User login

The Centre

Argyle House
Clarence Court, 5 Dee Road,
United Kingdom

Contact LTF

For enquiries please contact Tony Novissimo
Phone: 0208 408 1000


Health News from NHS Choices

Constantly updated health news across a range of subjects.

NHS Choices News

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

    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

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

    "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

  • Does happiness have a smell and is it contagious?

    "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

  • Middle age 'starts at 60' claims media

    “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

  • DNA changes in sperm may help explain autism

    "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