefore would not normally be detected.

They looked at total volume of the brain and also the volume of the specific parts of the brain using a magnetic resonance imaging (MRI) brain scan. The brain shrinks gradually with age, so the researchers were interested in whether pollution might have a similar effect. The MRI also identified whether the brain showed signs of a "silent stroke" – that is, parts of the brain tissue that had been damaged by having the blood supply interrupted.

These "covert brain infarcts" were not severe enough to cause symptoms, in the form of a stroke or mini-stroke. However, this damage suggests that the person may have some degree of blood vessel (vascular) disease. They are often seen in the brain scans of people who have vascular dementia.

The researchers used satellite data measuring the level of small particles (PM2.5) on the air in New England to assess average daily air pollution exposure at each participant’s current home address in 2001. They also assessed how close each home was to roads of different sizes. The researchers only looked at those living in urban and suburban areas in their main analyses.

They then looked at whether there were any links between estimated particulate matter exposure and distance from roads and brain findings.

They first took into account confounding factors that could affect results, including:

  • age
  • gender
  • smoking
  • alcohol intake
  • education

They then carried out a second analysis, taking into account a number of additional factors, such as:

  • diabetes
  • obesity
  • high blood pressure


What were the basic results?

Average (median) daily exposure to small particles in the air was about 11 microgrammes per cubed metre of air, and participants lived an average of 173 metres from a major road. The participants were, on average, 68 years old when they had their brain scan, and 14% showed signs of a "silent stroke" on the scans.

The researchers found that greater estimated exposure to air pollution was associated with a slightly smaller total brain volume. Each two microgramme per cubed metre increase in particulate matter was associated with a 0.32% lower brain volume. However, once this analysis was adjusted for conditions such as diabetes, this difference was no longer statistically significant.

Greater estimated exposure to air pollution was also associated with a higher likelihood of having signs of "silent stroke" damage to the brain tissue. Each two microgramme per cubed metre increase in particulate matter was associated with a 37% higher odds of this silent damage (odds ratio (OR) 1.37, 95% confidence interval (CI) 1.02 to 1.85).

They did not find differences in association across areas with different average income brackets. Distance from a major road was not linked to total brain volume or a "silent stroke" after adjustment for confounders.


How did the researchers interpret the results?

The researchers concluded that their findings "suggest that air pollution is associated with insidious effects on structural brain aging, even in dementia and stroke-free persons".



This cross-sectional study has suggested a link between exposure to small particles in the air (one form of pollution) and the presence of "silent stroke" in older adults – small areas of damage to the brain tissue that are not severe enough to cause obvious symptoms.

There are a number of limitations to be aware of when assessing the results of this study:

  • While there was an association between particulate matter in the air and total brain volume, this was no longer statistically significant after taking into account whether people have conditions such as high blood pressure, which can also affect their risk of stroke.
  • While the researchers did try to take into account factors such as smoking, alcohol intake and diabetes, which could be having an effect on risk, this may not remove their effect totally. There may also be various other unmeasured factors that could account for the association seen. This makes it difficult to be sure whether any link seen is directly due to the pollution itself.
  • The researchers could only estimate people’s air pollution exposure based on average air quality of where they lived in one year. This may not provide a good estimate of a person’s lifetime exposure.
  • While the news extrapolated these findings to suggest a link between air pollution and people’s risk of dementia, this is not what the study assessed. While areas of "silent stroke" can often be seen in people who have vascular dementia, none of the study participants had dementia, or a stroke or mini-stroke.

Overall, this study finds some evidence of a link between one measure of air pollution and "silent stroke", but the limitations mean that this finding needs to be confirmed in other studies.

It is also not possible to say whether the link exists because air pollution is directly affecting the brain.

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

Links To The Headlines

Air pollution could increase risk of dementia. The Daily Telegraph, April 23 2015

Living near busy roads 'can raise dementia risk': Exposure to sooty particles alters structure of the brain. Mail Online, April 24 2015

Links To Science

Wilker EH, Preis SR, Beiser AS, et al. Long-Term Exposure to Fine Particulate Matter, Residential Proximity to Major Roads and Measures of Brain Structure. Stroke. Published online April 23 2015

Categories: Medical News

New asthma treatment within five years, researchers hope

Medical News - Thu, 04/23/2015 - 14:50

"Asthma cure could be in reach," The Independent reports. Researchers have discovered that protein molecules called calcium-sensing receptors play a pivotal role in asthma. Drugs known to block these proteins already exist.

In asthma, the immune system mistakes harmless substances, such as pollen, as a threat. White blood cells and inflammatory proteins then collect in the airways. The inflammation causes the airways to constrict, leading to the breathing difficulties associated with asthma. This study found these proteins stimulate calcium-sensing receptors, which leads to further inflammation of the airways.

The research used mouse models of asthma and human airway tissue taken from asthmatic and non-asthmatic people. The researchers found increased numbers of these calcium-sensing receptors compared with healthy lung tissue. They concluded that this is one of the reasons for the exaggerated inflammatory response that occurs in asthma.

The drug calcityrol, which is used to treat osteoporosis, is known to block the actions of the receptors. It reduced inflammation of the airways when used in mice.

However, it is not clear that calcityrol could be a "cure" for asthma, as the initial inflammatory response by the immune system would still occur.

Though calcityrol pills are safe as a treatment for osteoporosis, it is not known whether the dose required to be effective in reducing the inflammation found in asthma would be safe.

The researchers plan to develop a version of the drug that can be inhaled to maximise its effectiveness and minimise side effects. They expect human trials to commence in a couple of years.

Where did the story come from?

The study was carried out by researchers from Cardiff University, the Open University, the Mayo Clinic, and the University of California, San Francisco School of Medicine in the US, and the University of Manchester and King's College London in the UK.

It was funded by Asthma UK, the Cardiff Partnership Fund, Marie Curie Initial Training Network, the Biotechnology and Biological Sciences Research Council, and the US National Institutes of Health.

Four of the authors report they are co-inventors of a patent for the use of calcium-sensing receptor antagonists for the treatment of inflammatory lung diseases.

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

The media reported the story accurately, although headlines saying that an asthma "cure" is five years away are a little premature. No clinical studies in people have been conducted yet, and there is no guarantee they will work. However, the "five-year cure" claim came from the researchers themselves.  

What kind of research was this?

This was a set of laboratory experiments involving mice models of asthma and samples of human lung tissue. The researchers aimed to better understand the inflammation that causes narrowing of the airways in asthma.

The inflammation is an exaggerated response to various triggers, such as pollen, infections and pollutants, but sometimes no cause is identified.

Recent research found that this inflammation results in the build-up of two proteins: eosinophilic cationic protein (ECP) and major basic protein. These proteins carry multiple positive electrical charges.

The researchers wanted to test the theory that the inflammation is driven by these proteins activating another type of protein molecule called calcium-sensing receptors (CaSR) on the surface of the smooth muscle cells that line the airways.  

What did the research involve?

The researchers conducted a variety of laboratory experiments, which involved looking at human lung tissue samples taken from people with asthma and comparing them with healthy lung tissue. They then performed several studies comparing mice with a type of asthma with healthy controls.

The researchers first compared the number of CaSRs in the lung tissue of people with asthma, compared with healthy lung tissue. They then measured how the CaSRs reacted to positively charged proteins and various chemicals involved in inflammatory response, such as histamine.

They repeated the experiments using a type of drug called a calcilytic, which blocks CaSRs. Calcilytic drugs were developed as a treatment for osteoporosis, as they increase the level of parathyroid hormone by targeting CaSRs. This helps to increase the level of calcium in the blood. 

What were the basic results?

The experiments indicated there are more CaSRs in people with asthma, which are required for inflammation. Calcilytic drugs blocked the receptors.

There were three times the number of CaSRs in biopsies of smooth muscle taken from the airways of people with asthma, compared with those who do not have asthma. The same was true for biopsies of mice with a form of asthma, compared with healthy controls.

In the laboratory setting, positively charged proteins and chemicals such as histamine activated the CaSRs, causing an inflammatory response. These receptors could be blocked by the calcilytic drugs.

Mice without CaSRs in their smooth muscle cells did not have an inflammatory response to the positively charged proteins. Healthy control mice did have an inflammatory response. Calcilytic drugs were able to reduce the effect of these proteins and other inflammatory stimulants tested. 

How did the researchers interpret the results?

The researchers concluded that there are more CaSRs in the lungs of people with asthma, and this contributes to the inflammation that causes narrowing of the airways.

They say that calcilytic drugs could reduce the number of CaSRs and reduce their responsiveness. This could both "prevent as well as relieve AHR [airways hyper-responsiveness]", which is found in asthma.

The researchers do not yet know if their findings would be true for all types of asthma. 


This piece of research has found that CaSRs play a role in the inflammatory response seen in asthma. The early results of laboratory experiments indicate that drugs called calcilytics can dampen this inflammatory response in asthmatic human lung tissue and in mice with asthma.

Though the media described this as a "cure" for asthma, the study has not proved this. It showed that there were more CaSRs in the human lung samples from people with asthma, and compared it with healthy lung tissue.

The researchers also have not shown that calcilytics can block the receptors. What is not known is how long this effect would last and whether it would stop the lungs producing more of the excessive numbers of receptors.

It remains unclear why people with asthma in this study had an increased number of receptors, and if this is true for everyone with asthma.

The researchers predict that if calcilytics prove to be effective in clinical trials, it will take around five years for them to become available as a treatment for asthma.

This is because, although this drug has been deemed a safe treatment for osteoporosis, the researchers intend to develop the drug so it can be used as an inhaler. This would deliver it straight to the lungs to maximise the effectiveness and minimise side effects.

Drug development will involve further animal trials to work out what dose would be required to achieve clinically meaningful results, and will also test its safety. If these trials are successful, the research will progress to human trials.

This is an exciting piece of research that may provide a new treatment for asthma, but it is still early days, so there are no guarantees.

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

Links To The Headlines

Asthma cure could be in reach as scientists make 'incredibly exciting' breakthrough. The Independent, April 22 2015

Asthma could be cured within five years after drug breakthrough. The Daily Telegraph, April 22 2015

Major asthma breakthrough as scientists discover root cause of the condition - and say a new treatment is less than 5 years away. Mail Online, April 23 2015

Cardiff University scientists discover asthma's root cause. BBC News, April 22 2015

Scientists discover root cause of asthma and believe bone drug could be cure. Daily Express, April 23 2015

Links To Science

Yarova PL, Stewart AL, Sathish V, et al. Calcium-sensing receptor antagonists abrogate airway hyperresponsiveness and inflammation in allergic asthma. Science Translational Medicine. Published online April 22 2015

Categories: Medical News

A magnet for mosquitoes? Blame your genes

Medical News - Thu, 04/23/2015 - 13:30

"Mosquitoes 'lured by body odour genes','' BBC News reports. Researchers tested a series of non-identical and identical twins, and found identical twins had similar levels of attractiveness to mosquitoes.

Researchers have long known that some people are more attractive to mosquitoes than others, and some think this is to do with body odour.

Body odour is, in part, inherited through our genes, so the researchers running this study wanted to find out whether twins with identical genes shared a similar level of attractiveness to mosquitoes.

They exposed the hands of sets of identical and non-identical twins to mosquitoes to see which twin the mosquitoes preferred.

The results showed identical twins were likely to have about the same level of attractiveness to mosquitoes, while non-identical twins' results differed more. This strongly suggests there is a genetic component, in the same way there is for height and IQ.

This could explain why one half of a couple is plagued by mosquitoes on holiday, while the other will be blissfully free of any bites. The research could eventually help scientists develop better insect repellents.  

Where did the story come from?

The study was carried out by researchers from the London School of Hygiene and Tropical Medicine, the University of Florida, the University of Nottingham and Rothamsted Research. It was funded by the Sir Halley Stewart Trust.

The study was published in the peer-reviewed medical journal PLOS One, which is an open-access journal, meaning the study can be read for free online.

Generally, the media reported the study accurately, but did not question the reliability of results from the fairly small sample size (a total of 74 participants).

The Daily Telegraph suggested that using insect repellent made no difference to people with a genetic disposition to being bitten, but the study did not look at insect repellent, so we don't know if that is true. 

What kind of research was this?

This was a laboratory-based twin study, which compared the relative attractiveness to mosquitoes of pairs of twins.

The researchers wanted to know whether identical twins, who share the same genes, were more likely to have the same level of attractiveness to mosquitoes as non-identical twins, whose genes are different.

Twin studies are useful ways to show how likely a particular trait is to be inherited. However, they can't tell us any more than that – for example, which gene is involved, or how genetics affects the trait. 

What did the research involve?

Researchers took 18 pairs of identical twins and 19 pairs of non-identical twins. They tested them for attractiveness to mosquitoes by releasing the insects into a Y-shaped tube with two sections.

The twins put their hand into the top of a section, and the researchers counted the numbers of mosquitoes that flew up each side of the tube. They then looked at whether results were closer for identical twins than for non-identical twins.

The researchers did a series of experiments, testing the twins individually against clean air, and also pairing them against each other. They tried to avoid bias in the study by using randomisation to decide which side of the tube was used by which twin, and which twin was tested first.

All the twins were women and over the age of menopause. The twins had also been asked to avoid strong-smelling food such as garlic or chilli, to avoid alcohol, and to have washed their hands with odour-free soap before the experiment.

The researchers also checked the twins' temperatures to see whether body temperature had any effect on the results. The researchers used Aedes aegypti mosquitoes, which is the strain that carries dengue fever.

They analysed the data in two sets – firstly, which twin was more attractive to mosquitoes when tested against clean air, and then which was more attractive when tested against the other twin.

As well as seeing which tube the mosquitoes flew into (used to measure relative attraction), the researchers also counted how many flew at least 30 centimetres up the Y-shaped tube (used to measure flight activity).

The researchers used an average of 10 measurements for each twin to come up with estimates of the proportion of the attractiveness that was down to heritability. 

What were the basic results?

The study found identical twins were much more likely to share the same level of attractiveness to mosquitoes than non-identical twins.

The study gives an estimate that 62% (standard error 12.4%) of relative attraction (the chances of the mosquitoes choosing that person's tube) was down to heritable factors, along with 67% (standard error 35.4%) of flight activity (the chance of the mosquitoes flying 30 centimetres up the tube).

The researchers say this would put attractiveness to mosquitoes at a level similar to height and IQ in terms of how much of it is inherited.

How did the researchers interpret the results?

The researchers say their results "demonstrate an underlying genetic component detectable by mosquitoes through olfaction". In other words, the study showed genetic differences account for at least some of the relative attractiveness of people to mosquitoes, and the difference is smelt by the insects.

They go on to suggest some people may have developed a body odour that is less attractive to mosquitoes, which could then have been handed down through natural selection of favourable genes, as it would protect against diseases such as dengue fever and malaria.

However, the researchers warn that the relatively small sample size and the nature of the experiment means they can't be precise about their conclusions. The standard error rates on their estimates of heritability are quite high, showing the level of uncertainty. 


This research suggests the genes you inherit from your parents may determine your chances of being bitten by mosquitoes. However, the small size of the study limits how confident we can be in the results.

The researchers suggest differences in body odour determine how attractive a person is to mosquitoes. We know body odour is partly down to inherited genetic factors, so it would make sense that inherited body odour can make you more or less attractive to mosquitoes.

However, the study doesn't tell us whether the mosquitoes were attracted to people because of their body odour, or for some other reason that wasn't researched.

A lot more research needs to be done into which inherited components of body odour are linked to attractiveness to mosquitoes before scientists can use this information to produce better mosquito repellents.

At this stage, we don't know whether people who get bitten less often have less of a mosquito-attractive chemical in their body odour, or more of a mosquito-repellent chemical.

If you get bitten by mosquitoes more than other people, and one or both of your parents does too, this research suggests you might have inherited the susceptibility to being bitten.

Unfortunately, at this stage, there's not much you can do about it, except for wearing insect repellent. Wearing light, loose-fitting trousers rather than shorts, and wearing shirts with long sleeves may also help. This is particularly important during the early evening and at night, when mosquitoes prefer to feed.

If you are travelling to an area where mosquitoes are known to carry malaria, it's vital to get medical advice about which type of antimalarial medication you should take. You may need to start taking the medication before you leave the country, so it's important to plan ahead.

Read more about antimalarial medication.

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

Links To The Headlines

Mosquitoes 'lured by body odour genes'. BBC News, April 23 2015

Do YOU always get bitten by mosquitoes? Blame your parents: Being attractive to bugs is genetic, scientists say. Mail Online, April 23 2015

Chance of being bitten by mosquito is written in genes. The Daily Telegraph, April 22 2015

Some people are BORN to be bitten by mosquitoes - genes can make us more attractive to the bugs. Daily Mirror, April 22 2015

Genes and body odour determine chance of mosquito bites, scientists find. Daily Express, April 23 2015

Mosquito Bite? It May Be Your Parents' Fault. Sky News, April 22 2015

Links To Science

Fernández-Grandon GM, Gezan SA, Armour JAL, et al. Heritability of Attractiveness to Mosquitoes. PLOS One. Published online April 22 2015

Categories: Medical News

Athlete’s foot cream could also treat multiple sclerosis

Medical News - Wed, 04/22/2015 - 14:10

"Two common drugs – one used for treating athlete's foot and another for alleviating eczema – may be useful therapies for multiple sclerosis," BBC News reports. The drugs have shown promise in lab and animal studies.

Multiple sclerosis (MS) is a neurological condition caused by damage to myelin. Myelin is a protein that acts as a protective layer to individual nerve fibres.

In this study researchers screened a number of drugs used for other conditions in the lab to see if any could produce mature cells to help replace damaged myelin.

One of the chemicals they identified as promising in their screen was miconazole, which is the active ingredient in some types of antifungal creams used to treat athlete’s foot. They found that it increased the number of mature myelin-producing cells in the brains of baby mice. It also helped repair damaged myelin in a mouse model of MS, and this made the mice’s symptoms less severe.

Clobetasol, a steroid cream used to treat psoriasis and eczema, also showed promise.

This is an early-stage study, and researchers hope they can eventually go on to test the drugs, or similar chemicals, in people with MS. Researchers will need to establish how safe this drug is if taken orally, and what effect it has in humans with the condition.


Where did the story come from?

The study was carried out by researchers from the Case Western Reserve University School of Medicine, and other research centres in the US. The study was funded by the US National Institutes of Health, New York Stem Cell Foundation, Myelin Repair Foundation, Mt. Sinai Health Care Foundation, the Case Comprehensive Cancer Center, the CWRU Council to Advance Human Health and philanthropic support from individual families. The authors declared that they did not have competing financial interests.

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

BBC News gives a good, balanced report of this study, noting the early stage of the findings, and warning of the potential risks of people self-medicating.

The Daily Telegraph reports the study reasonably well, but refers to the drug as a possible "cure", when it is too early to talk about the drug in these terms.


What kind of research was this?

This was laboratory and animal research that aimed to identify known human drugs that can prompt immature oligodendrocytes (called progenitor cells) to mature. Mature oligodendrocytes are the cells that "insulate" nerves with myelin. This myelin sheath helps nerves to send messages, and damage to the myelin sheath causes conditions such as multiple sclerosis (MS). One way to repair this damage might be to prompt the body to make more oligodendrocytes.

This type of screening of large amounts of chemicals at once is a quick way to find promising chemicals. These drugs need to be shown to be effective and safe in animal models before they can be used in humans. If a drug is already licensed for another condition in humans this can make progress to human trials quicker if it is going to be given at a similar dose and in the same way. However, if dose or how the drug is given are likely to differ for the new condition, safety would still need to be established in animals first.


What did the research involve?

The researchers tested more than 700 drugs on mouse oligodendrocyte progenitor cells in the lab. These immature cells are derived from stem cells, and the researchers singled out the drugs that caused them to develop into mature oligodendrocytes. They then tested their effects in brain tissue and in mice, including mouse models of MS, as well as on human oligodendrocyte progenitor cells in the lab.

In human MS, the immune system mistakenly attacks the body’s own myelin. The researchers used two different mouse models of the disease. In one "immune driven" model the mice’s immune system is actively attacking the myelin, and mimics the relapsing remitting form of MS. In the second model the immune system is not as active, and it is has more chronic progressive loss of myelin.


What were the basic results?

The research identified 22 drugs that prompted the oligodendrocyte progenitor cells in the lab to mature. They then picked the two drugs that were the best at getting the precursor cells to mature in brain tissue from young mice in the lab. These drugs were miconazole, which is currently used in antifungal creams, and clobetasol, which is a steroid used in creams (topical corticosteroid) for skin conditions such as psoriasis and eczema. They also found that drugs prompted human oligodendrocyte progenitor cells to mature in the lab. Of the two drugs, miconazole had the greater effect.

They found that giving the drugs to baby mice increased the number of myelin-producing cells in their brains. They also helped repair damaged myelin in the spinal cords of mice treated with a myelin-damaging chemical.

In the "immune driven" mouse model of MS, injections of clobetasol – but not miconazole – dampened down the immune response and reduced the severity of the mice’s symptoms. Steroids are known to affect the immune system, so the researchers had expected this. In the chronic mouse MS model, which has hind-leg paralysis, both clobetasol and miconazole injections helped to re-myelinate damaged nerves in the spinal cord and improved the mice’s movements.

Most existing MS drugs act by affecting the immune system, but miconazole did not appear to do this. Therefore the researchers felt this showed more promise as a new way to treat the disease. To show that their results were correct they had another lab confirm their miconazole results in the chronic MS mouse model.


How did the researchers interpret the results?

The researchers concluded that their screening system allowed them to rapidly identify drugs that have potential for re-myelination. This allowed them to identify two existing human drugs – miconazole and clobetasol – which increase re-myelination of nerves and "significantly reduce disease severity in mouse models of MS". They say that this "raises the exciting possibility that these drugs, or modified derivatives, could advance into clinical trials for the currently untreatable chronic progressive phase of MS".



This laboratory and mouse study has identified two drugs currently used for skin conditions – miconazole and clobetasol – that showed promise for treatment of conditions caused by myelin damage, such as MS.

If a drug is already licensed for another condition in humans, this can make progress to human trials quicker if it is going to be given at a similar dose and in the same way. However, as the researchers point out, these two drugs are licensed for use on the skin – not to be taken orally or injected into the system. This means more work will be needed to ensure the drugs are safe enough to be used in this way in humans. The drugs' chemical structures may need to be modified to make them work efficiently and reduce side effects.

Existing MS treatments act by dampening down the immune system, which attacks the myelin, so drugs that act in a different way, by repairing the myelin damage, could bring additional benefit. As yet, research into these drugs for MS is at an early stage, but many people will await with interest to see whether this early promise translates into better treatments.

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

Links To The Headlines

Athlete's foot drug may be MS therapy. BBC News, April 20 2015

Creams used to treat athlete's foot and eczema 'could REVERSE multiple sclerosis'. Mail Online, April 21 2015

Common athlete's foot cream 'could reverse multiple sclerosis'. The Daily Telegraph, April 20 2015

Links To Science

Najm FJ, Madhavan M, Zaremba A, et al. Drug-based modulation of endogenous stem cells promotes functional remyelination in vivo. Nature. Published online April 20 2015

Categories: Medical News

Coffee could make breast cancer drug tamoxifen more effective

Medical News - Wed, 04/22/2015 - 14:00

"A cancer-killing cocktail of the hormone drug tamoxifen and two coffees every day was found to reduce the risk of [breast cancer] tumours returning," the Mail Online reports. The same study also found evidence that caffeine slowed the cancer's growth.

The study looked at coffee consumption among 1,090 women with breast cancer, about half of whom were treated with tamoxifen.

Tamoxifen is a hormonal treatment used to treat cases of breast cancer known to be associated with the hormone oestrogen (known as oestrogen-dependent breast cancer).

The study found that women who reported drinking two to five cups of coffee a day had smaller primary tumours and a lower proportion of oestrogen-dependent tumours than those who drank one cup of coffee or less.

Women with oestrogen-dependent breast cancer who were treated with tamoxifen, and who drank at least two to five cups of coffee daily, had half the risk of the cancer recurring as those who drank less.

Researchers also carried out a laboratory study on the effect of two substances found in coffee – caffeine and caffeic acid (a compound found in coffee) – on breast cancer cells. They found that the substances suppressed the growth of breast cancer cells.

Although the results of this study are interesting, it cannot prove that coffee has an effect on breast cancer, as other factors, called confounders, could have influenced the results. 

There’s no harm in women being treated with tamoxifen for breast cancer drinking coffee in moderation. However, drinking excessive amounts can cause irritability, insomnia and indigestion.


Where did the story come from?

The study was carried out by researchers from Lund University and Skane University Hospital in Sweden, and the University of Bristol in the UK. It was funded by various grants from Swedish organisations, including the Swedish Cancer Society and the Swedish Research Council.

The study was published in the peer-reviewed journal Clinical Cancer Research.

The Mail Online’s reporting of the results implies it was proven that coffee prevents the return of oestrogen-dependent breast cancer or enhancing the action of tamoxifen. This is not the case, though the initial results are encouraging.

The Mail Online also did not include any comments on the study from independent experts. As a result, there is a risk that millions of women taking tamoxifen will start worrying about how much coffee they should drink.

There are no official UK guidelines on caffeine consumption, but regularly drinking more than 400 milligrams (mg) of caffeine a day (around four cups of brewed coffee or two "energy drinks") could cause side effects.


What kind of research was this?

This was a cohort study of 1,090 women with primary invasive breast cancer, living in Sweden. It is a follow-up study to one published in 2013 by the same researchers, which used a smaller number of women from the same cohort. The researchers say their previous study found an association between moderate to high coffee consumption and improved survival rates among women with breast cancer who were treated with tamoxifen. The researchers say the aim of the study is to investigate the association between coffee consumption, cancer characteristics and survival rates in a larger cohort of women with breast cancer.

Some breast cancer tumours rely on oestrogen to grow. These are called oestrogen-receptor (ER) positive cancers (the convention in classifying these types of cancer is to use the American spelling of oestrogen, which is estrogen; hence the ER).

Tamoxifen is the main hormonal therapy drug given for these types of breast cancer, as it blocks oestrogen from reaching the cancer cells. This reduces or stops the cells from growing.

The researchers also performed studies in the laboratory using human breast cancer cells to look at possible mechanisms by which two substances in coffee – caffeine and caffeic acid – may affect breast cancer growth.


What did the research involve?

For the cohort study, 1,090 women aged 24 to 99 who had been diagnosed with primary invasive breast cancer between 2002 and 2012 were recruited. Before undergoing surgery, the women’s body measurements and breast volume were taken and they were given an extensive questionnaire on their reproductive history, medication use and lifestyle factors, including smoking, alcohol and coffee consumption.

Coffee consumption was categorised into low (one cup or less a day), moderate (two to four cups a day) or high (five or more cups a day).

The researchers obtained information from pathology reports and medical records about tumour size and grade, whether it had spread to any lymph nodes, and if the tumour was hormone-receptor positive.

The women were followed until either their first breast cancer recurrence, their last disease-free follow-up or their death, whichever came first, before January 2013. Follow-up information on whether the breast cancer came back or whether the women had died was obtained from various official records. The results were analysed using standard statistical methods and adjusted for other factors, such as tumour size.

In their laboratory study, human breast cancer cells were exposed for 48 hours to caffeine or caffeic acid, with or without tamoxifen. The researchers used breast cancer cells that were ER positive, ER negative or cells that were resistant to tamoxifen. A minimum of three independent repeats were performed for each experiment.


What were the basic results?

The main results of the cohort study were:

  • women who reported a moderate to high coffee intake had smaller invasive primary tumours compared to those with low coffee consumption
  • moderate to high coffee intake was also associated with a lower proportion of ER positive tumours compared to patients with low consumption
  • moderate to high coffee consumption was associated with a 49% lower risk for breast cancer recurrence in women with ER positive tumours being treated with tamoxifen (adjusted hazard ratio 0.51; 95% confidence interval 0.26-0.97)

In the laboratory, caffeine and caffeic acid suppressed the growth of both ER positive and ER negative cancer cells. Caffeine and caffeic acid also had other effects on breast cancer cells, which led to slower cell growth and enhanced cell death.


How did the researchers interpret the results

The researchers say their findings demonstrate the various anticancer properties of caffeine and caffeic acid against both ER positive and ER negative breast cancers. In particular, they suggest that coffee may sensitise tumour cells to tamoxifen and therefore reduce breast cancer growth. It is possible, they say, that the substances in coffee switch off signalling pathways that cancer cells need to grow.



This study is interesting, but has several limitations. Its first finding was that women who report higher coffee consumption have smaller breast tumours, and also that their cancers are less likely to be ER positive. However, it seems that the women only reported their coffee consumption once, after diagnosis, and it is unclear from the write-up whether the questionnaire referred to their past or present coffee drinking habits. The women may also have under- or overestimated their coffee consumption, especially if they were asked to recall coffee consumption over a long period. The accuracy of coffee consumption is further hampered, as the study did not provide a standard definition for the size of a "cup" of coffee.

The second finding was that among women with ER positive cancer being treated with tamoxifen, higher coffee consumption was associated with better results. This sounds promising, especially when taken with the results of the laboratory study, but it is always possible that confounders might have affected the results.

Tamoxifen is normally only used in women with ER positive cancer who have not yet gone through the menopause. Therefore, it is unclear whether a similar effect would be seen in post-menopausal women who require a different type of hormonal treatments, such as aromatase inhibitors.

Further research is required on the possible association between coffee consumption and breast cancer risk, as it could lead to new treatments.

However, it should be noted that over-consuming coffee can have negative side effects. Regularly drinking more than five cups of coffee a day can cause insomnia, irritability, an upset stomach and palpitations.

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

Links To The Headlines

Coffee 'can cut risk of breast cancer tumours returning': Two cups a day found to reduce chance by half. Mail Online, April 21 2015


Links To Science

Rosendahl AH, Perks CM, Zeng L, et al. Caffeine and Caffeic Acid Inhibit Growth and Modify Estrogen Receptor and Insulin-like Growth Factor I Receptor Levels in Human Breast Cancer. Clinical Cancer Research. Published online April 15 2015

Categories: Medical News

Mindfulness 'as good as drugs for preventing depression relapse'

Medical News - Tue, 04/21/2015 - 16:00

"Mindfulness-based cognitive therapy may be as good as pills at stopping people relapsing after recovering from major bouts of depression," The Guardian reports.

Researchers wanted to see if a type of therapy known as mindfulness-based cognitive therapy (MBCT) could be an effective alternative treatment to antidepressants for people with major depression at high risk of relapse.

MBCT combines the problem-solving approach of cognitive behavioural therapy (CBT) with mindfulness techniques. These are designed to fix your awareness on the "here and now" instead of having unhelpful thoughts about the past and the future.

In a two-year clinical trial, people already taking antidepressants were assigned to a MBCT programme with a view to reducing or stopping their medication, or were asked to continue antidepressants alone. With support from their GP and therapist, around 70% of the mindfulness group were able to stop taking antidepressants.

The trial suggests MBCT might help some people with major recurrent depression reduce or cut out their medication. However, between four and five people out of every 10 in the trial relapsed within two years, regardless of their treatment. Depending on your perspective, the treatments were equally good or equally bad.

Research does suggest that mindfulness can benefit all of us, not just people with a history of severe depression. Read more about mindfulness for mental wellbeing

Where did the story come from?

The study was led by researchers from Oxford University and was funded by the National Institute for Health Research.

Two authors, including the first author, are co-directors of the Mindfulness Network Community Interest Company and teach nationally and internationally on mindfulness-based cognitive therapy. The other authors declare no competing interests.

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

The media generally reported the story accurately and overall took a positive spin on the results, with some exceptions. The Daily Telegraph, for example, added some balance by saying that, "Some experts warned that the trial was not large enough to come to a definitive conclusion and had not included a placebo group".

However, few sources mentioned the potential conflicts of interest. Some did not recognise that MBCT as well as antidepressants are already recommended treatment options in national guidelines on depression for England and Wales for the prevention of relapse.

The Mail Online's headline, "Meditation is as effective as drugs for treating depression", is also quite careless, as this may give the impression that this is the kind of meditation that may be practised in a yoga class, for example, when it was actually a structured programme of mindfulness-based cognitive therapy.  

What kind of research was this?

This was a single-blind randomised control trial (RCT) comparing mindfulness-based cognitive therapy with antidepressant treatments to prevent the relapse or recurrence of depression.

People with depression often have relapses, and an increasing number of past episodes or ongoing health or life problems can increase the risk of further relapses. People who have had three or more depression episodes are reported to have relapse rates as high as 80% over two years.

For people at high risk of relapse, taking antidepressants for at least two years is the current recommended treatment. However, psychological therapies, including mindfulness-based cognitive therapy (MBCT), are also a recommended option.

This may be given either alongside antidepressant treatment, as an alternative for people who cannot, or do not want to, take antidepressants for this long, or for people who have not responded to antidepressants.

MBCT is a psychosocial intervention specifically designed to teach people with recurrent depression the skills to stay well in the long term. It uses a combination of problem-solving techniques, as well as teaching people how to focus on their immediate environment instead of dwelling on the past or worrying about their future.

MBCT, say the study team, has been shown to reduce the risk of relapse or recurrence compared with usual care, but has not yet been compared with maintenance antidepressant treatment in an RCT.

The aim of the study was to see whether MBCT with support to taper or discontinue antidepressant treatment (MBCT) was better than taking antidepressants for the prevention of depressive relapse or recurrence over 24 months.

Randomised controlled trials are an appropriate and effective way of testing how well different treatments work, such as MBCT compared with antidepressants. 

What did the research involve?

The study analysed 424 adults from urban and rural areas in the UK. All had a diagnosis of recurrent major depressive disorder (currently in remission), had three or more previous major depressive episodes, and were taking maintenance antidepressants to prevent further relapses.

The recruits were randomly assigned to receive an eight-week MBCT class or continue on maintenance antidepressants (212 in each group). Recurrence of depression was assessed over the following two-year period.

Both groups took antidepressants to begin with. The MBCT intervention was added on top, and included efforts to lessen the use of antidepressants, in consultation with their GP, if they felt they didn't need them or needed less of them.

MBCT is intended to enable people to learn to become more aware of their bodily sensations, thoughts and feelings associated with depressive relapse or recurrence, and to relate constructively to these experiences.

Participants learn mindfulness practices and cognitive-behavioural skills both in sessions and through homework assignments. Therapists provide support to patients in learning to respond adaptively to thoughts, feelings and experiences that might otherwise have triggered a relapse.

The programme involved eight 2¼-hour group sessions, normally over consecutive weeks, with four refresher sessions offered roughly every three months for the following year.

Patients in the maintenance antidepressant group received support from their GPs to maintain a therapeutic level of antidepressant medication in line with prescribing guidelines for the two-year follow-up period.

The main success measure was the time to relapse or recurrence of depression, with patients followed up at five separate intervals over two years. Secondary measures of success were the number of depression-free days, residual depressive symptoms, psychiatric and medical comorbidity, quality of life, and cost effectiveness. 

What were the basic results?

Most people completed the two-year trial (86%). In the MBCT group, 13% did not lower their antidepressant dose, 17% did, and 71% stopped completely.

Time to relapse or recurrence of depression over 24 months did not differ between people in the MBCT group or those taking maintenance antidepressants alone (hazard ratio [HR] 0.89, 95% confidence interval [CI] 0.67 to 1.18). A total of 94 (44%) of 212 patients in the MBCT group relapsed, compared with 100 (47%) of 212 in the maintenance antidepressants group.

Nor did the number of serious adverse events differ. Five adverse events were reported, including two deaths in each of the MBCT and maintenance antidepressants groups. No adverse events were attributable to the interventions or the trial.

MBCT was no better than antidepressants for the number of depression-free days, residual depressive symptoms, psychiatric and medical comorbidity, and quality of life.

The cost effectiveness analysis showed MBCT is not more cost effective than maintenance antidepressants alone. 

How did the researchers interpret the results?

The researchers said that, "We found no evidence that MBCT [combined with support to reduce antidepressant treatment] is superior to maintenance antidepressant treatment for the prevention of depressive relapse in individuals at risk for depressive relapse or recurrence.

"Both treatments were associated with enduring positive outcomes in terms of relapse or recurrence, residual depressive symptoms, and quality of life." 


This trial showed that mindfulness-based cognitive therapy enabled many people at high risk of a relapse of depression to discontinue their medicines, and achieve similar levels of relapse over a two-year period.

The number of depression-free days, residual depressive symptoms, psychiatric and medical comorbidity, and quality of life ratings were also similar. This suggests the mindfulness programme in the trial may help those who can't, or do not want to, use antidepressant drugs over the long term.

These results are consistent with current national guidelines for the prevention of depression relapse in England and Wales.

These recommend that people with depression who are considered to be at significant risk of relapse – including those who have relapsed despite antidepressant treatment, or who are unable or choose not to continue antidepressant treatment – or who have residual symptoms should be offered one of the following psychological interventions:

  • individual cognitive behaviour therapy (CBT) – for people who have relapsed despite antidepressant medication, and for people with a significant history of depression and residual symptoms despite treatment
  • mindfulness-based cognitive therapy – for people who are currently well but have experienced three or more previous episodes of depression

The results remind us that treatments to prevent depression relapse in this high-risk group don't have a high success rate. Between four and five people out of every 10 in the trial relapsed, regardless of their treatment.

Depending on your perspective, the treatments were equally good or equally bad. This highlights that people at high risk of relapse need to receive tailored care and regular follow-up so they can find the best treatment approach for them.

But this study has a number of limitations. As the researchers say, the people in the trial were all willing to try a psychological treatment and try reducing their antidepressant dose. This may mean the results are not generalisable to all people at high risk of depression relapse.

The people in the study had also already tried antidepressants for relapse prevention. They are not the same as people who are considering relapse prevention for the first time and are discussing the first option to use in preventing further episodes.

There was also no control comparison to MBCT. That is, a control intervention where the person still received the same regular group sessions, but without the specific components of the MBCT intervention.

This means it is less able to provide solid proof that the mindfulness intervention is as good as antidepressants for most people with major depression, or whether it is just the regular attention and follow-up that has an effect.

Simply talking to a person could have a significant placebo effect that may improve mood. Larger and longer studies are needed to know this for sure.

This mindfulness intervention was designed specifically to prevent relapses of major depression in those considered to be high risk.

It is not designed or tested to prevent depression in the first place, prevent relapse in lower-risk groups (such as those with only one previous episode of depression), and was not being tested here as an initial treatment for depression.

If you are concerned you are depressed, it is usually recommended that the first person you talk to about your concerns is your GP.

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

Links To The Headlines

Mindfulness as effective as pills for treating recurrent depression – study. The Guardian, April 21 2015

Mindfulness can help prevent relapses of depression as well as anti-depressants, study claims. The Independent, April 21 2015

Mindfulness 'as good as anti-depressants for tackling depression'. The Daily Telegraph, April 21 2015

Depression: 'Mindfulness-based therapy shows promise'. BBC News, April 21 2015

Mindfulness therapy can treat depression as effectively as pills, doctors claim. Daily Mirror, April 21 2015

Meditation is 'as effective as drugs for treating depression': Mindfulness could be offered as an alternative to antidepressants, study claims. Mail Online, April 21 2015

Links To Science

Kuyken W, Hayes R, Barrett B, et al. Effectiveness and cost-effectiveness of mindfulness-based cognitive therapy compared with maintenance antidepressant treatment in the prevention of depressive relapse or recurrence (PREVENT): a randomised controlled trial. The Lancet. Published online April 20 2015

Categories: Medical News

Mistreatment of extreme morning sickness 'leading to abortions'

Medical News - Tue, 04/21/2015 - 13:50

"Extreme morning sickness causes 1k abortions a year, study finds," The Daily Telegraph reports. The report states that poor treatment of some cases of extreme morning sickness (hyperemesis gravidarum) is leading some women to terminate their pregnancy, despite there being safe and effective treatments available.

While morning sickness can be unpleasant, hyperemesis gravidarum (HG) can be extremely debilitating. It can cause feelings of constant nausea, frequent vomiting (some women have reported vomiting up to 50 times a day) and dehydration. Left untreated, it can even be life-threatening.

The "one thousand" figure quoted by the Telegraph comes from an unpublished survey reportedly finding that up to 10% of women with severe morning sickness terminate a pregnancy because of this. We are therefore not able to comment further on the representation of this survey or the validity of this figure.


What is the basis for these reports?

In a joint report called "I could not survive another day", The British Pregnancy Advisory Service and Pregnancy Sickness Support recount women's experiences of severe pregnancy sickness.

The report aims to improve treatment and tackle stigma for women with severe pregnancy sickness by outlining the experiences that led some to have an abortion. The report takes the form of a referenced discussion supported by anecdotes. However, no methods are given in the report, so we cannot know how the selected research has been identified, or whether all relevant information has been considered. We also don’t know how representative the sample is of all women with severe morning sickness, and it is not possible for us to verify the information they have given.


Sickness in pregnancy

Sickness in pregnancy is common. Around 7 out of every 10 pregnant women experience nausea and/or vomiting, and this doesn't just occur in the morning. The medical term for morning sickness is nausea and vomiting in pregnancy.

For most women, this improves or disappears completely by around week 14, although it can last longer for some women.

However, some pregnant women experience severe nausea and vomiting. They might be sick many times a day and be unable to keep food or drink down, which can have a negative impact their daily life. Many women with this condition are unable to leave their house, go to work or look after their other children.


What is severe pregnancy sickness?

Severe pregnancy sickness, called HG, is a severe pregnancy complication characterised by extreme nausea and vomiting. Symptoms in addition to the nausea and vomiting can include ptyalism (excessive saliva production), headaches, heightened and warped sense of smell, and extreme fatigue.

Poor management of HG can lead to complications, including but not limited to, dehydration and malnutrition, tears of the food pipe, burst blood vessels, pressure sores, deep vein thrombosis and placental abruption. In addition to the physical complications, HG can lead to depression and social isolation, as well as financial and relationship problems for those experiencing it, and women feel they are less effective parents due to the condition. These complications can lead to post-traumatic stress disorder, and the condition is known to limit family size.


What evidence does the report discuss?

The report is based on the experiences of 71 women who had terminated a pregnancy while suffering HG over the past 10 years. The report documents their experiences and discusses what can be done to improve care for women in this situation and better support their choices.

Most women surveyed (over 85%) believed that healthcare professionals did not understand their condition or believed how ill they were. For the majority of women, it was the impact that HG had on their ability to care for their existing children that was a key factor in their decision.

A significant proportion of women who ended wanted pregnancies were reportedly not offered the full range of treatment options. They were said to be "expected either to put up with the sickness or undergo an abortion".

There were also said to be struggles accessing medication. The report suggests that doctors’ previous awareness of the thalidomide tragedy may have led them to fear of medicating during pregnancy. Thalidomide was marketed first as a sleeping pill, then as an aid for morning sickness during the 1950s. It was soon found to cause severe and often fatal birth defects.

They say that most effective medications for nausea and vomiting are not licensed in pregnancy because pharmaceutical companies usually exclude pregnant women from drug trials, and doctors who prescribe medication for pregnant women do so off-label.

Stigma and misapprehensions were documented. A number of women surveyed commented on the difficulty talking about their decision, fearing judgement for terminating a wanted pregnancy "just for morning sickness".


How accurate is the media reporting of the study?

The media reporting was generally accurate and represented the information given in the report. Many quoted figures suggesting that around 10,000 women suffered HG, and 10% of these decide to terminate their pregnancy as a result. This figure comes from an unpublished survey reportedly finding that up to 10% of women with severe morning sickness terminate a pregnancy because of this. We are therefore not able to comment further on the representation of this survey or the validity of this figure.


What recommendations were made?

The report says that any woman who has made an appointment to discuss her symptoms should have her concerns taken seriously and any risks of medication must be weighed against the larger picture of the risks both for mother and baby of not treating HG, especially if symptoms become so bad that the mother considers terminating the pregnancy.

The report says the stigma and guilt that surrounds abortion for severe sickness should also be confronted. Many women continue to "blame themselves for being unable to carry their pregnancy to term, or feel that they should have fought harder to get help".

The report concludes: "No woman should ever be judged, feel ashamed or a failure for deciding that abortion is the best course of action for her, or pressured into accepting medication when she believes ending the pregnancy is what she needs to do. But women with pregnancies they wish to keep deserve prompt access to treatments that may enable them to do just that."

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

Links To The Headlines

Extreme morning sickness causes 1k abortions a year, study finds. The Daily Telegraph, April 20 2015

Morning sickness report: 1,000 abortions a year in Britain due to extreme form of illness during pregnancy. The Independent, April 20 2015

1,000 abortions each year are linked to severe pregnancy sickness also suffered by Kate Middleton because women fail to get help. Mail Online, April 20 2015

Severe morning sickness? ‘Put up with it or get an abortion’. Metro, April 20 2015

Categories: Medical News

Why you should drink (water) before you drive

Medical News - Mon, 04/20/2015 - 15:30

"Not drinking enough water has same effect as drink driving," The Daily Telegraph reports. A small study found participants made more mistakes on a driving simulator task when they were mildly dehydrated than when they had plenty of fluids.

This was a small trial of 12 men, studying the effect of mild dehydration on performance during a driving task. The men had a day of being hydrated or fluid-restricted prior to spending two hours in a driving simulator showing a view of a monotonous dual carriageway.

This was a crossover trial, meaning that all men acted as their own control, undertaking both hydrated and dehydrated conditions one week apart.

The researchers found men in the dehydrated state made around double the number of driving errors during the two-hour drive compared with the hydrated group.

Overall, the detrimental effects of dehydration on wellbeing and physical and mental performance are well-publicised, so the results are entirely plausible. But the study has many limitations, so it cannot provide solid proof.

These include the very small sample size and the fact that spending two hours in a driving simulator in an enforced state of dehydration or hydration may not be the same as driving in real life. The participants could have driven less carefully because they knew it was only a simulation.

Still, when you are in charge of several tonnes of metal moving at high speed, anything that could impair your concentration is a concern. We recommend topping up with food and water if you are going on a long drive, as well as taking regular breaks. 

Where did the story come from?

The study was carried out by researchers from Loughborough University and was funded by the European Hydration Institute.

It was published in the peer-reviewed journal, Physiology and Behaviour.

The UK media reliably reports the main theme of this research, but does not point out that, though based on an entirely plausible hypothesis, this small study actually provides very little conclusive proof. 

What kind of research was this?

This was a small randomised crossover trial looking at the effect of mild dehydration on driving performance during a long, monotonous driving simulation.

As the researchers explain, mild dehydration can cause symptoms such as headache, weakness, dizziness, fatigue, lethargy, and reduced alertness and ability to concentrate. This could affect both physical and mental performance in a variety of tasks, including driving.

The study was particularly interested in any possible link between dehydration and vigilance or response times during a driving simulation. The crossover design meant participants acted as their own controls, performing the task in both hydrated and dehydrated conditions.  

What did the research involve?

The study included 12 healthy men with an average age of 22, who were all tested in a driving simulator. After an initial visit to familiarise themselves with the set-up, the participants attended the lab on two separate occasions seven days apart. The hydrated and dehydrated conditions were given in a random order.

Each man filled in a food and drinks diary the day before each visit. They went to the test laboratory after a 10-hour overnight fast, where urine and blood samples were taken.

Subjective feelings of thirst, hunger, concentration and alertness were assessed on a visual analogue scale, where you plot yourself on a 100mm line from good to bad, such as "not thirsty" to "dire thirst".

The men went away for a day with the instruction to repeat their food intake of the previous day, with differences in fluid intake.

The hydrated group drank at least 2.5 litres of fluid throughout the day, while the dehydration group only had 25% of this fluid intake (expected to cause a 1% reduction in body weight over 24 hours).

The following morning, they returned to the test lab after another overnight fast and the blood, urine and visual scales were repeated. They were then given breakfast, along with water to drink – 500ml in the hydrated group and 50ml in the dehydrated group.

They were fitted with electrodes to measure their brain activity (an electroencephalogram, or EEG) and then completed a two-hour driving task in the driving simulator.

The car gave a computer-generated road projection of a monotonous dual carriageway with long straight sections and gradual bends.

Slow-moving vehicles were met occasionally and had to be overtaken. Otherwise, the driver was instructed to stay in their lane. After one hour of the task, 200ml of fluid was given to the hydrated group and 25ml to the dehydrated group.

After the driving trial, blood samples were taken and an assessment was again made of subjective feelings of thirst, throat dryness, hunger, concentration and alertness. 

What were the basic results?

Data is only reported for 11 of the 12 participants. One was excluded from the results for "displaying a high propensity to fall asleep during the driving task (perhaps caused by sleep deprivation)".

The day of fluid restriction caused a 1.1% reduction in body mass, compared with a 0.1% reduction in the people who drank normally on that day. Examination of their blood and urine samples also confirmed that they were less hydrated.

The two-hour driving test was split into four 30-minute sections. Both groups made more and more driving errors as the test progressed. However, the number of errors was consistently higher in the dehydrated group than in the hydrated group – significantly so after the first 30 minutes.

These were minor errors, and included drifting, car wheels crossing the rumble strip or lane line, and late braking. There were four major incidents (such as hitting the barrier or another car), but these were evenly distributed between the two groups.

Overall, there were 101 major or minor errors in the dehydrated group, compared with 47 in the hydrated group – a statistically significant difference.

There was no significant difference in brain activity between the groups throughout the trial, as measured by the EEG.

At the end of the trial, people in the dehydrated trial rated worse for feelings of thirst, throat dryness, hunger, concentration and alertness. 

How did the researchers interpret the results?

The researchers concluded that, "The results of the present study suggest that mild [dehydration] produced a significant increase in minor driving errors during a prolonged, monotonous drive, compared to that observed while performing the same task in a hydrated condition."

They say the magnitude of decrement was similar to that observed when driving after drinking alcohol (to a blood alcohol concentration of approximately 0.08%, which is the current UK legal driving limit), or while sleep-deprived. 


This small randomised crossover study suggests that men make more minor driving errors when dehydrated, similar to the effect of being over the alcohol limit or sleep-deprived.

The idea that dehydration worsens driving ability is plausible. However, despite the plausibility of these results, there are several important limitations, meaning that this study does not actually provide firm evidence.

Representation of the sample

The study included only 12 young healthy males, and one of them was excluded as it was thought his performance wasn't reliable enough during the trial. The performance of these 11 remaining men cannot be extrapolated to the general population, as there are too many potential variables, such as age, gender, and varying general driving abilities, alertness and concentration levels.

Sample size

With only 11 men analysed, it is possible that the results could have been completely different if a larger sample had been studied. As the researchers acknowledge, the small sample size means their study did not have the statistical power to examine how the number of driving errors was related to the degree of hydration.

The artificial scenario

Spending two continuous hours in a driving simulator viewing a monotonous computer-generated screen while in an enforced state of dehydration or hydration may not be the same as driving in real life. For example, in real life:

  • you know you are in a serious situation where errors can mean life or death
  • there are variations in scenery and other distractions, which could have either beneficial or detrimental effects (such as fresh air or loud noise) 
  • if you know you are feeling unwell, you can actually stop, have a break, have something to eat or drink, for example 
Unproven comparisons

Though the study – and hence the media – has made a comparison between dehydration, alcohol and sleep deprivation, these are indirect comparisons.

Overall, despite the study's limitations, the detrimental effects of dehydration on wellbeing and physical and mental performance are recognised. That this applies to driving is entirely plausible, but was not proven by this study.

But if you are driving and feel thirsty, it is highly recommended that you take a break and rehydrate. Anything that can impair your concentration while driving is a potential risk to health.

As this study points out, worldwide, an estimated 1.2 million people die and a further 50 million people are injured each year in road traffic accidents. Driver error is the leading cause of accidents.

Read more about road traffic safety.

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

Links To The Headlines

Not drinking enough water has same effect as drink driving. The Daily Telegraph, April 18 2015

Driving while dehydrated can be just as dangerous as drink driving, study suggests. The Independent, April 19 2015

Dry drivers who are dehydrated behind the wheel 'make as many mistakes as drinkers'. Mail Online, April 20 2015

Scientists: 'Drinking makes you a better driver'. Metro, April 19 2015

Links To Science

Watson P, Whale A, Mears SA, et al. Mild hypohydration increases the frequency of driver errors during a prolonged, monotonous driving task. Physiology and Behavior. Published online April 16 2015

Categories: Medical News

There are six different types of obesity, study argues

Medical News - Mon, 04/20/2015 - 14:00

"Researchers have identified six 'types' of obese person," The Independent reports. It's argued that each type would benefit from a targeted treatment programme for obesity, rather than a "one-size-fits-all" approach.

This study looked at data from more than 4,000 obese adults taking part in the Yorkshire Health Study. It aimed to see whether it was possible to categorise obese individuals according to common health and lifestyle characteristics.

The study reported six clusters of obese individuals. These were:

  • young healthy females – women who were obese, but generally had fewer obesity-related complications, such as type 2 diabetes
  • heavy-drinking males – as above, but with higher alcohol intake
  • unhappy and anxious middle-aged – predominantly women with poor mental health and wellbeing
  • affluent and healthy elderly – generally positive health, but defining characteristics of higher alcohol intake and high blood pressure
  • physically sick but happy elderly – older people with more chronic diseases such as osteoarthritis, but good mental health
  • poorest health – people who were the most economically deprived and had the greatest number of chronic diseases

This research suggests it may be better to recognise subgroups of obesity, rather than put all obese people into one category, which may help tailor interventions and treatments more effectively. The current study does not prove this hypothesis, though it is worth further investigation.  

Where did the story come from?

The study was carried out by researchers from the University of Sheffield in the UK and the Harvard School of Public Health in the US. No sources of financial support are reported.

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

The UK media reports the study's findings accurately, but could, in general, do with emphasising this is theory-generating research only.

On its own, it does not provide firm evidence that there are six categories of obesity or that these people would benefit from different treatments. 

What kind of research was this?

This was an analysis of data collected as part of an ongoing UK cohort study, the Yorkshire Health Study, which aimed to see whether it was possible to categorise different subgroups of obese people according to health, sociodemographic, or behavioural characteristics.

The researchers suggest that using a single classification of obesity – simply all those with a body mass index (BMI) of 30 or over – fails to recognise the variations seen in obese people.

Some may have different levels of metabolic fitness and require different interventions. For example, some people's obesity may be related to their alcohol intake, while for others it is the result of a lack of exercise and a poor diet.

This is a useful initial study for trying to identify whether there may be different obesity types, but it can't tell us more than that. Without further study, we won't know whether these are stable subtypes with different health risks who might benefit from different treatments. 

What did the research involve?

The study used data collected from the Yorkshire Health Study between 2010 and 2012. The study aimed to examine the health needs of individuals in Yorkshire.

Participants were sent questionnaires by their GP, and data on 27,806 people (16% response rate) was collected, 4,144 of whom were obese with a BMI of 30 or more.

The questionnaire included information on age, sex, ethnicity, socioeconomic status and health conditions. A validated questionnaire (EuroQoL EQ5D) assessed health-related quality of life.

Behavioural assessments gathered information on smoking status, alcohol consumption, physical activity, and whether the person had engaged in active management of their weight, such as using slimming clubs, controlling their portion sizes, or over-the-counter remedies.

The main analysis looked for different clusters of people with common characteristics. 

What were the basic results?

The average age of the study group was 56 years, 58% were women, and the average BMI was 34. Most (95%) were white, and generally came from more deprived areas of the region.

On analysing the data, the researchers found there were six distinct clusters of obese individuals. These were defined as:

  • heavy-drinking males
  • younger healthy females
  • physically sick but happy elderly
  • affluent healthy elderly
  • unhappy anxious middle-aged
  • poorest health

The largest of these groups was the young healthy females, who displayed the most positive characteristics when comparing the different variables across the groups.

For example, they drank slightly less alcohol than others, had fairly good life satisfaction scores, and managed their weight slightly more actively.

Heavy-drinking males were similar to the young healthy females with the exception of their alcohol intake (average 11.86 units per week versus 4.98).

Other characteristics differed for the different groups. For example, the unhealthy anxious middle-aged predominantly included women with poor mental health, low quality of life and sense of wellbeing.

Physically sick but happy elderly included those with low levels of mental health problems but other chronic health problems, such as arthritis and high blood pressure.

The poorest health group were those who were the most deprived, and had the most chronic health problems and unhealthier lifestyle behaviour. 

How did the researchers interpret the results?

The researchers concluded that, "It is important to account for the important heterogeneity [variation] within individuals who are obese.

"Interventions introduced by clinicians and policy-makers should not target obese individuals as a whole, but tailor strategies depending upon the subgroups that individuals belong to." 


The researchers appropriately describe their study as being "exploratory and hypothesis-generating". The study used a large population sample of more than 4,000 obese individuals from Yorkshire.

It looked at whether there were patterns of health, sociodemographic and lifestyle characteristics that were common to these people. The study found six distinct categories that best fitted this group. However, as the researchers say, the study "may be used to drive future research" but "cannot identify causation".

The study identified six categories for this Yorkshire-based sample, but we do not know whether the same six categories would be identified if other samples of obese people were examined – for example, those of different ages, ethnicities, from different counties in the UK, or different countries. Other samples may yield fewer, more, or different categories.

Even if the different obesity categories are accurate, we can't say anything about how they relate to different health risks. For example, though some chronic diseases were more common in certain obesity categories, we can't say from this snapshot in time whether their obesity contributed to causing these diseases. By the same measure, we can't say whether any of the lifestyle characteristics measured has contributed to causing the obesity.

The study authors say all the individuals in the study would benefit from weight loss, but weight loss may not be a priority for all groups. They say, for example, that "among the poorest health group, weight loss may be less of an issue compared with the chronic health issues associated with the cluster. This is in contrast to other groups such as younger healthy females or affluent healthy elderly, where weight loss could be a priority".

However, we can't say from this research whether any of these obese groups is "healthier" or "unhealthier" than any other. Obesity is known to be associated with several adverse health effects, including risk for cardiovascular diseases and certain cancers. Research has so far not established a "healthy" type of obesity. Obesity means a weight that is unhealthy.

Although it may well be true that different types of people with obesity may respond better to different types of intervention (such as exercise interventions or behavioural support groups), this cannot be determined by this study, which has not examined different interventions.

As the researchers say, their research provides an interesting avenue for further study in ways to tackle the obesity epidemic. However, for now, the best advice is to aim for a healthy weight and lifestyle through a balanced diet, regular exercisenot smoking and moderating your alcohol intake.

Following the NHS weight loss plan may be one way you can bring your weight down to a healthy level through a combination of diet and exercise.

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

Links To The Headlines

Six types of obese individual, researchers find. The Independent, April 18 2015

Six categories of obesity, and just as many ways to treat it. The Times, April 18 2015

Obese people fall into six distinct categories, study suggests. The Daily Telegraph, April 17 2015

Obesity affects six different types of people, researchers say. The Guardian, April 18 2015

Revealed: The SIX different types of obese person from glowing girls to heavy-drinking males. Daily Mail, April 18 2015

Scientists identify 6 different obesity models in new study: Do you fall into one of the categories? Daily Mirror, April 18 2015

Scientists call for stop to 'one-size-fits-all' weight loss plans. BBC News, April 18 2015

Links To Science

Green MA, Strong M, Razak F, et al. Who are the obese? A cluster analysis exploring subgroups of the obese. Journal of Public Health. Published online April 18 2015

Categories: Medical News

Study doesn't prove e-cigs make quitting smoking harder

Medical News - Fri, 04/17/2015 - 11:46

"E-cigs don’t help smokers quit fags – in fact they make it harder to stop," the Daily Mirror reports, apparently turning on its head the common view that using e-cigarettes can help you quit smoking conventional cigarettes.

The Mirror’s report – echoed in the Daily Mail – was based on surveys of American smokers’ habits and intentions to quit. The study found that people who had ever used e-cigarettes were about half as likely to have reduced their smoking or quit one year later compared to those who said they would never use them.

This might look like a significant finding considering the controversy over whether e-cigarettes are a useful aid to quitting. But we don’t know whether the people who used e-cigarettes were actually using them to try and quit, or whether they actually used them between the first and second surveys. There may be many factors including lifestyle and use of other smoking cessation therapies, which were not considered by the researchers.

Ideally, a well-conducted randomised controlled trial would be needed to examine the effect of e-cigarette use on the success of people wanting to quit, comparing success rates between e-cigarette users and those using other smoking cessation methods.

The studies – and debate – into the pros and cons will continue, but this study does not prove that e-cigarettes make it harder to stop.

Where did the story come from?

The study was carried out by researchers from the University of California and San Diego State University. The California Department of Public Health supported data collection for the California Smokers Cohort but no other further sources of financial support are reported.

The study was published in the peer-reviewed medical journal, the American Journal of Public Health.

The media coverage takes these study findings as conclusive and does not consider the important limitations of this study. For one thing, saying that e-cigarettes "make quitting smoking harder" is not demonstrated by this study. That’s because we don’t know whether the people who reported ever using e-cigarettes were using them as a way of trying to quit in the first place. Also, the researchers don’t report whether or how often this group of people used e-cigarettes in the year between surveys.

What kind of research was this?

This was a longitudinal study of Californian smokers who were surveyed twice (12 months apart). The researchers wanted to see if people who had ever used electronic cigarettes were more likely to quit than those who had never used e-cigarettes.

Using e-cigarettes, or "vaping", is a hotly debated area. E-cigarettes and associated products are a relatively new phenomenon and they have not been extensively studied. Currently, it is unclear whether they are of any benefit for quitting smoking, or whether they may even be harmful to society in introducing a new form of nicotine addiction.

This type of study cannot answer the question for us. It can only look at associations between reported e-cigarette use at one point in time and quitting later. It cannot tell us whether e-cigarette use is directly causing the quitting (or lack of quitting) or what other factors may be involved. High-quality randomised controlled trials would be needed for that.

What did the research involve?

This study used the California Smokers Cohort (CSC), a longitudinal survey designed to investigate factors that predict "cigarette cessation behaviour" in current and former smokers in California.

The researchers carried out a baseline telephone survey of Californian residents and identified 1,000 people aged 18-59 years who were current smokers. These people were re-interviewed using the same survey one year later.

Current smokers were defined as those who had smoked at least 100 cigarettes in their lifetime, and were smoking on at least some days at the time of the survey. Frequency of smoking was recorded only as daily or non-daily (on some days). Smokers were questioned about nicotine dependence by deeming those who needed a cigarette within 30 minutes of waking up as a sign of greater addiction.

The smokers were asked about their intention to quit, with options being:

  • never expect to quit
  • might quit in the future but not in the next six months
  • will quit in the next six months
  • will quit in the next month

The first two groups were combined as "no current intention to quit", the last two as "intending to quit in the next six months".

The smokers were also asked if they had heard of e-cigarettes, and if they had they were asked "what describes you best regarding your use of e-cigarettes: you have used e-cigarettes, you might use e-cigarettes, or you will never use e-cigarettes?"

The outcomes the researchers were interested in were:

  • whether smokers had achieved a self-reported 20% reduction in the number of cigarettes smoked each month
  • any self-reported quit attempts in the past year
  • current abstinence from cigarette use (those reporting abstinence of one month or longer)

The researchers took into account potential confounding factors of intention to quit, level of addiction, age, gender, ethnicity and years of education.

What were the basic results?

In the first survey, around a quarter of people had used e-cigarettes, and roughly a third each said they might use them, or would never use them. The remainder had never heard of them.

Sixty per cent of the sample had greater addiction in terms of needing a cigarette within 30 minutes of waking, and just over half of the sample (57%) said they had no intention of quitting smoking in the next six months.

At follow-up, 41% had made a quit attempt in the past year, a third had reduced their consumption, and 9% had achieved abstinence, quitting smoking completely.

People who said they had ever used e-cigarettes were about half as likely to have reduced monthly consumption one year later compared to those who said they would never use them (odds ratio [OR] 0.51, 95% confidence interval [CI] 0.30 to 0.87).

Factors significantly associated with increased likelihood of reduced smoking were younger age (18-44 versus 45-59 years), being a daily smoker (rather than an occasional smoker), and reported intention to quit in the next six months.

People who had ever used e-cigarettes were also less likely to be abstinent at 12 months compared to those who said they would never use them (OR 0.41, 95% CI 0.18 to 0.93).

Intention to quit was associated with a significantly increased likelihood of quitting smoking, and people who were daily smokers were significantly less likely to quit than occasional smokers.

How did the researchers interpret the results?

The researchers conclude that: "Smokers who have used e-cigarettes may be at increased risk for not being able to quit smoking. These findings, which need to be confirmed by longer-term cohort studies, have important policy and regulation implications regarding the use of e-cigarettes among smokers."


This study found that people who have used e-cigarettes may be less likely to quit smoking, but it can’t prove that’s the case. There are limitations to the findings and confirmation is needed from other studies.

The two surveys can only look at factors associated with quitting, but we can’t be certain that the e-cigarette use had any direct influence upon this. There are likely to be many unmeasured factors that could be influencing the results, including lifestyle factors and use of other smoking cessation therapies. We also don’t know whether the smokers actually used e-cigarettes as a quitting aid during the year between the first and second surveys.

The researchers did assess people’s intentions to quit smoking in the first survey, and adjusted for this in their analyses. However, it may be difficult to fully capture people’s intentions, and these may have changed. It may be that the people who used e-cigarettes were not doing so to quit or were less serious about quitting, while those who were, chose to use other smoking cessation therapies.

Ideally, high-quality randomised controlled trials looking particularly at people who want to quit and whether they use e-cigarettes or other smoking cessation methods are needed. These trials would also need to carefully follow people at intervals and take scientifically validated, in-depth assessments of their smoking status, rather than just relying on people’s self-reported smoking status in a telephone survey, which may not give reliable results.

Other limitations to this study include that the sample of Californian residents may be unrepresentative of other populations worldwide.

The use of e-cigarettes, including whether they actually help people to quit, or whether they may have harmful effects, such as introducing a new form of addiction, will continue to be studied and debated.

Read more about treatment and support to quit smoking.  

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

Links To The Headlines

E-cigarettes make quitting smoking HARDER, study claims. Daily Mail, April 16 2015

E-cigs DON'T help smokers quit fags - in fact they make it harder to stop. Daily Mirror, April 16 2015

Links To Science

Al-Delaimy WK, et al. E-Cigarette Use in the Past and Quitting Behavior in the Future: A Population-Based Study. American Journal of Public Health. Published April 16 2015

Categories: Medical News

Discovery could 'boost immune system's cancer fighting ability'

Medical News - Fri, 04/17/2015 - 11:46

The media is awash with news of a breakthrough that is "turbocharging the immune system to kill all cancers" (The Daily Telegraph) and a "game-changing new way to fight cancer" (The Independent).

Both of these vivid headlines are debatable – the first because the technique has only been looked at in one type of cancer, and the second because it has only been examined in lab mice.

Researchers were actually looking at a way to overcome "exhaustion" of the body's immune system when its killer cells (called CD8 T cells) have too much to deal with. They wanted to find out how to increase the number of these killer cells, and memory cells that help the immune system "remember" cancers and viruses.

The researchers used genetic techniques in mice to study CD8 T cells. They discovered a protein, lymphocyte expansion molecule (LEM), which helps increase the number of CD8 T cells, improving the mice's ability to fight viruses or cancer cells. The LEM protein is a new discovery, and the researchers hope they can produce treatments for human diseases based on it.

Discovery aside, research on this protein is at its first stage. A balance of the beneficial and harmful effects of boosting the immune system with this protein would need to be struck before it can start being tested on people.

So we now know more about the human immune system, but it is – as is often the case – too early to say if it will lead to a truly "game-changing" treatment for cancer. 

Where did the story come from?

The study was carried out by researchers from Imperial College London, Queen Mary University of London, Harvard Medical School, and ETH Zurich, a specialist science university in Switzerland.

The study received various sources of funding, including from the Wellcome Trust, Cancer Research UK, and the US National Institutes of Health.

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

The news stories give representative coverage of this laboratory study overall, but their headlines talking about a "breakthrough" give premature hopes about research that is still in the very early stages.

The Mail Online's estimate that a drug based on the findings "could be tested on humans in three years" appears to be based on this press release from Imperial College London. However, it would be many years of further research before any treatment becomes widely available.

The press release, which describes "boosting immunity to viruses and cancer", is likely the basis for the "turbocharging" and "game-changing" metaphors used in much of the media coverage. 

What kind of research was this?

This laboratory and animal research examined the workings of the immune system, specifically looking at CD8 T cells. T cells are a type of white blood cell (lymphocytes) that play a key role in defending the body against infection from foreign organisms such as viruses and bacteria.

T cells also destroy abnormal or cancerous cells. The T cells that have this "killing" ability are sometimes called killer T cells, or cytotoxic T cells. Because they carry a receptor for the CD8 protein, these particular cells are called cytotoxic CD8 T cells.

But the very fact humans get infections and cancer is evidence that the CD8 T cell immunity is a bit flawed. A possible reason for this flaw is that because there are so many virally infected or cancerous cells, the CD8 T cells may in some way become inactivated – a kind of "immune exhaustion".

This exhaustion causes a failure of the immune response in the short term, but also hinders the development of "memory" CD8 T cells. These are T cells that "remember" how to recognise abnormal cells for future immune response.

In this study, the researchers looked at the immune response of genetically mutated mice infected with a virus. They wanted to see whether they could identify ways to encourage more cytotoxic CD8 T cells and memory cells to grow. 

What did the research involve?

The research involved both normal mice and mice carrying different genetic mutations to see whether some of the mutant mice had a better immune response.

The mice were infected with a virus called lymphocytic choriomeningitis virus (LCMV C13). This is said to be an established animal model for chronic viral infection in humans. It results in a very high level of virus in the body, causing "immune exhaustion" of CD8 cells and blocking memory cell development.

About a week after infecting the mice, levels of cytotoxic CD8 cells and memory cells were measured to see which mice were producing more of them.

The researchers furthered their study of viral infection by also looking at the response when mice were given cancer (melanoma) cells.

In the mice with enhanced immune response, the researchers then identified what gene was causing this heightened response. 

What were the basic results?

The researchers found a particular type of mutant mouse (called "Retro" mutant mice) had increased CD8 T cell levels ten times that of normal mice. These cells had increased virus-killing ability when studied in the lab.

However, the researchers found all Retro mice died two weeks after infection, whereas the normal mice survived the infection. They thought this was because the increased immune response in the Retro mice led to a fatal breakdown of the blood vessels.

The Retro mice also demonstrated increased production of CD8 memory cells. When mice were injected with a second dose of the LCMV virus later on, the Retro mice again had a very enhanced CD8 T cell response compared with the normal mice.

Similarly, when injected with melanoma cells, the Retro mice demonstrated three times higher CD8 T cell levels, and four times fewer tumours, compared with normal mice injected with melanoma.

The Retro mice were found to have a mutation in a gene that codes for a protein called lymphocyte expansion molecule (LEM). The researchers confirmed that this gene and protein were involved in the enhanced immunity in a further study, where mice were genetically engineered to lack this gene variant or the cellular activity of the protein was blocked.

Researchers also identified the human equivalent of the LEM protein and found it was produced in higher levels in human T cells responding to infection. Increasing the amount of LEM the human T cells were making in the lab caused them to divide and produce more T cells. 

How did the researchers interpret the results?

The researchers say they have "discover[ed] LEM at the heart of a pathway that, when up-regulated, not only restores CD8 T cell immunity to chronic viral infection and tumour challenge, but also increases memory cell development".

They say that, "LEM therapy has the potential to both globally expand CD8 T cells". 


This laboratory study in mice has looked at how CD8 T cell immunity might be enhanced. Researchers hoped to find ways to increase the numbers of "killing" cells that can destroy infected or abnormal cells and avoid a state of "immune exhaustion", which leads to humans succumbing to infection or the progression of cancer.

Studying normal and genetically mutated mice, they identified a previously overlooked protein they called LEM, which is involved in increasing the numbers of these cells. The researchers hope it could one day lead to the production of LEM therapy.

While they do not specify treatment use in their research article, an accompanying press release spells out that they hope the research will be used to develop cancer treatments.

The study is at a very early stage and many questions remain unanswered. The main problem is that nobody appears to have looked into the role of LEM protein in humans yet.

Another problem that can't be ignored is that all the Retro mice died after infection as a result of their greatly enhanced CD8 T cell proliferation. This shows there is a delicate balance to be struck in enhancing LEM activity and immune cell proliferation, while keeping side effects to a minimum.

The study in mice is, so far, also limited to the study of a particular virus and melanoma cancer cells. We don't yet know whether the same CD8 T cell proliferation would be seen with all infections or all cancer. It's also not clear whether the levels of proliferation seen would completely remove or prevent viral infection or cancer.

Overall, the research genuinely furthers our understanding of how the immune system fights infections and cancer, but it is too early to know if this will lead to a treatment breakthrough for cancer. 

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

Links To The Headlines

'Game-changing' new way to fight cancer discovered. The Independent, April 17 2015

Cancer fighting protein discovered by chance offers fresh hope for cure. Daily Express, April 17 2015

Mystery protein could help us ward off disease. The Times, April 17 2015

New cancer treatment which supercharges the body's ability to fight disease is hailed as having an 'astonishing' effect – and could be tested on humans in three years. Mail Online, April 16 2015

Scientists find key to 'turbo-charging' immune system to kill all cancers. The Daily Telegraph, Published April 16 2015

Links To Science

Okoye I, et al. The protein LEM promotes CD8+ T cell immunity through effects on mitochondrial respiration. Science. Published April 17 2015

Categories: Medical News

Does happiness have a smell and is it contagious?

Medical News - Thu, 04/16/2015 - 17:00

"Humans can smell when other people are happy, researchers discover," The Independent reports; somewhat over-enthusiastically.

In a new study, Dutch researchers investigated where happiness could be "spread" to others, via body odours, through a process known as "chemosignalling".

Nine men provided sweat specimens during three sessions that aimed to make them feel happy, fearful or neutral. Film and TV clips were used to induce these feelings.

Thirty-five female students were then asked to smell the samples and their reactions were captured.

The women were more likely to have a happy facial muscle response if the sample was taken while the men watched happy clips. A fearful response was more likely if the sample was taken in the fear condition. Women seemed to be able to tell if the sweat had come from men in the happy or fearful condition compared to the neutral condition, but not from each other.

It is not possible from such a small study to be able to say with certainty that any changes were due to the smell.

The hypothesis that emotions could be spread via odours may be plausible to anyone who has been in a sweaty mosh-pit, rave, or the middle-aged equivalent, a post-wedding disco.

But while interesting, this study does not prove that body odours can transmit happy or sad feelings to others.


Where did the story come from?

The study was carried out by researchers from Utrecht University in the Netherlands, Koç University in Turkey, the Institute of Psychology in Lisbon and Unilever research institutes in the UK and Netherlands. It was funded by Unilever, the Netherlands Organisation for Scientific Research and the Portuguese Foundation for Science and Technology. (We seriously hope Unilever are not considering bringing any sweat-based products to market).

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

The UK media reported the research accurately in terms of the actual story, though it seems some headline writers went out on a limb. For example, The Daily Telegraph’s headline "You can actually smell joy", while a delightful prospect, is unproven.

Also, the media did not explain any of the limitations in the study design.


What kind of research was this?

This was an experimental study of the effect of body odours in transferring human emotion from one person to another. Previous research has suggested that negative emotions, especially fear, can be conveyed to others through bodily odours, so-called chemosignals.

Chemosignalling is a recognised phenomenon in some animal species, such as rodents and deer. It is still a matter of debate whether chemosignalling occurs in humans.

The researchers aimed to see if positive emotions can also be transferred through chemosignals. In essence, whether smelling the sweat from someone in a happy state could induce happiness.


What did the research involve?

Sweat samples were taken from men during conditions designed to make them feel fearful, happy or neutral. Women were then asked to smell the samples and their emotional reaction was measured by their facial expression and reported emotion. Their level of attention was also tested, as researchers say that "happiness broadens the attentional scope" while fear narrows it.

Nine healthy Caucasian men of average age 22 provided sweat samples. The samples were collected using armpit pads during three separate sessions, each one week apart.

In the first session the researchers tried to induce fear in the men by showing them nine film clips.

The second session aimed to make the men feel happy, and included a clip of the "Bare Necessities" from the Jungle Book and the opera scene from The Intouchables (a "feelgood" film about the growing friendship between a disabled man and an ex-prisoner).

The final session involved neutral TV clips such as weather reports. The men washed their armpits before the sessions commenced and the pads were frozen after the sessions.

The men were asked to abstain from the following activities for two days before each session to avoid "contamination" of the sweat samples:

  • drinking alcohol
  • sexual activity
  • eating garlic or onions
  • excessive exercise

Whether the sessions induced the desired emotional effect in the men was assessed using a Chinese symbol task and a questionnaire. The Chinese symbol task involves looking at Chinese symbols and rating them on a scale from pleasant to unpleasant compared to the average Chinese character. The task is meant to give an indication of the state the viewer is in when they see the characters, rating them as more pleasant when in a happier mood. The questionnaire asked the men to rate how angry, fearful, happy, sad, disgusted, neutral, surprised, calm or amused they felt, each on a scale of one (not at all) to seven (very much). The men were paid 50 euros for participating.

The sweat pads were thawed, cut up and placed in vials to create happy, neutral or fearful samples. Each sample type was placed under the nose of 35 female students. Their facial expressions in the five seconds after smelling the vials was captured using electromyographic (EMG) pads. These devices are used to capture electrical activity produced by muscles and moving bones (e.g. whether they smiled or grimaced).

The students also completed the Chinese symbol task and other tests to measure their level of attention while smelling each vial.

After all vials had been smelled, the women were asked to rate them for how pleasant and how intense they found them. They were also asked to say whether they thought the samples came from happy, fearful or neutral individuals. They were paid 12 euros for participating.

All men and women recruited were heterosexual – to try and standardise chemosignals emitted by the men, and response from the women.


What were the basic results?

The combined test results for the men suggested that mainly positive feelings were induced by the happiness condition and negative feelings for the fear condition:

  • the men reported feeling happier and more amused in the happy condition
  • feelings of fear and disgust were higher in the fear condition
  • the men had lower levels of arousal in the neutral condition

In the females, a happy facial muscle EMG response was more likely if the male sample was taken in a happy condition. If the sample was taken in the fear condition, the EMG was more likely to show a fear response in the women. The women performed better in the tests measuring wider attention ability when they smelled sweat provided in the happy condition. The sample condition had no effect on the Chinese symbol task or the reported odour intensity. Women could tell if the sweat had come from men in the happy or fearful condition compared to the neutral condition.


How did the researchers interpret the results?

The researchers concluded that: "exposure to sweat from happy senders elicited a happier facial expression than did sweat from fearful or neutral senders". They say: "humans appear to produce different chemosignals when experiencing fear (negative affect) than when experiencing happiness (positive affect)".



The findings from this small experimental study suggest that smelling sweat produced during different emotional states can influence people’s feelings.

However, the study has many limitations and cannot prove this theory. It only looked at sweat samples from nine men, and all of the testers were female students. The researchers say this was deliberate because men sweat more and women have a better sense of smell and greater sensitivity to emotional signals. Nevertheless, this means that we do not know if similar results would be found for men smelling female sweat or within the same sex. We also don’t know whether results would be similar if the women had been with the men at the time and smelling the sweat directly from their body, rather than in a vial that has been placed under their nose.

The study aimed to assess the feelings induced by the smell through facial muscle changes, reported mood and attention. It is not possible from such a study to be able to say with any certainty that any changes were due to the smell.

Other confounding factors could have caused the effects.

In real-life situations, where people are together and more than just smell is involved, emotional responses are due to a combination of thoughts, feelings, environmental factors and all of the senses.    

While interesting, this study does not prove that body odours can transmit happy or sad feelings to others.

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

Links To The Headlines

Humans can smell when other people are happy, researchers discover. The Independent, April 16 2015

Why happiness is infectious: you can actually smell joy. The Daily Telegraph, April 15 2015

Links To Science

De Groot JHB, Smeets MAM, Rowson PJ, et al. A Sniff of Happiness. Psychological Science. Published online April 13 2015

Categories: Medical News

Middle age 'starts at 60' claims media

Medical News - Thu, 04/16/2015 - 14:45

“Middle age begins at 60, say researchers,” The Times reports. A new population modelling study estimates that due to increased lifespan, what was once regarded as elderly should be seen as middle-aged, and this trend will continue into the future.

Traditionally, medical professionals, particularly epidemiologists, regarded 65 as the age at which somebody becomes elderly. This was based on the expectation that they probably only had a few years left to live.

As this study argues, however, this expectation is no longer valid.

Improvements in life expectancy and health mean that categorising someone as old because they've turned 65 no longer makes sense.

Instead, they suggest looking at how long a person may have left to live, based on average life expectancy, which in the UK is currently around 79 years for men and 82 for women (this is expected to rise in the future).

This means that people in their late 60s with a life expectancy of 10 to 15 years would not count as old, and the proportion of the population considered old would be smaller.

While healthy living may contribute to longer lifespans, the study doesn't suggest that we hit middle age later. Using the new definitions, middle age lasts longer, with old age postponed to our last decade-and-a-half of life.


Where did the story come from?

The study was carried out by researchers from Stony Brook University in the US and the International Institute for Applied Systems Analysis in Austria. It was funded by the European Research Council.

The study was published in the peer-reviewed medical journal PLOS One, which is an open-access journal, meaning that it can be read for free online.

The media focused on the comments made by the researchers to explain why they had done the study, rather than the content of the research paper itself, with much discussion of how people now stay healthier for longer. The Times' headline said that middle age now starts at 60, which is not claimed anywhere in the study. The Daily Telegraph seems to think that living longer stops you ageing – "baby boomers refuse to grow old" – sadly, this is not the case.

The Mail Online did a better job of explaining the arguments behind the research, although they said that "the proportion of old people actually falls over time" using the new analysis. However, this was not borne out by the figures.


What kind of research was this?

This was an analysis of population data using the cohort component method. It involved making different calculations of possible future scenarios, from information about the age and sex of European populations. The researchers used assumptions about future birth rates, death and migration, and how they could change over time. The results and conclusions all relate to what happens to ageing at population level, so can't be used to predict what might happen to individuals.


What did the research involve?

Researchers took international population data and calculated what would happen to the proportion of people in a country considered old, and to the median (average) age of the population. They first used conventional measures, then their own new measures. The new measures are designed to take into account the fact that older people now, and in the future, are likely to be healthier, with a longer life expectancy, and are less dependent on others than they used to be. The researchers wanted to see what effect these new measures would have on how we think about the age of a population.

Researchers based their calculations on information from the European Demographic Data Sheet 2014, which includes statistics about the populations of European countries. Conventional measures of old age and median age are based on chronological age in years, with 65 often taken as the point at which someone is classed as old. Because life expectancy is rising, by this measure, the proportion of the population classed as old will go up over time, and will rise faster as life expectancy improves.

However, people aged 65 and over may be fit, independent and working, so this measure may not be useful for governments wanting to plan future pension provision or health and care costs.

The researchers call their new measure "prospective age". They say that people should only be considered old when their remaining life expectancy falls below 15 years, because it is in the last remaining years of life that people are most likely to be dependent and to have health problems.

Life expectancy varies for different countries, because it is calculated based on the average age of death for men and women in that country. It usually rises over time, as medicine and healthcare improves.

They also looked at median age, which is the average age of the population. As people live longer, the median age increases. However, the researchers argue, this does not take into account changing life expectancy. Instead, they calculate prospective median age, which is a measure of how long people have left to live, not just how long they have already lived.

Prospective median age is the age where remaining life expectancy is the same as the median age in a specific year. Again, this changes over time.

The researchers compared the conventional measures and the prospective measures of the percentage of the German population considered old in 2013, 2030 and 2050, under three scenarios:

  • one in which life expectancy did not increase
  • one in which it increased by 0.7 years per decade
  • one in which it increased by 1.4 years per decade

The European Demographic Data Sheet assumes a 1.4 years per decade increase. The researchers also calculated the median age and the prospective median age of the German population under those three scenarios.


What were the basic results?

The proportion of people considered old in the future would be smaller, based on the researchers' prospective age measures, compared to current measures based on chronological age.

Using standard measures, the proportion of the German population considered old would rise from 20.7% in 2013 to 27.8 in 2050 with no increase in life expectancy, or to 33% with the predicted life expectancy increase. However, using the prospective old age (when people had a life expectancy of 15 years or less), the proportion considered old would be 14.8% in 2013, 20.5% in 2050 with no increase in life expectancy, or 19.7% with the predicted life expectancy increase.

Conventional median age of the German population would rise from 46.5 years in 2013 to 49.3 with no increased life expectancy, or 52.6 with predicted life expectancy improvements. Using prospective median age, taking into account time left to live, it would actually fall to 45.6 by 2050 with predicted improvements in life expectancy.


How did the researchers interpret the results?

The researchers say their results demonstrate that conventional measures of population ageing are "incomplete" because they do not take into account rises in life expectancy and what this means for people's lifestyles. In their measures, the old age threshold changes over time as life expectancy changes.

They say their prospective measures show that "faster increases in life expectancy lead to lower population ageing". In other words, although people live longer, they don't hit the threshold of being considered old as soon – so the population as a whole is middle-aged for longer.

They admit that some of the thresholds chosen for their study are arbitrary. For example, they could have used 60 for the conventional old age threshold, or used a prospective old age threshold of 10 remaining years of life. They say that the "major trends" would have been the same if they had done that, although they do not show this data.



This study is an interesting analysis of population data, which shows how looking at figures from a different perspective can change our view. We are used to hearing about "ageing Britain" and how the increasing numbers of older people could be a drain on the country's resources. This study considers whether our definitions of old age are too rigid and need to be revisited.

In the paper, the researchers focus on results for Germany, but they have done calculations for 40 European countries, including the UK. This shows that the proportion of people in the UK aged 65 or over, given expected improvements in life expectancy, would rise from 17.2% in 2013 to 24.9% in 2050. However, the proportion in the last 15 years of their life would rise from 10.9% in 2013 to 13.7%. That still represents a large and increased proportion of the population considered old.

While it’s true that, on average, people are living longer, healthier lives than in the past, the study can only make predictions based on assumptions that may or may not turn out to be correct. The paper did not go into those assumptions, so we don't know whether, for example, they factored in the possible impact of being unable to treat infections because of rising antibiotic resistance, or the increased numbers of people with diabetes due to obesity.

Studies like these make for interesting headlines and give governments a new way of thinking about how to plan for our ageing population. However, they are no predictor of what will happen to any of us on an individual basis as we get older.

While there is no guarantee of your future lifespan, you can try to live longer by reducing your risks of getting some of the most common causes of premature death:

Read about reducing your risk of premature death.

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

Links To The Headlines

Middle age begins at 60, say researchers. The Times, April 16 2015

Why 60 is the new middle age: Our longer, healthier lives means we aren't classed as elderly until at least 70. Mail Online, April 16 2015

Sixty is the new 40: Healthy living means we now hit middle age later. Daily Mirror, April 15 2015

Middle age now lasts until 74 as baby boomers refuse to grow old. The Daily Telegraph, April 15 2015

Links To Science

Sanderson WC, Scherbov S. Faster Increases in Human Life Expectancy Could Lead to Slower Population Aging. PLOS One. Published online April 15 2015

Categories: Medical News

DNA changes in sperm may help explain autism

Medical News - Wed, 04/15/2015 - 15:30

"DNA changes could explain why autism runs in families, according to study," The Independent reports. Research suggests a set of changes in a father's DNA – known as methylation – is linked to autism spectrum disorder (ASD) in their offspring.

Methylation is a chemical process that can influence the effects of genes on the body (gene expression), essentially turning off certain genes. This process can lead to both positive and negative changes in DNA. These types of changes are known as epigenetic changes.

In this small study of 44 men and their offspring, researchers scanned for epigenetic changes at 450,000 points on the DNA molecule. They compared the DNA results with the child's score on an ASD prediction test at one year of age, and then looked for regions of DNA where changes were linked to a higher or lower risk of ASD.

The researchers found 193 areas of DNA from the men's sperm where methylation levels were associated with a statistically significant increased risk of developing ASD.

Researchers hope the study will help them see how epigenetic changes might affect ASD risk. At present, there is no genetic test for ASD and the causes are poorly understood. The study suggests ways ASD risk could be handed down in families without specific gene mutations being involved.

We're still a long way from understanding the causes of ASD, and many cases can occur in children with no family history of the condition, but this study gives researchers new avenues to explore.  

Where did the story come from?

The study was carried out by researchers from Johns Hopkins University and Bloomberg School of Public Health, the Lieber Institute for Brain Development, George Washington University, Kaiser Permanente research division, the University of California and Drexel University.

It was funded by the US National Institutes for Health and the charity Autism Speaks.

The study was published in the peer-reviewed medical journal the International Journal of Epidemiology.

Both The Independent and Mail Online covered the study well, explaining the research and outlining its limitations.  

What kind of research was this?

This was an observational study that compared changes to the chemicals attached to DNA in father's sperm (epigenetic changes) with early signs that a baby may go on to develop ASD.

It also looked at the DNA of people who had died to see whether the same changes were associated with having ASD.

This small study investigated links between epigenetic changes and the risk of ASD among children whose parents already had at least one child with the condition. However, it can't tell us whether these DNA changes cause ASD.  

What did the research involve?

Families who already had at least one child with ASD and where the mother was pregnant with another child were enrolled into the study.

The researchers took sperm samples from 44 fathers. 12 months after the babies were born, they were tested for early signs suggesting they might have ASD.

The researchers analysed the sperm samples and looked for differences between the DNA of the fathers whose children's test results showed a higher risk of ASD, and compared them with those at lower risk.

They chose to study families with at least one child with ASD, because the condition is thought to run in families. They wanted a group of children who were more likely than the general population to have ASD, so they could do a smaller study and still get useful results.

The babies were tested using the ASD Observation Scale for Infants (AOSI). This test does not show whether or not the babies have ASD. It looks at behaviour such as eye contact, eye tracking, babbling and imitation, and gives scores from 0 to 18, with a higher score meaning the baby is at higher risk of having ASD.

Other studies have found that babies with high AOSI scores at around 12 months are more likely to be diagnosed with ASD when they get older, but the test is not a 100% effective screening tool.

The fathers' sperm was analysed for epigenetic changes – these are changes to the chemicals attached to the DNA molecule, but not the genes themselves. These chemicals can affect how the genes work.

In this case, researchers looked for methylation of DNA. They used two different methods of analysing sperm, so they could check the accuracy of the primary method.

The researchers used a technique called "bump hunting" to search for regions of DNA where the levels of methylation were associated with the AOSI scores of the children.

Once they had identified the regions, they looked at DNA in samples of brain tissue taken from people after death, some of whom had ASD, to see if they could spot similar patterns. 

What were the basic results?

The researchers found 193 areas of DNA from the men's sperm where methylation levels associated with AOSI scores were statistically significant. In 73% of these regions, an AOSI score showing a higher risk of ASD was linked to lower levels of methylation.

Looking at these regions, the researchers found they overlapped genes that were important for the formation and development of nerve cells and cell movement.

They also found some – but not all – of the DNA regions identified as important in sperm analysis could also be associated with having ASD in DNA taken from brain tissue.  

How did the researchers interpret the results?

The researchers say they saw a strong relationship between epigenetic changes and increased chances of having ASD within this group of children. They said the difference in methylation was "quite substantial" and concentrated in areas of DNA associated with nerve cell development.

They point to a region of DNA that contains a group of genes thought to cause Prader-Willi syndrome, a genetic condition that has some similarities to ASD but is much rarer (affecting no more than 1 in every 15,000 children). This was one of the regions strongly associated with epigenetic changes.

The researchers say the results suggest that epigenetic changes to the father's DNA in this region "confer risk of autism spectrum disease among offspring, at least among those with an older affected sibling". 


This study found that epigenetic changes to a father's DNA seem to be linked to an increased chance of his child developing ASD in families where there is already one child with the condition.

ASD tends to run in families, and some studies have identified genes that may increase the chances of developing the condition. However, there is no clear genetic explanation in most cases of ASD. Research like this helps scientists to investigate other ways that the condition could be handed down.

The study raises a lot of questions. It can't tell us what causes the epigenetic changes to the DNA, or how they affect the way DNA works. Also, when the researchers looked at epigenetic changes to DNA in people's brains, they didn't find changes in many of the regions identified in the sperm analysis.

This was a fairly small study, relying on only 44 sperm samples. The researchers themselves say the results need to be confirmed in larger studies. We also can't say whether these results would apply to the general population. They may only be valid for families where one child already has the condition. 

Learning more about the genetics of ASD will hopefully lead to new treatments. This study may offer up one more piece of a very complicated, yet-to-be-solved, puzzle.

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

Links To The Headlines

DNA changes could explain why autism runs in families, according to study. The Independent, April 15 2015

Sperm 'may hold clues to autism': Link is found between father's DNA and symptoms. Mail Online, April 15 2015

Links To Science

Feinberg JI, Bakulski KM, Jaffe AE, et al. Paternal sperm DNA methylation associated with early signs of autism risk in an autism-enriched cohort. The International Journal of Epidemiology. Published online April 14 2015

Categories: Medical News

Paracetamol may blunt feelings of pleasure as well as pain

Medical News - Wed, 04/15/2015 - 11:44

"Paracetamol may dull emotions as well as physical pain, new study shows'," The Guardian reports.

The story comes from research testing whether over-the-counter painkiller paracetamol can blunt not just the feeling of pain, but also emotions.

Half the study’s 80 participants were given a normal dose of paracetamol, while the other half took a placebo pill. They were then asked to view photos commonly used by researchers to test both positive and negative emotional responses. These included, for instance, unpleasant pictures of crying, malnourished children and pleasant images, such as children playing with cats.

The study found that those who had taken paracetamol reported slightly less intense reactions to the photos than those who had taken a placebo pill. They also found the photos less emotionally arousing.

The researchers speculated that paracetamol may affect signalling pathways inside the brain, which may have an effect on mood.

However, far more research is needed before any conclusions can be drawn as to whether the painkiller can dull emotional reactions, particularly real life events.

If you are taking paracetamol on a long-term basis due to a chronic pain condition, and feel that you are less emotionally engaged than you used to be, you could discuss alternative treatment options with your GP.


Where did the story come from?

The study was carried out by researchers from Ohio State University and was funded by the National Science Foundation Graduate Research Fellowship and the National Center for Advancing Translational Sciences.

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

Most newspapers reported the research accurately, if uncritically, although The Guardian mentioned at the end of its story that the differences between the two groups were not large.

Confusingly for UK readers, the Mail Online’s report used the US generic name for paracetamol, which is acetaminophen, and also the US brand Tylenol. Although these were the names used in the US paper, it is usual practice to use UK generic names when reporting research for a UK audience.


What kind of research was this?

This was a randomised controlled trial (RCT) to test whether taking paracetamol can blunt emotional reactions to negative and positive images.

The authors say the drug has recently been shown to blunt people’s reactions to a range of emotionally negative stimuli, in addition to reducing physical pain. For example, they say it has been found to blunt feelings of hurt in social relationships and reduce the discomfort felt in making difficult decisions. They suggest that this may be due to its neurochemical effects on the brain, and the drug may reduce positive reactions as well as negative ones.


What did the research involve?

The researchers carried out two studies involving 82 college students in the first and 85 in the second. The students were randomly assigned to be given either 1,000 milligrams of paracetamol (the maximum dose) or an identical-looking placebo, both in liquid form. They then waited 60 minutes for the drug to take effect.

Participants then viewed 40 photographs selected from a database (International Affective Picture System) used by researchers to elicit emotional responses. These consisted of 10 extremely unpleasant photos (such as crying, malnourished children), five moderately unpleasant, 10 "neutral" images (such as a cow in a field), five moderately pleasant images and 10 extremely pleasant images (for example, young children playing with cats).

In the first study, after viewing each photo, participants were asked to rate how positive or negative the photo was on a scale of -5 (extremely negative) to +5 (extremely positive). They were then asked to view all 40 images again in a different, random order and asked to rate how much the photo made them feel an emotional reaction, from 0 (little or no emotion) to 10 (an extreme amount of emotion).

In the second study, participants saw all the images again in a different randomised order and were asked to make the same judgments of evaluation and emotional reactions as in the previous study. Additionally, participants in this second study also reported how much blue they saw in each photo, using an 11-point scale from 0 (the picture has no blue colour) to 10 (the picture is 100% blue). This was to test whether paracetamol blunts individuals' broader judgments "of magnitude", not just of emotional content.

The researchers then calculated average scores for participants’ evaluations and emotional arousal toward all 40 pictures, and for evaluation and emotional arousal towards neutral, positive and negative images.


What were the basic results?

Results in both studies showed that, overall, participants who took paracetamol rated all the photographs less intensely than those in the placebo group.

In other words, they evaluated unpleasant stimuli (anything that triggers a psychological or physical response) less negatively, and pleasant stimuli less positively than those who took a placebo.

They also rated both positive and negative images as less emotionally arousing than those taking a placebo.

There was no difference between the two groups in the rating of the degree of colour in each image.


How did the researchers interpret the results?

The researchers conclude that paracetamol reduces the intensity of both negative and positive emotions. "Rather than being labelled as merely a pain reliever, acetaminophen [paracetamol] might be better described as an all-purpose emotion reliever," they argue.

They speculate that the drug elicits neurochemical changes which affect evaluative psychological processes and that it might change sensitivity to emotional stimuli more generally – for example, causing someone to feel less joy at a wedding.



This small study found some slight differences in the way a group of people taking paracetamol reacted to a range of images, compared to a group of people taking a placebo.

Though an RCT is the "gold standard" of studies for determining whether a medication causes an effect, both groups need to be evenly matched for a variety of potentially confounding factors.

There is no information about the participants, other than the impression that they are all students, as they were given course credits for partaking in the study. It is not clear whether the groups were matched in terms of age, sex, ethnicity, whether they had children, or indeed whether they liked cats. 

The study is interesting, but no conclusions can be drawn as to whether paracetamol can dull emotional reactions to real life events.

While learning more about different chemicals’ effects on the brain and mood could lead to new treatments, this research has no immediately obvious clinical implications.

Therefore, further research is required into the potential side effects of this popular and effective painkiller.

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

Links To The Headlines

Paracetamol may dull emotions as well as physical pain, new study shows. The Guardian, April 14 2015

Paracetamol kills feelings of pleasure as well as pain. The Daily Telegraph, April 14 2015

Paracetamol can dull positive and negative emotions, study finds. The Independent, April 14 2015

Paracetamol dulls pleasure as well as pain. The Times, April 15 2015

How Tylenol blunts your emotions: Popular painkiller can reduce feelings of sadness AND happiness, claims study. Mail Online, April 14 2015

Links To Science

Durso GRO, Luttrell A, Way BM. Over-the-Counter Relief From Pains and Pleasures Alike - Acetaminophen Blunts Evaluation Sensitivity to Both Negative and Positive Stimuli. Psychological Science. Published online April 10 2015

Categories: Medical News

No proof that bad relationships raise blood pressure

Medical News - Tue, 04/14/2015 - 15:00

"If you have ever blamed your partner for making your blood boil, a new study could be the evidence you need to prove it's true," Mail Online reports. But the association between stress and blood pressure is much less clear-cut than the Mail suggests.

The study involved 1,356 older married couples in the US. They completed two sets of assessments four years apart. The assessments asked questions about their stress levels and marital satisfaction, and also measured their blood pressure. The researchers then looked at how these factors were related to each other. 

The results were quite a mixed bag, which makes it difficult to draw any firm conclusions from them. They generally suggest that husbands had higher blood pressure if their wives were more stressed.

If wives were stressed, their blood pressure was lower if their husbands were also stressed. Poor relationship quality was only detrimental to blood pressure if both partners felt negative about the relationship.

But this study has many limitations, including the difficulty in establishing whether blood pressure changes were definitely seen after stress or relationship problems. We also cannot tell whether a person actually had clinically high blood pressure.

Overall, this study will be of interest to social scientists, but provides no proof that the stress of a bad relationship causes high blood pressure. 

Where did the story come from?

The study was carried out by researchers from the University of Michigan. Data for the study was drawn from the Health and Retirement Study, which is funded by the US National Institute on Aging.

It was published in the Psychological Sciences and Social Sciences series of The Journals of Gerontology.

Mail Online took the results of this study at face value and did not consider its limitations, or explain that there is no proof of cause and effect. 

What kind of research was this?

This was an ongoing cohort study that gathered data on marital status and psychosocial health at one time point, and then looked at whether this was associated with changes in blood pressure over time.

Stress in its various forms has often been thought to have various detrimental effects on health and wellbeing. This study aimed to look at chronic stress associated with a poor marital relationship, and specifically how this was associated with changes in blood pressure.

The researchers expected to see evidence that more stress was linked to higher blood pressure, but also wanted to see if the effects differed between men and women.

The main problem with a study like this is that it can't prove cause and effect, as there are likely to be many other unmeasured factors involved (confounders)

What did the research involve?

The study used participants in the ongoing nationally representative Health and Retirement Study (HRS) in the US, which includes people born before 1954.

Participants are interviewed every two years. In 2006, psychosocial questionnaires were given in face-to-face interviews. These included an assessment of partner relationships and stress. Participants also had body measures taken, including blood pressure.

Chronic stress was assessed by asking the people involved about whether seven stressful events had been ongoing for at least 12 months:

  • physical or emotional problems (in a spouse or child)
  • problems with a family member's alcohol or drug use
  • difficulties at work
  • financial strain
  • housing problems
  • problems in a close relationship
  • helping at least one sick, limited, or frail family member or friend on a regular basis

They responded either "no", "it didn't happen", or "yes, it did". If they responded "yes", they rated this as "not", "somewhat", or "very upsetting".

They also completed a set of questions specifically looking at relationship quality, including the following questions:

  • How often does your spouse or partner make too many demands on you?
  • How often does he or she criticise you?
  • How often does he or she let you down when you are counting on them?
  • How often does he or she get on your nerves?

This study used data from the repeat assessments taken four years later in 2010 to see if blood pressure and psychosocial factors changed over time, and how they were associated with each other.

The researchers took the potential confounders of age, ethnicity, education, length of marriage and use of blood pressure medication into account. 

What were the basic results?

A total of 1,356 married couples completed the two assessments in 2006 and 2010. The average age for men was 66 and 63 for women, and they had been married for an average of 36 years.

Average blood pressure (looking at only the upper systolic figure) was slightly higher for husbands (132 in 2006 and 134 four years later) than for wives (127 to 129).

Just over a third of husbands and just under a third of wives were classified as having high blood pressure at both time points. Blood pressure was shown to significantly increase over time in both partners.

Overall, couples reported low levels of chronic stress and low relationship quality, though wives tended to report more of both of these problems than husbands.

The most common problems were the ongoing health problem of a spouse or child, ongoing financial strain, and helping at least one sick or disabled person.

The researchers also found significant associations between reported chronic stress, gender and blood pressure. Some of the findings included:

  • husbands had higher blood pressure when their wives reported higher stress
  • husbands reporting greater stress had lower blood pressure if their wives reported lower stress
  • wives reporting greater stress had lower blood pressure if their husbands reported more stress

This was interpreted as meaning that husbands appear to be more stressed by their wives' stress than the reverse. Wives' stress, meanwhile, seemed to be "buffered" by more stress in the husband.

Looking specifically at questions on relationship quality, the researchers found that if one partner reported negative relationship quality, their blood pressure was higher if the other partner also reported negative relationship quality.

Blood pressure was lower if the partner reported less negative relationship quality. There were no significant effects by gender.

The researchers interpreted this as meaning that higher levels of negative relationship quality are only detrimental when both partners feel negative about the relationship. 

How did the researchers interpret the results?

The researchers concluded that their findings indicate that in a marriage, "(a) stress and relationship quality directly affect the cardiovascular system, (b) relationship quality moderates the effect of stress, and (c) the [two] rather than only the individual should be considered when examining marriage and health". 


Overall, this study looking at the relationships between reported chronic stress, relationship quality and blood pressure in a group of married couples will be of interest to social researchers. But readers should not read too much into these findings.

Though it is quite plausible that ongoing stress can have a detrimental effect on your health (particularly your mental health), this study does not prove that the stress of a bad relationship affects blood pressure.

This study had many limitations:

  • It only looked at general associations between stress and relationship quality and blood pressure. It doesn't tell us whether psychosocial factors were associated with clinically meaningful changes in blood pressure, such as a person developing high blood pressure and requiring medication.
  • It is difficult to establish a clear temporal relationship by only assessing psychosocial factors and blood pressure at just two time points. For example, we cannot say if a change in blood pressure was caused by the onset of stress or relationship quality problems. 
  • The study was only able to ask fairly general questions about chronic stress and satisfaction in the relationship. These questions are unlikely to be able to capture the true nature of these issues and the extent of the effect this is having on the partner.
  • It has not been able to take into account the complex influence that personality, physical and mental health, and lifestyle factors are likely to be having on any association between stress, marriage quality and health.
  • This was a specific population sample of older married couples from the US who were married for a considerable length of time. The results may not apply to other nationalities, younger people, people married for less time, or people (of any genders) in a committed relationship who are not married.

This study provides no reliable evidence that you can blame your partner for your high blood pressure, as the media suggests.

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

Links To The Headlines

High blood pressure? Blame your partner! Chronic stress of a bad relationship can negatively affect your health, experts warn. Mail Online, April 13 2015

Links To Science

Birdtt KS, Newton NJ, Cranford JA, Ryan LH. Stress and Negative Relationship Quality among Older Couples: Implications for Blood Pressure. The Journals of Gerontology. Published online April 7 2015

Categories: Medical News