UK life expectancy expected to rise to late 80s by 2030

Thursday April 30 2015

Life expectancy is expected to rise thanks to improved public health

"Life expectancy is rising faster than thought, with 90 expected to become the norm in some affluent areas of the country by 2030," The Guardian reports. The same predictions led the Daily Mail to warn of a "life expectancy timebomb".

A new modelling study looking at trends in life expectancy estimated that male babies born in 2030 could live to an average of 85.7 years, with females living an average of 87.6 years.

The study also flagged up the potential effects of health and socioeconomic inequalities on life expectancy. For example, it estimated life expectancy in the affluent London borough of Kensington and Chelsea would be five to six years higher than the working class area of Tower Hamlets.

It remains to be seen if the increase in life expectancy would be a blessing or a burden. Elderly people contribute to society in many meaningful ways, such as helping out with childcare or volunteering for charity work. But they may also have complex health needs that could require significant resources to treat.

Assuming the model is accurate, the study produces some interesting results about trends in life expectancy and inequalities, and how they may change over time.  

Where did the story come from?

The study was carried out by researchers from the department of epidemiology and biostatistics at the School of Public Health and MRC-PHE Centre for Environment and Health, the UK Small Area Health Statistics Unit, Imperial College London, Northumbria University, and GlaxoSmithKline. It was funded by the UK Medical Research Council and Public Health England.

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

Most of the media reported the results of the research well, although they did not question the accuracy of the predictions much. Different outlets focused on different aspects of the research.

The Daily Telegraph and the Mail focused on the headline figure that the study predicted higher life expectancies than official estimates. In its headline, the Telegraph claimed people would live "up to four years longer" than official estimates, although the study shows a difference of 2.4 years for men and one year for women.

BBC News highlighted the narrowing gap between men and women's life expectancies, while The Guardian and The Independent were more concerned with the widening gap between rich and poor.  

What kind of research was this?

This modelling study analysed death rates and population data for 375 districts of England and Wales. Researchers used the data to construct mathematical models to predict life expectancy from 1981 to 2030 for each of the districts, looking at men and women separately.

The study aimed to give reliable district-level information about life expectancy to help with future planning for health, social service and pension needs. The figures are all averages for the districts and cannot be used to predict individual lifespans. 

What did the research involve?

Researchers looked at records of deaths in England and Wales between 1981 and 2012 by local authority district. They combined this with population data to develop five statistical models that could predict future death rates and life expectancy.

The researchers tested the models to see which best predicted actual death rates during the last 10 years of the data, then used the best-performing model to predict future life expectancy at the local and national level.

The data in the study came from the Office for National Statistics. The models incorporated features of death rates in relation to people's age, trends of death rates in people who were born within or close to the same five-year period, changes to death rates over time, and by local area.

The test of the five models found one model, which gave greater importance to trends in those born within adjacent time periods, worked better than the others, with forecast errors of 0.01 years for men and women.

This model was best able to predict death rates for 2002-12 using the first 21 years of the data. The researchers therefore chose this model to predict life expectancy from 2012-30.

While the geographical areas of the districts remained the same over the study, people living in these areas obviously change. The researchers looked at trends for each district, including birth rates and migration, so they could factor this in.

They looked at how relative levels of deprivation for each district affected the mortality rates and life expectancy. Taking account of all this data, they then predicted how life expectancy at birth could change from babies born in 2012 to babies born in 2030.

Rates for men and women were calculated separately, as life expectancy differs by gender. As far as we can tell from the paper, the analysis was done using reasonable assumptions about population trends.  

What were the basic results?

The study found life expectancy in England and Wales is expected to continue to rise from the 2012 average of 79.5 years for men and 83.3 for women, to 85.7 (95% credible interval 84.2 to 87.4) for men and 87.6 (95% credible interval 86.7 to 88.9) for women by 2030.

This is higher than predictions from the Office of National Statistics. However, this will come at the cost of increasing inequality between districts.

Improvements in life expectancy from 1981-2012 varied a great deal between districts. In 1981, men in districts with the best life expectancies could expect to live 5.2 years longer than those in the areas with the lowest life expectancies (4.5 for women).

By 2012, this had increased to a difference of 6.1 years for men and 5.6 years for women. The study says this trend is expected to accelerate, so that by 2030 the difference in life expectancy between the best and worst districts could reach 8.3 years for both men and women.

Most of the districts with the lowest life expectancies now and in 2030 were in south Wales and the northeast and northwest of England. The areas with the highest life expectancy were mostly in the south of England and London. However, London districts varied from the highest to the lowest life expectancy levels.

The gap between men and women's life expectancy is expected to shrink further. It has already shrunk from 6 years in 1981 to 3.8 years in 2012, and by 2030 it could be only 1.9 years. In some areas, there may be no difference between men and women's life expectancy at all.  

How did the researchers interpret the results?

The researchers say their results are a more accurate prediction of how life expectancy will increase than official figures, and are the first to look consistently at changes in life expectancy at the district level over a long period of time.

They say the increase is likely to be the result of better survival in people over the age of 65. They say men's life expectancy will rise faster than women's, partly because of the effect of social trends such as smoking among middle-aged and older women.

The researchers claim the data will allow local authorities to plan better for the future, especially as much health and social care is now the responsibility of local areas. However, they also say the figures provide a warning that inequality in England and Wales will continue to rise.  

Conclusion

This analysis of population data provides some fascinating information about how life expectancy has changed over the past 30 years, and how it may change in the future.

It found life expectancy for men and women will continue to rise. However, it also found the existing trends of the difference in life expectancy between different districts will continue to rise, which is of concern.

Although the data shows more deprived areas have seen less of an improvement in life expectancy, the study cannot inform us what factors are responsible for the differences in life expectancy.

There is one big limitation of any study that predicts life expectancy in the future: the figures are always based on trends from death rates in the past, and assume that past trends will continue into the future.

These types of studies cannot account for unexpected events or major social changes that could have a huge effect on life expectancy. For example, they can't build into their models the potential for unlikely events such as a big natural disaster, changes within the healthcare system, or even a major health breakthrough, such as a cure for heart disease or cancer.

It's worth remembering, too, that life expectancy figures represent the life expectancy of a baby born in that particular year. So the life expectancy figures for 2012 don't represent life expectancy for adults alive in 2012, but for babies born that year. This means the figures for 2030 don't yet apply: they are only predictions for babies born in the future.

The study can't be used by individuals to predict how long they may live, but it does provide useful data to plan for pensions and health and social provisions in the future.

If you are keen to live to 2030 and beyond, your best bet is to take steps to reduce your risk of the five leading causes of premature death:

Read more about the top five causes of premature death.

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

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Parents 'may pass anxiety on to their children'

Monday April 27 2015

Children may 'learn' anxious behaviour from their parents

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.   

Conclusion

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.

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

Monday April 27 2015

Chimpanzees are our closest living non-human relative

"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."

Conclusion

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.

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Air pollution linked to silent strokes

Friday April 24 2015

Air pollution could affect the flow of blood through the brain

"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".

Conclusion

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 Twitter. Join the Healthy Evidence forum.

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A magnet for mosquitoes? Blame your genes

Thursday April 23 2015

Mosquitoes are the world's deadliest animal

"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. 

Conclusion

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 Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

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Why you should drink (water) before you drive

Monday April 20 2015

Dehydration can cause loss of concentration

"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. 

Conclusion

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.

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Aspirin May Help Ward Off Gastro Cancers, Study Finds

By Steven Reinberg

HealthDay Reporter

SUNDAY, April 19, 2015 (HealthDay News) -- Taking aspirin regularly over several years may help prevent gastrointestinal cancers, a new study suggests.

There was a 20 percent lower risk of cancers of the gastrointestinal tract, especially in the colon and rectum, among people taking aspirin, said lead researcher Yin Cao, a postdoctoral research fellow at the Harvard School of Public Health in Boston.

But Cao doesn't think people should start taking aspirin to prevent cancer until more research is done. "The results of ongoing research to develop more tailored treatment based upon a personalized assessment of risks and benefits is critical before recommending aspirin for preventing cancer," she said.

Moreover, patients and their doctors need to consider the potential risks of taking aspirin, including stomach bleeding, Cao said.

However, "if considered alongside the known benefits of aspirin in the prevention of heart attacks and strokes, our data suggest the possibility that long-term regular aspirin use may have a significant benefit in prevention of the two leading causes of sickness and death in the U.S. and much of the world," she said.

The results of the study were to be presented Sunday at an American Association for Cancer Research meeting in Philadelphia. The data and conclusions should be viewed as preliminary until published in a peer-reviewed journal.

For the study, Cao and her colleagues collected data on 82,600 women enrolled in the Nurses' Health Study in 1980 and 47,650 men enrolled in the Health Professionals Follow-up Study in 1986. The researchers collected data on aspirin use, risk factors for cancer and diagnoses of cancer.

After up to 32 years of follow-up, about 20,400 women and 7,570 men developed cancer, the investigators found. Among men, prostate cancer was excluded.

Cao's team found that men and women who took a regular dose of aspirin (325 milligrams) two times a week or more had a lower risk of cancer overall than people who did not regularly take aspirin. The reduced risk was largely due to fewer cases of gastrointestinal cancers, including colon cancer, rectal cancer and esophageal cancer.

Regular aspirin use was not associated with a reduced risk of other cancers. Specifically, no link was found between aspirin use and a lower risk of breast cancer, advanced prostate cancer or lung cancer, the researchers said.

Moreover, the benefit of aspirin in reducing overall cancer risk appeared to depend on how much one took. So the more aspirin taken, the more the risk was reduced. Amounts ranged from less than one aspirin a week to 15 or more, the researchers said.

Getting the biggest benefit from aspirin required taking it for at least 16 years. The benefit was no longer seen within four years of stopping it, the researchers found. And the study only showed an association between aspirin use and gastrointestinal cancer risk, not a cause-and-effect relationship.

The association of aspirin with reduced cancer risk was the same for women and men regardless of race, history of diabetes, family history of cancer, weight, smoking, regular use of other painkillers or taking multivitamins, the study authors added.

Eric Jacobs, strategic director of pharmacoepidemiology at the American Cancer Society, said the new study "confirms the now well-established link between regular aspirin use and lower risk of developing certain cancers of the gastrointestinal tract -- cancers of the colon, rectum and esophagus."

Some, though not all, previous studies have indicated that aspirin might slightly lower risk of certain other cancers, including breast cancer, prostate cancer and lung cancer, he added.

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Safety Tips Hot Off the Grill

By Robert Preidt, HealthDay Reporter

SATURDAY, April 18, 2015 (HealthDay News) -- This barbecue season, make sure the only thing at risk of getting burned is the food.

Protect yourself with an apron and mitts, and pay attention to your surroundings, a doctor advises.

"The primary type of burn you get around the grill is a thermal burn caused by heat or fire from the grill itself. Extreme heat can be toxic to the skin, lead to inflammation, and if serious cause scarring," said Dr. Joshua Zeichner. He's an assistant professor of dermatology at the Icahn School of Medicine at Mount Sinai, in New York City.

"Mild burns lead to skin redness, affecting only the most superficial layers of skin. More severe burns can damage the deep skin layers and, in some cases, can lead to permanent, disfiguring scars," he explained in a hospital news release.

Zeichner outlined safety measures to take when using a barbecue.

Keep the flame low and don't pour oil, alcohol, or other flammable items near the grill. "Aerosol spray sunscreens have been reported to light on fire when used near an open grill, so make sure to use them far from the open fire," he advised.

Never barbecue in your bathing suit. Cover your skin to reduce the risk of suffering burns if oil or grease from the food splatters.

If you do suffer a burn while barbecuing, immediately run cold water over the burn, and then apply a cool compress consisting of skim milk and ice cubes in a wash cloth. Proteins in the milk reduce skin inflammation. Raw egg whites contain similar proteins, Zeichner said.

Aloe vera -- either gel or straight from the plant -- helps hydrate and soothe burns. Over-the-counter cortisone ointment reduces inflammation from the outside in, and aspirin or other non-steroidal anti-inflammatory pills reduce inflammation from the inside out.

If you have blistering or open skin, it means that the deeper layers are affected and you should seek medical attention. If you have an open wound, apply over-the-counter bacitracin ointment or another first-aid ointment to it, Zeichner said.

More information

The American College of Emergency Physicians has more about burn prevention.

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Women With Grandkids May Leave Workforce Sooner

By Robert Preidt, HealthDay Reporter

FRIDAY, April 17, 2015 (HealthDay News) -- Women with grandchildren are more likely to retire early, according to a new study.

Researchers looked at more than 47,000 retirement-age women in the United States. They found that those with grandchildren were 9 percent more likely to retire early, presumably to care for the youngsters. That's about the same percentage who retire early due to health problems.

The investigators also found that older women who have flexible work arrangements -- such as reducing the number of hours they work -- are less likely to retire. This finding suggests that many want to keep working.

But it's not clear from this study whether women retire early to care for grandchildren out of choice or necessity, according to the researchers.

Early retirement can be a bigger problem for many women because they tend to have lower incomes than men while they're working, the researchers noted. Women also may have fewer years in the workforce than men, which usually means smaller retirement accounts, Social Security benefits and pensions, according to study co-author Robin Lumsdaine, a professor of international finance at American University in Washington, D.C.

If people are making retirement decisions based on family considerations, such as the arrival of grandchildren, current policies meant to extend the number of years Americans spend working may have a limited effect, Lumsdaine said in a university news release.

Instead, policies to improve access to child care for younger people could help reduce the grandchild-related care demands on retirement-age workers and keep them in their jobs longer, she said.

The study was published recently in the journal Demography.

More information

The American Academy of Pediatrics offers child care tips for grandparents.

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Remote Amazon Tribe Members Have Greater Germ Diversity in Their Bodies

By Amy Norton

HealthDay Reporter

FRIDAY, April 17, 2015 (HealthDay News) -- In a discovery that could eventually shed light on some diseases that plague modern society, a tribe in a remote part of the Amazon jungle in Venezuela appears to have the most diverse collection of bodily bacteria ever found.

The study suggests that modern living has decreased the diversity of the typical Westerner's "microbiome" -- the trillions of bacteria and other microbes that normally dwell in the body.

And that could be having wide-ranging consequences for people's health, researchers say.

In particular, there is growing evidence that a less-diverse microbiome may contribute to disorders related to the immune system and metabolism, said Maria Gloria Dominguez-Bello, the senior researcher on the study and an associate professor of medicine at NYU Langone Medical Center, in New York City.

Those conditions include obesity, asthma, and autoimmune diseases such as type 1 diabetes -- where the immune system mistakenly attacks the body's own tissue.

One recent study, for example, focused on young children at high genetic risk of type 1 diabetes. Researchers found that the children typically showed a drop in the diversity of the gut microbiome about one year before they developed diabetes.

The new study, published April 17 in the journal Science Advances, offers a view of what the human microbiome looks like if it is untouched by modern, "Western" living, Dominguez-Bello said.

To get that snapshot, the researchers studied bacterial samples from an isolated tribe of Yanomami Indians living in southern Venezuela. Their village was originally spotted by helicopter in 2008, then visited by Venezuelan health workers.

Dominguez-Bello said the tribe had no known contact with non-Yanomami people. They speak their own language, and largely subsist on fish, plantains and cassava -- a plant with a starchy root that the villagers sometimes drink as a fermented beverage, Dominguez-Bello said.

It turned out that the typical Yanomami microbiome had nearly twice the diversity of the typical American's microbiome.

It was also more diverse than those of two rural groups -- one from Venezuela and one from the African nation of Malawi.

According to Dominguez-Bello, the findings suggest that, with every step toward modernization, there is a decline in the body's microbial diversity.

"Basically, our microbiome may be missing some members that our ancestors had," said Lita Proctor, program director for the Human Microbiome Project at the U.S. National Institutes of Health.

And that's concerning, according to Proctor, who was not involved in the new research.

Scientists are still trying to understand the critical roles that bacteria and other germs play in the human body. But, Proctor said, the microbes' jobs include regulating immune function, digesting food, and helping to produce vitamins, anti-inflammatory compounds and even neurotransmitters -- chemicals that relay messages among brain cells.

Why are Americans' microbiomes lacking in diversity?

Much of that decline may come early in life, Dominguez-Bello said.

C-sections and lack of breast-feeding are thought to be two factors. C-sections deprive newborns of beneficial bacteria from the birth canal -- and breast milk, Proctor said, "is nature's way of feeding (gut) bacteria."

Overuse of antibiotics, in medicine and agriculture, is another major contributor -- as is the Western diet, Proctor said. Processed foods are, in essence, partially digested, whereas whole foods make the digestive system work, she said.

And do the Yanomami benefit from their greater bacterial diversity?

Because the tribe is so isolated, little is known about their rates of various diseases, Proctor acknowledged.

Unsurprisingly, they're not overweight, Dominguez-Bello said. They do not seem to be malnourished, she noted, though they are "very short."

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California Declares Measles Outbreak Over

By HealthDay staff, HealthDay Reporter

FRIDAY, April 17, 2015 (HealthDay News) -- The California measles outbreak that began last December at two Disney parks was officially declared over Friday by state health officials.

A total of 131 people in California were diagnosed with measles during the outbreak, according to the state's Department of Public Health.

However, additional cases were reported outside of California, and the U.S. Centers for Disease Control and Prevention said Thursday that the latest total in the outbreak was 159 cases.

"We are pleased this outbreak is over, but caution that measles can be reintroduced in California at any time when an infected person brings it to the state," Dr. Karen Smith, director of the California Department of Public Health, said in a news release. "The best defense for protection against the highly infectious measles is vaccination."

The outbreak reignited a debate over the anti-vaccine movement, because a significant number of people infected had not been vaccinated against the highly contagious disease or had only received one dose of the vaccine that protects against measles. Two doses are recommended.

According to the CDC, more than 80 percent of all the cases in the outbreak occurred among people who were unvaccinated or had an unknown vaccination status. The Disney outbreak accounted for 70 percent of all measles cases nationwide this year, the agency added.

California health officials said that of the patients for whom they had documentation, 57 of the 131 cases were unvaccinated, while another 25 had one or more doses of the measles vaccine.

Health officials have explained that vaccination rates must be very high to protect an entire population against an infectious disease like measles, but they said the anti-vaccine movement had lowered those rates.

Although measles was declared eliminated from the United States in 2000, "approximately 20 million measles cases occur [worldwide] annually, and importations to the U.S. will continue to place unvaccinated populations at risk for measles," CDC researchers reported in the April 17 issue of the Morbidity and Mortality Weekly Report, an agency publication.

Therefore, "measles transmission in pockets of unvaccinated persons increases the risk for transmission to vulnerable groups, such as those who cannot be vaccinated because of underlying medical conditions, or infants too young to be vaccinated," the researchers said.

"The continued risk for importation of measles into the United States and occurrence of measles cases and outbreaks in communities with high proportions of unvaccinated persons highlight the need for sustained, high vaccination coverage across the country," corresponding author Nakia Clemmons, and colleagues at the CDC, concluded.

Measles symptoms can include fever, cough and watery eyes followed by a telltale rash.

A measles outbreak is considered over when 42 days -- or two incubation periods -- have passed since the last onset of the rash, according to the California Department of Public Health.

More information

Visit the U.S. Centers for Disease Control and Prevention for more about measles.

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1 in 3 Teen Boys Sexually Assaulted Tries Suicide, Study Finds

By Robert Preidt, HealthDay Reporter

FRIDAY, April 17, 2015 (HealthDay News) -- Teen boys who have been a victim of sexual assault are likelier to attempt suicide, a new study says.

University at Buffalo researchers analyzed data from more than 31,000 American teens, aged 14 to 18, who took part in surveys in 2009 and 2011.

Among healthy-weight boys, 3.5 percent of those with no history of sexual assault attempted suicide within the past year, compared with more than 33 percent of those who had been sexually assaulted, the investigators found.

The percentage was also about 33 percent for overweight boys who had been sexually assaulted, which shows that weight alone is not a significant risk factor for suicide attempts among teen boys, the researchers said.

Stigma, shame and lack of support are among the possible reasons for the higher rate of attempted suicides among teen boys who are sexually assaulted, said study author Laura Anderson, a psychologist and assistant professor at the University at Buffalo School of Nursing in New York.

"The stigma is often not addressed; it's a silent issue in society," she said in a university news release. "Very rarely does programming address boys. It's often presumed to be an issue for girls. The results highlight the need to educate the public and develop preventive programming and support for male and female sexual assault survivors."

Among healthy-weight girls, 5.8 percent of those with no history of sexual assault attempted suicide in the past year, compared with about 27 percent of those who had been victims of sexual assault, the study found.

Among overweight girls, 8.2 percent of those with no history of sexual assault attempted suicide, compared with more than 26 percent of those who had been sexually assaulted, the findings showed.

Suicide is the third leading cause of death among American teens.

The study was published online in the journal Suicide and Life-Threatening Behavior.

More information

For more on teen suicide, visit the National Alliance on Mental Illness.

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Gene Variation Could Spur Longer Smoking, Earlier Cancer

By Robert Preidt, HealthDay Reporter

FRIDAY, April 17, 2015 (HealthDay News) -- A gene variation associated with smoking longer and getting lung cancer at a younger age has been identified by researchers.

People usually are screened for lung cancer based on how much they smoke and their age, the researchers said. But this new study supports the idea of using genetic information to target people who might not be screened otherwise, said study first author Dr. Li-Shiun Chen, of Washington University School of Medicine in St. Louis.

The researchers analyzed more than 24 studies that included over 29,000 smokers of European ancestry. They found that people with a certain variation in a nicotine receptor gene called CHRNA5 were more likely to keep smoking for four years after those without the variation had quit.

The average age that people quit was 52 among those without the variation and 56 among those with the variation.

People with the variation in the CHRNA5 gene also inhaled deeper when they smoked and had a higher risk of being diagnosed with lung cancer four years earlier than those without the variation, the study found. The average age of diagnosis was 61 among those with the variation and 65 for those without the variation.

The findings suggest that people with the variation should undergo lung cancer screening at a younger age, said Chen.

The study was published April 14 in the Journal of the National Cancer Institute.

A previous study by Chen and her colleagues found that people with the CHRNA5 variation are more likely to respond to medications to help them stop smoking.

"The same people with this high-risk gene are more likely to respond to smoking-cessation medications, such as nicotine-replacement patches, lozenges or gum," she said in a university news release.

"Although it's clear the gene increases the chances a person will develop lung cancer at a younger age, it also is clear that the risk can be reversed with treatment," Chen concluded.

More information

The U.S. Department of Health and Human Services explains the health effects of smoking.

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Brain Scans Give Clues to Link Between Alzheimer's, Down Syndrome

By Mary Elizabeth Dallas, HealthDay Reporter

FRIDAY, April 17, 2015 (HealthDay News) -- It's long been known that people with Down syndrome are at higher risk for Alzheimer's disease.

Now, research suggests that changes in the brains of people with Down syndrome, as seen on brain scans, might help lead to promising treatments that could delay or prevent Alzheimer's.

"We and other researchers have been interested in detecting and tracking Alzheimer's, starting before the onset of cognitive [thinking] impairment in individuals at genetic risk for the disease," study senior researcher Dr. Eric Reiman, executive director of Banner Alzheimer's Institute, said in an organization news release.

"We have used this approach to help launch Alzheimer's prevention trials in people with other genetic risk factors, and we hope that the same approach can help empower people with Down syndrome in the fight against this disease," he explained.

Along with medical advancements that have enabled people with Down syndrome to live longer, there's also come the realization that they face an 80 percent risk of developing Alzheimer's disease, according to the news release.

That's because people with Down syndrome carry three copies of chromosome 21, which carries a gene for the so-called amyloid precursor protein. This leads to the overproduction of amyloid, a protein strongly linked to Alzheimer's disease, as well as thinking and memory problems at a young age.

For people with Down syndrome, brain changes that are tied to Alzheimer's are seen on scans beginning around the ages of 35 to 40, Reiman's team found.

"The number of people with Down syndrome who go on to Alzheimer's symptoms has tripled in the last 20 years," said the study's lead researcher, Marwan Sabbagh, director of Banner Sun Health Research Institute. "There is a growing need to find interventions to treat and prevent Alzheimer's in these individuals, and there is an opportunity to do so in a way that could help find effective Alzheimer's prevention therapies for everyone."

The study, published online recently in Alzheimer's & Dementia, involved five people with Down syndrome who had already developed symptoms of Alzheimer's, 12 people with Down syndrome who had no symptoms of Alzheimer's, and nine "control" participants who did not have Down syndrome or Alzheimer's disease.

The investigators used brain-imaging technology, known as PET scans, to look for signs of beta-amyloid accumulation and patterns of reduced brain activity associated with Alzheimer's.

The researchers also used MRI scans to measure the volume of "gray matter" in the study participants' brains.

The study found that the people with Down syndrome who also had Alzheimer's symptoms had much greater buildup of beta-amyloid, less activity in parts of the brain known to be affected by Alzheimer's, and smaller gray matter volumes than people from the other two groups.

Moreover, the people with Down syndrome who didn't yet develop symptoms of Alzheimer's had more amyloid protein than the control group, the findings showed.

The researchers believe that the buildup of this protein begins early on, before memory and thinking problems develop. The authors suggested that the findings could help researchers design new prevention trials among people with Down syndrome.

More information

The U.S. National Institute on Aging has more about Alzheimer's disease.

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U.S. Boy's Death Highlights Rare Mosquito-Borne Infection

By Steven Reinberg

HealthDay Reporter

FRIDAY, April 17, 2015 (HealthDay News) -- The death from encephalitis of a 6-year-old Tennessee boy has led researchers to a better understanding of the mosquito-borne virus that killed the child.

La Crosse virus, transmitted by the bite of an infected mosquito, often causes no symptoms. But severe cases may involve encephalitis, a type of brain inflammation usually triggered by infection.

"When [the La Crosse virus] does cause disease, it can cause fatal illness or make children very sick," said Amy Lambert, a research microbiologist with the U.S. Centers for Disease Control and Prevention.

"The disease is almost exclusively among children," added Lambert, lead researcher of the new paper published in the May issue of the journal Emerging Infectious Diseases.

In this case, the 6-year-old Union County boy was hospitalized in July 2012 after suffering two seizures and other symptoms associated with viral encephalitis. His condition deteriorated rapidly, and he was dead within five days.

Illness from La Crosse virus, which was identified in 1963 in La Crosse, Wis., is uncommon. Cases each year in the United States number just 80 to 100, Lambert said.

Still, these infections have increased in parts of the southeastern United States, including eastern Tennessee, where the boy was living, the CDC pointed out.

"Historically, the known center of La Crosse virus activity was in the Midwest and Atlantic states," the researcher said.

Possible reasons for the increase in infections in the Southeast include more of the virus-carrying mosquitoes -- known as Aedes triseriatus -- or a new more potent strain of La Crosse virus in this area, Lambert said.

After an autopsy, researchers compared the strain of virus that killed the boy with strains of virus collected from mosquitoes in woods near his home. They also compared these strains to samples collected from mosquitoes in different areas of the country over more than 40 years.

The fatal strain in the Union County, Tenn., case was the same strain seen in other cases of La Crosse infection, Lambert said.

"This strain of La Crosse is the only known strain in the entire history of human cases that has been associated with severe human illness and fatal outcomes," she said. "Further, that was the strain that was present in mosquitoes native to the U.S., not to mosquitoes recently introduced to the country."

Dr. Marc Siegel, a professor of medicine at NYU Langone Medical Center in New York City, said the study has merit.

"La Crosse virus will remain relatively uncommon, reliant as it is on mosquito transmission," he said.

Where this study shows a big advance is in understanding the genetic structure of the subtype of the virus that leads to more severe illness, he said.

"This can have big implications in tracking deadly strains and figuring out where the biggest emphasis on prevention and destruction of mosquito eggs should go," Siegel said.

Symptoms of La Crosse virus infection include fever, headache, nausea, vomiting and fatigue. Although seizures during the illness are common, most patients recover completely, according to the CDC. Less than 1 percent of cases result in death.

Lambert said Aedes triseriatus mosquitoes live in wooded areas, making their home in tree holes. The best way to protect yourself from a bite when outdoors is to use insect repellent and wear pants and a long-sleeved shirt, she said.

More information

For more about La Crosse virus, visit the U.S. Centers for Disease Control and Prevention.

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Higher Altitude States Have Fewer Kids With ADHD, Study Reveals

By Dennis Thompson

HealthDay Reporter

FRIDAY, April 17, 2015 (HealthDay News) -- The thin air of America's higher-elevation regions may reduce the risk of attention-deficit/hyperactivity disorder (ADHD), a new study suggests.

Researchers reported that the occurrence of ADHD decreases substantially as altitude increases. For example, Utah has an average state elevation of 6,100 feet. That state's ADHD rate is half that of states at sea level, they said.

It's important to note though that the current study's design can only show a link between altitude and a lower incidence of ADHD. It can't prove a cause-and-effect relationship.

Still, the researchers suspect that brain chemistry may be affected by the lower oxygen levels at higher elevations.

In particular, levels of dopamine -- one of the brain's chemical messengers (neurotransmitters) -- increase as someone adapts to oxygen-depleted air, said Dr. Douglas Kondo, a child psychiatrist and brain imaging researcher at the University of Utah's Brain Institute and University Neuropsychiatric Institute.

One of dopamine's jobs is to help regulate emotional responses. Previous research has associated lower levels of the hormone with ADHD, Kondo said. Most drugs used to treat ADHD work through the dopamine system.

Kondo and his colleagues have theorized that as dopamine levels increase with elevation, the risk for developing ADHD diminishes.

"The idea is that if your symptoms are on the borderline of clinical ADHD -- it's affecting your family life and your academic life -- the effects of high altitude are beneficial," Kondo said.

So, should parents in low-lying states pack up their ADHD kids and set out for a Rocky Mountain high? Not necessarily, Kondo added.

"That kind of very life-changing clinical recommendation, we're not there yet," he said. "We're just asking the question at this point."

Kondo doesn't even recommend visiting places like Utah or Nevada solely to see whether the high altitude can positively affect an ADHD kid. Just the novelty of being in the mountains or being on vacation, along with the additional physical activity involved, likely would improve a child's symptoms, he said.

The research was published online in the Journal of Attention Disorders.

For the study, the research team relied on elevation data gathered during a NASA space shuttle mission. This mission created a highly detailed topographical map of the 48 contiguous United States.

The investigators then paired that with data on ADHD collected during two surveys conducted by the U.S. Centers for Disease Control and Prevention.

Researchers found that for every 1-foot increase in elevation, the likelihood of being diagnosed with ADHD by a health care provider decreased by 0.001 percent.

North Carolina, with an average elevation of 869 feet above sea level, had the highest percentage of children diagnosed with ADHD -- nearly 16 percent. Delaware, Louisiana and Alabama, all states with an average elevation of less than 1,000 feet, followed closely behind North Carolina with high percentages of ADHD.

Nevada has an average elevation of more than 5,500 feet above sea level, and the lowest percentage of ADHD children at less than 6 percent. Utah also had one of the lowest rates of ADHD, at less than 7 percent, the findings showed.

All of the western mountain states rated well below average for the percentage of children diagnosed with ADHD. That was true even after the researchers adjusted the data to control for other factors that could affect ADHD risk, such as birth weight, ethnic background and gender.

Mark Stein, a clinical pediatric psychologist at Seattle Children's Hospital, called the findings "very interesting and provocative."

"A clear implication is that youth with ADHD should be encouraged to participate in outdoor activities, including higher altitude ones if available and safe, as opposed to sedentary activities. More summer treatment programs and physical exercise," Stein suggested.

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Spring Allergy Season Could Be a Bloomin' Nightmare

By Serena Gordon

HealthDay Reporter

FRIDAY, April 17, 2015 (HealthDay News) -- If you've got seasonal allergies, you probably already know that spring has finally arrived. And, some experts are predicting that this allergy season may be one of the worst in years.

After a long, cold, wet winter, trees and flowers all seem to be blooming at once, and that means a sudden, big burst of all different types of pollen at the same time.

Some experts are even predicting a "pollen vortex."

The one bright spot? Because the pollen season started later, it's likely to be shorter, according to Dr. Joseph Leija, an allergist with the Loyola University Health System's Gottleib Memorial Hospital in Chicago. Leija has also been in charge of measuring the Midwest's official pollen count for the U.S. National Allergy Bureau for the past two decades.

"The allergy season has been slow to start this year, but now we're seeing a high pollen count from trees. They're all pollinating together. This will be a heavy season, but since the pollination started quite late, it will be shorter," Leija said.

Dr. Beth Corn, director of Clinical Immunology Faculty Practice Associates at Mount Sinai Hospital in New York City, said it's difficult to quantify from year-to-year exactly how bad an allergy season might be, particularly from a patient's perspective.

"Allergy season was bad last year, and it will be bad this year. People are very symptomatic now. But, remember, up until last week, we were still in winter coats in New York. People are noticing the stark contrast. Things have abruptly changed and people notice it," she said.

The cities hit hardest by rough weather this winter may not see the worst of allergy season, according to the Asthma and Allergy Foundation's Top Five Spring Allergy Capitals list. To make the allergy capitals list, a city has to have higher than average pollen counts along with higher than average medication use.

The cities given this dubious distinction for 2015 are: Jackson, Miss.; Louisville; Oklahoma City; and Memphis and Knoxville, Tenn.

But, no matter where you live or what the pollen count might be, you can take steps to ease your allergy symptoms.

The first step, said Corn, is to see an allergist and get tested so you know exactly what causes your allergy symptoms.

"It's important to know what it is you're treating, and when you're seen by a specialist, they can tailor your treatment. You'll get the most effective cocktail of medications," Corn said.

Both over-the-counter and prescription allergy medicines are also available. And steroid nasal sprays can help relieve allergies, while eye drops can help control eye symptoms, according to Corn.

Leija pointed out that "controlling your environment as much as possible is important. Keep your windows closed and run the air conditioner inside the house, and when you're driving, too. If you get pollen in your hair and clothing, don't bring it into the bedroom."

Leija also said it's a good idea to change clothes before you come inside, or at least not in your bedroom. And, if possible, wash pollen out of your hair before getting into bed.

More information

Learn more about what causes allergies from the Allergy and Asthma Foundation of America.

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