Did the English smoking ban stop 90,000 children getting ill?

Friday May 29 2015

Smoking in public places was banned in 2007

"90,000 children spared illness by smoking ban," reports the Daily Mail. This impressive-seeming statistic is based on research looking at how many under-14s ended up in hospital with respiratory infections in the years before and after the July 2007 smoking ban in England and Wales.

Researchers analysed data on more than 1.6 million children who were admitted to NHS hospitals for respiratory infections – excluding asthma cases – between 2001 and 2012. To put this into context, children are unlikely to be admitted to hospital with a mere cold or sniffle – these are likely to be children very ill with bronchitis, pneumonia, laryngitis or tonsillitis.

The researchers calculated the rate of admission for any respiratory tract infection reduced by 3.5% immediately after the introduction of the smoking ban. It then continued to reduce by 0.5% each year.

The biggest immediate reduction in admissions was for lower respiratory tract infection (such as pneumonia), which reduced by 13.8%.

While this study can't prove the smoking ban definitely caused the drop in the numbers of children needing hospitalisation, the research appears robust and we have confidence that the findings are likely to be accurate. The researchers accounted for potential confounding factors, including the introduction of the pneumococcal vaccine in 2006.

And while this study shows the smoking ban is associated with around 11,000 fewer hospital admissions for respiratory tract infections in children a year, it cannot tell us the potential wider benefits of the smoking ban on children's health.

Now is the best time to quit smoking. 

Where did the story come from?

The study was carried out by researchers from Maastricht University and Sophia Children's Hospital, both in The Netherlands; Brigham and Women's Hospital in the US; and the University of Edinburgh and Imperial College London in the UK.

It was funded by the Thrasher Research Fund, the Netherlands Lung Foundation, the International Pediatric Research Foundation, and The Commonwealth Fund.

The study was published in the peer-reviewed European Respiratory Journal.

The media reported the study accurately, though some did not point out the limitations of this type of study, in that it cannot prove cause and effect.

The Guardian's figure of 11,000 children a year saved from hospital admissions reflects the estimates in the research. The Mail's figure of 90,000 appears to be an extrapolation of this figure over the eight years since the ban. The research only went up to 2012, so this figure can't be verified, but the Mail's headline claim is unlikely to be wildly inaccurate. 

What kind of research was this?

This was an observational study looking at the number of admissions for respiratory tract infections in children before and after the smoking ban was introduced in July 2007. This type of study is useful when it is not feasible to perform a randomised trial, though it cannot prove cause and effect.

The scientists knew secondhand smoke exposure was a major risk factor for respiratory tract infections. However, no-one had yet studied the direct impact of the smoking ban in England on children's health in this way. 

What did the research involve?

The researchers used the Hospital Episode Statistics database to collect data. They looked at the monthly number of hospital admissions for children aged 0 to 14 in England and Wales with respiratory tract infections between January 1 2001 and December 31 2012. 

The researchers calculated the rate of admissions according to the number of admissions divided by the number of children at risk of admission to account for any changes in the number of children in the population over time.

The rate of admission to hospital before and after the smoking ban was introduced on July 1 2007 was compared, taking some potential confounding factors into account.

The results were adjusted using standard statistical analysis to take into account:

• age group (0 to 4, 5 to 9 and 10 to 14 years)
• gender
• socioeconomic deprivation
• level of urbanisation
• region
• introduction of the pneumococcal vaccine in 2006  

What were the basic results?

There were 1,660,652 admissions for acute respiratory tract infections among 0 to 14 year-olds during the study period. Most occurred in children up to age four (85%), and admission was more likely with increased deprivation.

Overall, respiratory tract infection admissions reduced by 3.5% immediately after the introduction of the smoking ban (admission rate -3.5%, 95% confidence interval [CI] -4.7 to -2.3%). The rate continued to reduce each year thereafter by 0.5% (admission rate -0.5%, 95% CI -0.9 to -0.1%).

The biggest immediate reduction in admissions was for lower respiratory tract infections (such as pneumonia) – these were reduced by 13.8% (admission rate -13.8%, 95% CI -15.6 to -12%).

The smoking ban was associated with an estimated 54,489 fewer hospital admissions over the next five years. 

How did the researchers interpret the results?

The researchers concluded that, "The introduction of national smoke-free legislation in England was associated with ~ [around] 11,000 fewer hospital admissions per year for RTIs in children."

They say their research demonstrated "an immediate reduction in lower RTI admissions, and a more gradual, incremental reduction in upper RTI admissions". 

Conclusion

This observational study found an association between the introduction of the 2007 smoking ban in public places in England and Wales, and a reduction in children's hospital admissions for respiratory tract infections.

The study included data on a large number of admissions for respiratory tract infections in children, using nationwide official hospital statistics to gather this information. This gives us confidence in how well these findings may be generalisable because it limits selection bias.

The researchers took several potential confounding factors into account when analysing their results, including:

• the introduction of the pneumococcal vaccine for children in 2006
• seasonal variations
• temperature 
• levels of air pollution

They only included children up to the age of 14 in an attempt to limit the effect of adolescent first-hand smoking. A cut-off point had to be used, though recognising there will be children under the age of 14 who smoke.

However, this study has limitations because of its design. As it is a "before and after" type of study, there may have been other factors that changed that may have influenced the results.

• Hospital admissions may have reduced over time as a result of improvements in the treatments available for respiratory tract infections in children – for example, at home, through a pharmacist, GP or A&E services, or because of preventative measures.
• Private hospital admissions were not included and their use may have changed over the study period. However, this is believed to be less than 1% of total admissions.
• Admissions for children with asthma were excluded so they did not bias results, but children with other conditions that increase their risk of respiratory tract infections were included. The number of children with these conditions – such as cystic fibrosis – may have changed over the study period.
• Epidemics such as H1N1 (swine) flu in 2009 will have increased the number of admissions. The authors say that despite this increase in infections in the "after" stage of the study, there was still an overall reduction in the number of admissions for respiratory tract infections in children after the smoking ban.

The study could not directly measure the impact the smoking ban had on people smoking in their homes or cars, which is one of the main sources of secondhand smoke for children.

However, the authors cited several credible studies that found the number of smoke-free homes increased significantly after smoking bans.

Overall, this study shows the smoking ban is associated with around 11,000 fewer hospital admissions for respiratory tract infections in children a year.

If you still haven't given up smoking, now is as good a time as any and you can get free help to quit from the NHS.

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Traffic and aircraft noise exposure linked to bigger bellies

Tuesday May 26 2015

Could noise pollution lead to stress and overeating?

"Living near a main road causes people to gain weight with the risk of obesity," is the slightly dubious claim in The Daily Telegraph. While a Swedish study did find an association between noise pollution and obesity, cause and effect has not been proved.

The study involved more than 5,000 adults. It looked at the traffic noise exposure where participants lived and whether they were obese according to measurements such as their body mass index (BMI) or waist circumference. The researchers also looked at exposure to road, rail and aircraft noise.

Researchers found people with more exposure to traffic noise from any of the sources had greater waist circumferences. The more sources of traffic noise a person was exposed to, the more likely they were to be obese around the waist. However, there was no link between traffic noise exposure and being obese based on BMI measurement.

Because this study measured noise exposure and obesity at around the same time, it's not possible to say whether noise could contribute towards causing obesity. While the researchers did try to take into account factors (confounders) such as people's lifestyles and socioeconomic status, these factors could still be influencing the results.

The link between noise exposure and health outcomes is likely to continue to be studied, but for now a healthy diet and being physically active are the best ways to maintain a healthy weight. 

Where did the story come from?

The study was carried out by researchers from the Karolinska Institute in Sweden and other research centres in Sweden and Norway.

It was funded by the Swedish Research Council for Health, Working Life and Welfare, the Swedish Heart and Lung Foundation, Stockholm County Council, the Swedish Research Council, the Swedish Diabetes Association, Novo Nordisk Scandinavia and GlaxoSmithKline.

The study was published in the peer-reviewed journal Occupational and Environmental Medicine on an open-access basis, so it is free to read online or download as a PDF.

The Daily Telegraph, along with the Daily Mirror and the Daily Express, overstates what can be concluded based on the findings of this study. For example, the first sentence in the Telegraph's story states that traffic noise "causes people to gain weight".

We cannot say for certain whether this is the case, or whether people were already obese before they were exposed to road noise. We also can't say that moving to less urban environments would help people lose weight, as the paper suggests.

It also says at one point that: "Living under a flight path doubled the rate of obesity."

To its credit, however, a balanced comment from an expert was included at the end of the article noting that: "It's definitely too soon to be able to blame your increasing waistline on traffic noise!".

Other UK newspapers, such as The Guardian and The Independent, were more reserved, explaining that a causal relationship has not been proven. 

What kind of research was this?

This cross-sectional study looked at whether exposure to traffic noise was linked to obesity. Some studies have suggested that this is the case. The suggestion is that this may relate to noise exposure increasing stress hormones such as cortisol, or disrupting sleep.

Other studies have also suggested that traffic noise may be linked to cardiovascular disease, and a link with obesity might be one way this might occur.

But the evidence so far is limited, and studies have not looked at whether the different types of traffic noise (road, rail or aeroplane) show differing associations with obesity. 

What did the research involve?

The researchers studied 5,075 adults in suburban and semi-rural areas of Stockholm County. They assessed the participants' exposure to noise from road traffic, railways and aircraft at their homes, and took various measurements of the participants' fatness, such as their weight and waist circumference. They then analysed whether there was a relationship between these factors.

The participants were taking part in the Stockholm Diabetes Prevention Program, which looked at risk factors for type 2 diabetes. About half were selected to participate because of a family history of type 2 diabetes, but none had the condition at the start of the study.

The assessments for the current study took place when participants were followed up between 2002 and 2006, when they were aged between 43 and 66 years. Participants filled out questionnaires on their lifestyles and health, and had a medical examination by trained nurses.

The researchers obtained information on where the participants lived since 1991 from various national sources. They combined this information with maps of road traffic noise exposure from the local regions to assess exposure, and also calculated exposure to railway noise and aircraft noise based on distance from rail lines or Stockholm's Arlanda airport flight paths. The average exposure between 1997 and 2002 for each participant was estimated, taking into account if they moved house.

The researchers analysed whether there were links between the different forms of traffic noise (road, rail or aeroplane) and measures such as BMI, waist circumference and waist to hip ratio. Individuals were considered to have "central obesity" if they had a:

• waist circumference of 88cm or above for women and 102cm or above for men
• waist to hip ratio of 0.85 or above for women and 0.90 or above for men

In their analyses, the researchers took into account confounders such as the participants':

• age
• gender
• physical activity
• dietary habits
• self-reported noise sensitivity
• self-reported annoyance with road traffic noise
• road traffic air pollution
• socioeconomic status (based on household income)

What were the basic results?

The researchers found that:

• 62% of participants were exposed to road traffic noise of 45 decibels (dB) or higher – 45dB is just a bit louder than a bird call
• 22% of participants were exposed to airplane traffic noise of 45dB or higher
• 5% of participants were exposed to rail traffic noise of 45dB or higher
• 30% of participants were classified as having no exposure to traffic noise of 45dB or higher

Fewer people were obese based on BMI measurement (19% of men and 17% of women) than based on waist circumference (23% of men and 36% of women) or waist to hip ratio (63% of men and 50% of women).

All forms of traffic noise were linked to waist circumference – every 5dB increase in exposure was associated with a:

• 0.21cm increase in waist circumference for road traffic noise
• 0.46cm increase in waist circumference for rail traffic noise
• 0.99cm increase in waist circumference for aircraft traffic noise

Road and aircraft traffic noise were linked to waist to hip ratio, but rail traffic noise was not. None of the traffic noise sources was linked with BMI.

The odds of having central obesity based on waist circumference and waist to hip ratio was significantly higher in those exposed to any traffic noise source of 45dB or higher, with the odds increasing with the more sources of traffic noise participants were exposed to.

For example, exposure to all three traffic noise sources was associated with almost twice the odds of central obesity based on waist circumference (odds ratio [OR] 1.95, 95% confidence interval [CI] 1.24 to 3.05).

Obesity based on BMI measurement was not significantly associated with any traffic noise source of 45dB or higher. 

How did the researchers interpret the results?

The researchers concluded that their results "suggest that traffic noise exposure can increase the risk of central obesity" and that, "combined exposure to different sources of traffic noise may convey a particularly high risk". 

Conclusion

This cross-sectional study found a link between traffic noise exposure from cars, railways or aircraft and obesity around the waist (central obesity – having a bigger belly), but not obesity defined by a high BMI (30 or over).

The main limitation of this research is that, as it is cross-sectional, it cannot determine whether the exposure to the traffic noise came before the central obesity. Therefore, we cannot say the traffic noise definitely causes the obesity.

Factors other than traffic noise (confounders) may be contributing to the link seen. The researchers did try to take a number of these factors into account, but their impact may not be removed completely.

For example, where a person lives is likely to be strongly linked to their socioeconomic status, and this is in turn likely to be linked to a range of lifestyle behaviours. Likewise, areas with high levels of noise pollution tend to be located in the poorer parts of towns and cities, and poverty is known to be associated with a higher risk of obesity. Disentangling these factors to identify the exact impact of each is very difficult.

The estimation of traffic noise exposure was based on the person's place of residence, but did not take into account whether they had noise-reducing measures such as double or triple glazing. It also did not assess noise exposure from other sources – for example, at work.

One way that results were expressed (odds ratios) can make it sound like the differences are greater than they are when you look at the groups. Adjusting for other factors does help to remove their effects, but can contribute to this. "Twice the odds" of being obese might not actually translate to twice as many people being obese when you look at the actual numbers.

So, while 33% of women who were exposed to less than 45dB of road traffic noise had central obesity based on their waist circumference, 36% of those experiencing 45-55dB fell into this category and 39% of those experiencing more than 55dB. These are increases, but are not as drastic as the "doubling" figure might suggest.

While the study suggests a link likely to warrant further investigation, we cannot as yet say for certain that noise pollution causes obesity.

You can take other steps to reduce your waist circumference if it is moving into the danger zone (94cm or more for men, 80cm or more for women). The NHS Choices Weight loss plan uses a combination of healthy diet choices and exercise to get your belly back to a healthier size.

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Holidays and parties mean we may drink more than we think

Friday May 22 2015

People may forget about holidays and parties

"The amount of alcohol people in England drink has been underestimated by the equivalent of 12 million bottles of wine a week," BBC News reports.

It has long been known that there is a big gap between the amount people say they drink in national surveys, like the Health Survey for England, and the amount of alcohol known to be sold in England.

In this new survey researchers set out on the assumption that while people may accurately report their standard drinking patterns from week to week, they may forget the drinking they do on special occasions, such as bank holidays, parties, weddings, wakes or big sporting events (which for many England fans is akin to a wake).

The study used a large phone interview to estimate the amount of extra drinking going on during these types of occasions. They found this accounted for an extra 12 million bottles of wine per week in England – just under a staggering eight and a half million litres, which is more than enough to fill three Olympic-size swimming pools.

The results seem plausible. As the scientists point out: "The impact of atypical and special occasion drinking is reflected in evening presentations to emergency units, which peak on weekends but also sports events, bank holidays, and even commemorative occasions such as Halloween."

If you are concerned about whether you may be drinking more than you should you can download the Change4Life Drinks Tracker app, which is available for iOS and Android devices.

Where did the story come from?

The study was carried out by UK researchers from Cardiff University, Bangor University, Liverpool John Moores University and London School of Hygiene and Tropical Medicine. It was funded by Alcohol Research UK.
 
The study was published in the peer-reviewed medical journal BioMed Central. This is an open-access journal, so the study is free to read online or download as a PDF.

The UK media reported the story accurately.

What kind of research was this?

This was cross-sectional survey aiming to provide a more accurate picture of how much alcohol people in England drink.

The researchers say there is a big gap between the amount people report drinking in national surveys and the amount of alcohol being sold in England. So are we a nation of liars in denial about our drinking habits?

Rather than fibbing, the researchers suspected people might be being asked the wrong type of questions on alcohol surveys. You are usually asked what your average alcohol consumption is, over say a week. People might not think to include special events in this estimate, such as drinking at a wedding or a birthday party, because they are not typical.

The scientists designed a large telephone interview study to see whether the special occasion drinking might make up the shortfall between estimates of typical drinking and alcohol sales.

What did the research involve?

The team conducted a large-scale telephone survey between May 2013 and April 2014 of people aged 16 years or over living in England. Respondents (n = 6,085) provided information on typical drinking (amounts per day, drinking frequency) and changes in consumption associated with routine atypical days (e.g. Friday nights) and special drinking periods (e.g. holidays) and events (e.g. weddings).

The team acknowledged it did not collect a representative sample of alcohol consumers and abstainers on a national basis, but instead used national population estimates and stratified drinking survey data to weight responses to match the English population.

The analysis looked to identify additional alcohol consumption associated with atypical or special occasion drinking by age, sex and typical drinking level.

What were the basic results?

Accounting for atypical and special occasion drinking added more than 120 million units of alcohol/week (equivalent to 12 million bottles of wine) to population alcohol consumption in England.

The greatest impact was seen among 25- to 34-year-olds with the highest typical consumption, where atypical/special occasions added approximately 18 units/week (144g) for both sexes.

Those reporting the lowest typical consumption (≤1 unit/week) showed large relative increases in consumption (209.3%) with most drinking associated with special occasions.

In some demographics, adjusting for special occasions resulted in overall reductions in annual consumption. For example, women aged 65 to 74 years in the highest typical drinking category.

The Health Survey for England, a nationally representative survey, estimate of alcohol consumption only accounted for 63.2% of sales. The new survey, including the special occasion drinking, accounted for 78.5%.

How did the researchers interpret the results?

The research team concluded: "Typical drinking alone can be a poor proxy for actual alcohol consumption. Accounting for atypical/special occasion drinking fills 41.6% of the gap between surveyed consumption and national sales in England."

From a public health perspective they said: "These additional units are inevitably linked to increases in lifetime risk of alcohol-related disease and injury, particularly as special occasions often constitute heavy drinking episodes.

"Better population measures of celebratory, festival and holiday drinking are required in national surveys in order to adequately measure both alcohol consumption and the health harms associated with special occasion drinking."

Conclusion

This large telephone survey sought to generate a more accurate estimate of England’s alcohol consumption by taking account of atypical drinking days like Friday nights, holidays and events such as weddings. They found atypical and special occasion drinking added more than 120 million units of alcohol/week (about 12 million bottles of wine) to population alcohol consumption in England

This accounted for some of the discrepancy between self-reported alcohol consumption and alcohol sales, but not all. The Health Survey for England, a nationally representative survey, estimate of alcohol consumption only accounted for 63.2% of sales. The new survey, improved this to 78.5%.

This begs the question, where is the other 21.5% going. There are many potential explanations for this. One is that people are pretty bad at estimating how much they drink, and generally underestimate it, for whatever reason, when asked. An alternative, rather worrying, explanation is that a significant portion could be consumed by under-16s – who were excluded from the survey. And there could be people who just can’t help downplaying the amount they drink, whether consciously or unconsciously, even to strangers on the telephone.

The research team highlighted a number of limitations of its own research.

First, the survey did not attempt to generate a representative sample of alcohol consumers and abstainers on a national basis. The scientists say their survey acts as a proof of concept, and a larger nationally representative survey is needed to test the usefulness of this methodology as a national alcohol monitoring tool. For example, participation rates were quite low (just 23.3% of those contacted) and the sample had more women, older people and people of white ethnicity than is true for England as a whole.

The estimates also might be imprecise. For example, the team didn’t know if special drinking events were instead of or as well as the normal drinking days. In their analysis they opted for a conservative measure by removing an average drinking day’s consumption for each special event day reported.

The results make sense. As the scientists point out: "The impact of atypical and special occasion drinking is reflected in evening presentations to emergency units, which peak on weekends but also sports events, bank holidays, and even commemorative occasions such as Halloween."

If you find yourself regularly drinking more than the recommended daily limits (3-4 for men, 2-3 for women) you may have an alcohol misuse problem that may require treatment

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Quarter of sun-exposed skin samples had DNA mutations

Friday May 22 2015

Skin cancer rates have risen in the UK

A sobering BBC News headline greets sun worshippers on the eve of the spring bank holiday: "More than a quarter of a middle-aged person's skin may have already made the first steps towards cancer."

Sunlight is made up of ultraviolet (UV) radiation. Low levels of exposure to UV light are actually beneficial to health – sunlight helps our bodies produce vitamin D.

But prolonged exposure can change (mutate) the DNA in the cells. Over time the mutations accumulate, turning the skin cells cancerous, which can lead to either non-melanoma or melanoma skin cancer.

As part of a study into skin cancer, researchers analysed skin removed from the eyelids of four people aged 55 to 73 known to have a varying history of sun exposure (but not a history of cancer) to see what DNA mutations had built up.

To their surprise they found hundreds of normal cells showing DNA mutations linked to cancer, called "mutant clones", in every 1sq cm (0.1 sq in) of skin, and there were thousands of DNA mutations per cell.

The results were based on skin cells from the eyelids of just four people, so we don't yet know if the same would be found in other skin areas, or in other people, or what proportion of the mutated cells would eventually progress to skin cancer. 

Where did the story come from?

The study was carried out by researchers from The Wellcome Trust Sanger Institute in the UK, and was funded by The Wellcome Trust and the Medical Research Council.

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

The BBC and the Daily Mail reported the story accurately and reiterated the best ways to lower your risk of getting skin cancer. 

What kind of research was this?

This was a genetics study looking at changes in the DNA of normal skin cells to see what proportions were linked to cancer.

Skin cancer is one of the most common forms of cancer. There are two main types of skin cancer:

• non-melanoma skin cancer – where cancer slowly develops in the upper layers of the skin; there are more than 100,000 new cases of non-melanoma skin cancer every year in the UK
• melanoma skin cancer – a more serious type of skin cancer; there are around 13,000 new cases of melanoma diagnosed each year in the UK and 2,000 deaths

Radiation from too much sun exposure causes damage to the DNA of skin cells. When certain combinations of mutations accumulate, the cell can become cancerous, multiplying and growing uncontrollably. 

Scientists know about lots of skin cancer mutations, but these tend to have been studied using samples of cancerous skin cells. Researchers don't know what combination of mutations is needed to transform healthy skin cells into cancer, or in what order.

Approaching the problem from a different direction, this team looked at healthy skin cells to see what mutations might be accumulating in a pre-cancerous stage. 

What did the research involve?

The scientists analysed the DNA of healthy eyelid skins cells removed from four people during plastic surgery (blepharoplasty). They looked for DNA mutations they knew were linked to cancer later on. The removed eyelid skin was reported to be normal and free of any obvious damage.

The team used eyelid skin because of its relatively high levels of sun exposure and because it is one of the few body sites to have normal skin removed.

They say this procedure is performed for age-related loss of elasticity of the underlying skin, which can cause eyelid drooping sometimes severe enough to disrupt vision, although the epidermis remains otherwise normal.

The skin sample donors were three women and one man, aged 55 to 73. Two had low sun exposure, one moderate and one high. Three were of western European origin and one was of south Asian origin. It was not clear how sun exposure was assessed.  

What were the basic results?

The researchers found a lot more cancer-related mutations in the normal cells than they were expecting. In all, their analysis pinpointed 3,760 mutations. The pattern of DNA mutations "closely matched" those expected for UV light exposure and that seen in skin cancers. 

DNA is made up of a code of letters known as base pairs. The team estimated people have around two to six mutations per million base pairs per skin cell. This, they said, was lower than the number of mutations usually found in skin cancer, but higher than found in other solid tumours.

Overall, they estimated around 25% of all skin cells carried a certain type of cancer-linked mutation called NOTCH mutations. While not enough to cause cancer on their own, if other mutations accumulate on top of the NOTCH mutations, they may cause cancer in the future. 

How did the researchers interpret the results?

Dr Peter Campbell, head of cancer genetics at Sanger, told the BBC News website: "The most surprising thing is just the scale; that a quarter to a third of cells had these cancerous mutations is way higher than we'd expect, but these cells are functioning normally."

He added: "It certainly changes my sun worshipping, but I don't think we should be terrified … It drives home the message that these mutations accumulate throughout life, and the best prevention is a lifetime of attention to the damage from sun exposure." 

Conclusion

This study estimated around 25% of normal skin cells have DNA mutations that could prime them to develop into skin cancer in the future. This was a lot higher than the scientists expected.

The genetic analysis of the study was robust, but used skin samples from just four people. This severely limits the generalisablity of the findings to the general population. For example, the results might be different for people of different ages, sun exposures and skin colours, so we don't know if this is true for most people.

Similarly, the researchers only used eyelid cells. There may be something unique about eyelid tissue that is linked to this higher than expected mutation rate. This may or may not be true for skin from other areas. At the moment, we don't know if the one in four estimate applies to other skin areas.

The good news is there are simple and effective ways of reducing your risk of skin cancer. The best way to prevent all types of skin cancer is to avoid overexposure to the sun and to keep an eye out for new or changing moles.

A few minutes in the sun can help maintain healthy levels of vitamin D, which is essential for healthy bones, but it's important to avoid getting sunburn. Wearing protective clothing such as sun hats, seeking shade, and wearing sun cream of at least SPF 30 are all advised.

Read more about how to enjoy the benefits of the sun without exposing your skin to damage

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Mildly cold weather 'more deadly' than heatwaves or very cold snaps

Thursday May 21 2015

Mildly cold weather could weaken the immune system

"Mildly cold, drizzly days far deadlier than extreme temperatures," The Independent reports. An international study looking at weather-related deaths estimated that moderate cold killed far more people than extremely hot or cold temperatures.

Researchers gathered data on 74,225,200 deaths from 384 locations, including 10 in the UK. The results showed that the days most countries have the fewest deaths linked to temperature are those with warmer temperatures than average.

Therefore, the researchers calculate, the majority of "excess deaths" occur on days that are colder than average. Because extreme temperatures occur on only a few days a year, they have an impact on fewer deaths than the majority of moderately cold days.

Overall, the researchers say, 7.71% of all deaths can be attributed to temperature based on their statistical modelling.

One hypothesis offered by the researchers is that exposure to mild cold may increase cardiovascular stress while also suppressing the immune system, making people more vulnerable to potentially fatal conditions.

The researchers suggest that their findings show public health officials should spend less time planning for heatwaves, and more time thinking about how to combat the effect of year-round lower than optimum temperatures.  

Where did the story come from?

The study was carried out by researchers from 15 universities and institutes in 12 countries led by a team from the London School of Hygiene and Tropical Medicine.

It was funded by the UK Medical Research Council. The study was published in the peer-reviewed medical journal The Lancet and has been made available on an open-access basis, so it is free to read online or download as a PDF.

The media reports focused on the finding that moderately cold weather – such as that experienced in the UK for much of the year – caused more deaths than hot weather or extremely cold weather. The Daily Telegraph gave a good overall summary of the research.

The Independent's claim that "mildly cold, drizzly days" are "far deadlier than extreme temperatures" is an extrapolation, as the study didn't look at drizzle or rain as a risk factor, just temperature.

The Guardian includes a number of reactions from independent experts, such as Sir David Spiegelhalter's, presumably tongue-in-cheek, suggestion that "perhaps they are really saying that the UK climate is killing people". 

What kind of research was this?

This study was a meta-analysis of data on temperatures and deaths around the world to find out what effect temperature has on the risk of death, and whether people are more likely to die during cold weather or hot weather.

The researchers used statistical modelling to estimate the proportions of deaths in the regions studied that could be attributed to heat, cold, and extreme heat and cold. This type of study can tell us about links between variables such as temperature and death rates, but not whether one causes the other. 

What did the research involve?

Researchers collected data on temperature and mortality (74,225,200 deaths) from 384 locations in 13 different countries, during time periods from 1985 to 2012. They used statistical analysis to calculate the relative risk of death at different temperatures for each location.

The countries included were Australia, Brazil, Canada, China, Italy, Japan, South Korea, Spain, Sweden, Taiwan, Thailand, the UK and the US. About one-third of the locations sampled were in the US.

The researchers were not able to adjust figures to take account of the potential effects of other factors, such as income levels in the different countries, although they used air pollution data when it was available.

The researchers divided the temperature data from each location into evenly spaced percentiles, from cold to hot days. This was so the temperatures for the coldest days would be in the lowest percentiles of 1 or 2, while the highest temperatures would be at the top range, 98 or 99.

They defined extreme cold for a location as below the 2.5th percentile, and extreme heat as above the 97.5th percentile. They looked for the "optimum" temperature for each location, being the temperature at which fewest deaths attributable to temperature were recorded.

They calculated the deaths linked to temperatures above or below the optimum, and sub-divided that again to show deaths linked to extreme cold or heat.

The statistical analysis used a complex new model developed by the researchers, which allowed them to take account of the different time lag of different temperatures.

The effects of very high temperatures on death rates are usually quite shortlived, while very cold temperatures may have an effect on deaths for up to four weeks. 

What were the basic results?

Across all countries, colder weather was linked to more excess deaths than warmer weather – approximately 20 times as many (7.29% deaths in colder weather compared with 0.42% in warmer weather). 

For all countries, the optimum temperature – when there were fewest deaths linked to weather – was warmer than the average temperature for that location.

In the UK, for example, the average temperature recorded was 10.4C, while optimum temperature ranged from 15.9C in the north east to 19.5C in London. The optimum temperature for the UK was in the 90th centile, meaning that 9 out of 10 days in the UK are likely to be colder than the optimum.

The proportion of all deaths linked to extremely hot or cold days was much lower than that linked to less extreme hot or cold. The researchers say extreme heat or cold was responsible for 0.86% of deaths according to their statistical modelling (95% confidence interval 0.84 to 0.87).

However, the relative risk of dying at extremes of temperatures was increased, with a sharp increase in deaths at the hottest temperatures for most countries.  

How did the researchers interpret the results?

The researchers say their results have "important implications" for public health planning, because planning tends to focus on how to deal with heatwaves, whereas their study shows that below-optimal temperatures have a bigger effect on the number of people who die.

They say deaths from cold weather may be attributed to stress on the cardiovascular system, leading to more heart attacks and strokes. Cold may also affect the immune response, increasing the chances of respiratory disease.

They say their results show that public health planning should be "extended and refocused" to take account of the effect of the whole range of temperature fluctuation, not just extreme heat. 

Conclusion

Many of the headlines focus on the finding that moderate cold may be responsible for more deaths than extreme hot or cold weather.

Perhaps more interesting is the finding that the optimum temperature for humans seems to be well above the temperatures we usually experience, especially in colder countries like the UK. If this is true, then the finding that most deaths occur on days colder than the optimum is unsurprising, as most days are colder than the optimum temperature.

The relative unimportance of very hot or very cold days in terms of mortality is interesting, because most research and public health planning has focused on extreme weather. However, this depends partly on the definition of extreme temperature.

The researchers used 2.5 upper and lower percentiles to decide on what was extreme for a particular location, so by definition these temperatures are experienced on very few days. Even though the relative risk of death is increased on those days, the absolute number of deaths is nowhere near as high as on the majority of days.

That doesn't mean it's not worth planning for the increased risk of deaths during extreme temperatures. In London, for example, the relative risk of death is more than doubled on days with temperatures below 0C, compared with days at the optimum temperature of 19.5C.

Read more advice about coping with heatwaves as well as very cold snaps.

There are some limitations to the study we should be aware of. First, although it sampled data from 13 countries from very different climates, it didn't include any countries in Africa or the Middle East. This means we can't be sure the findings would apply worldwide.

Second, the study did not take into account some confounders that could affect how many deaths occur in warmer or colder periods – for example, levels of air pollution, whether people have access to shelter and heating, the age make-up of a population, and whether people have access to nutritious food all year round.

This also makes it difficult to know how governments or public health bodies can make plans using this new data, as we don't know whether the effects of moderate cold on mortality could be affected by public health measures.

In the UK, the NHS already plans for more hospital admissions during the winter months, taking account of factors such as the amount of flu-like illness circulating in the population, as well as the temperature.

Read more advice about winter health.

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Single mothers have 'worse health in later life'

Friday May 15 2015

There are around 1 million single parents in the UK

The Daily Telegraph today tells us that: "Single mothers in England [are] more likely to suffer ill health because their families 'do not support them'."

This is a half-truth. The large international study – involving 25,000 people from England, the US and 13 other European countries – behind the headline found a link between single motherhood between the ages of 16 and 49 and worse health in later life. But it did not find this was because families do not support them.

It would appear that this claim is prompted by a trend spotted in the study by the researchers. It found that health risks were more pronounced in northern European countries and the US. While in southern European countries the risk was less pronounced.

The researchers speculated that in southern European countries there is more of a tradition of informal support services, where grandparents, aunts, uncles, cousins etc all pitch in with childcare duties. Or as the proverb puts it "It takes a village to raise a child".

While this hypothesis is plausible it is also unproven and was not backed up with any new robust data on social support as part of the study.

The study was very large and diverse so the mother health link appears real. However, the reasons and causes behind it are still to be worked out.

Where did the story come from?

The study was carried out by researchers from US, Chinese, UK and German universities and was funded by the US National Institute on Aging.

The study was published in the peer-reviewed Journal of Epidemiology & Community Health.

The media reporting was generally partially accurate, as most took the finding about social support at face value. The link between single motherhood and later ill health was supported by the body of this study, but the study did not collect any information on social support, so this explanation, although plausible, was not based on direct evidence. 

What kind of research was this?

The study investigated if single motherhood before the age of 50 was linked to poorer health later in life, and whether it was worse in countries with weaker "social [support] safety nets". To do this they analysed data collected from past cohort and longitudinal studies across 15 countries.

The researchers say single motherhood is known to be linked to poorer health, but didn’t know whether this link varied between countries.

Analysing previously collected data is a practical and legitimate study method. A limitation is that the original information was collected for specific reasons that usually differ from the research aims when coming to use it later. This can mean some information that would ideally be analysed is not there. In this study, the researchers couldn’t get information on social support networks, which they thought might explain some of their results.

What did the research involve?

The research team analysed health and lifestyle information on single mothers under 50 collected from existing large health surveys. The single mothers' health was documented into older age and compared across 15 countries.

Data was available from 25,125 women aged over 50 who participated in the US Health and Retirement Study; the English Longitudinal Study of Ageing; or the Survey of Health, Ageing and Retirement in Europe (SHARE). Thirteen of the 21 countries represented by SHARE (Denmark, Sweden, Austria, France, Germany, Switzerland, Belgium, The Netherlands, Italy, Spain, Greece, Poland, Czech Republic) had collected relevant data. With the US and England on board, this gave 15 countries for final analysis.

The researchers used data on number of children, marital status and any limitations on women's capacity for routine daily activities (ADL), such as personal hygiene and getting dressed, and instrumental daily activities (IADL), such as driving and shopping. Women also rated their own health.

Single motherhood was classified as having a child under the age of 18 and not being married, rather than living with a partner.

What were the basic results?

Single motherhood between the ages of 16 and 49 was linked to poorer health and disability in later life in several different countries. The risks were highest for single mothers in England, the US, Denmark and Sweden.

Overall 22% of English mothers had experienced single motherhood before age 50, compared with 33% in the US, 38% in Scandinavia, 22% in western Europe and 10% in southern Europe.

While single mothers had a higher risk of poorer health and disability in later life than married mothers, associations varied between countries.

For example, risk ratios for ADL limitations were significant in England, Scandinavia and the US but not in western Europe, southern Europe and eastern Europe.

Women who were single mothers before age 20, for more than eight years, or resulting from divorce or non-marital childbearing, had a higher risk.

How did the researchers interpret the results?

The researchers' concluded that: "Single motherhood during early adulthood or mid-adulthood is associated with poorer health in later life. Risks were greatest in England, the US and Scandinavia."

Although they didn’t have good data to back it up, they suggested that social support and networks may partially explain the findings. For example, areas like southern Europe, which the researchers say have strong cultural emphasis on family bonds, were not associated with higher health risks.

They add: "Our results identify several vulnerable populations. Women with prolonged spells of single motherhood; those whose single motherhood resulted from divorce; women who became single mothers at young ages; and single mothers with two or more children, were at particular risk."

Conclusion

This large retrospective study of over 25,000 women linked single motherhood between the ages of 16 and 49 with worse health in later life. This is not a new finding. What was new was that the link varied across different countries. Risks were estimated as greatest in England, the US and Scandinavia for example, but were less consistent in other areas of Europe.

The research team thought this might be caused by differences in how social networks supported single mothers in different countries, such as  being able to rely on extended families. But they had no data to directly support this. They did not have information on, for example, socioeconomic status, social support or networks during single motherhood, so could not analyse whether these were important causes. They also did not know whether any of the women they classed as single were actually in non-marital or same-sex partnerships, which may have affected results.

Health status in later life is likely to be linked to a complex number of interrelated factors. Being a single mum may be one, social networks might be another. But based on this study we don't yet know for sure, or the mechanisms by which this could lead to worse health.

Studies that collect information on levels of social support alongside health outcomes for single women would be able to tell us whether this is the likely cause, but getting this data may not be easy.

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

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Study finds seasons may affect immune system activity

Wednesday May 13 2015

Some patterns of immune activity come with drawbacks

"Winter immune boost may actually cause deaths," The Guardian reports. A new gene study suggests there may be an increase in inflammation levels during winter, which can protect against infection but could also make the body more vulnerable to other chronic diseases.

The study looked at gene expression (the process of using a gene to make a protein) in blood samples taken from 1,315 children and adults in different months throughout the year in a range of different countries. The researchers found increased activity of some of the genes involved in inflammation during the winter, and decreased activity in the summer.

The authors concluded that this seasonal change in the immune system could, for example, contribute to the worsening of some autoimmune disorders during the winter, such as rheumatoid arthritis.

But the immune system is extremely complex, and different genes showed different seasonal expression patterns. There were also important discrepancies in expression patterns in different parts of the world. Saying the immune system is "weaker" in certain seasons at this stage is therefore oversimplifying the findings of this research.

It is also likely these seasonal changes could at least in part be a response to changes in infections and allergens, such as pollen in the summer, but this type of study cannot prove cause and effect. Further research into this area is required before any practical application of these results can be found. 

Where did the story come from?

The study was carried out by researchers from the University of Cambridge and the London School of Hygiene and Tropical Medicine in the UK, and the Technical University of Munich and the Technical University of Dresden in Germany.

It was funded by various institutions, including the National Institute for Health Research, Cambridge Biomedical Research Centre, the UK Medical Research Council (MRC), The Wellcome Trust, and the UK Department for International Development.

The study was published in the peer-reviewed journal Nature Communications. This is an open-access journal, so the study is free to read online.

The media, on the whole, reported the story accurately, though the total number of people who had gene expression analyses was 1,315, not more than 16,000, as reported.

Many of the news sources talked of the immune system being "stronger", "weaker" or "boosted". These terms are, arguably, overly simplistic and not representative of the findings of this research. It is probably better to think of the overall pattern of immune activity changing from season to season, rather than the immune system going from "weak" to "strong", and back to "weak" again.

The Mail Online also reported that it is believed the amount of daylight we get "plays a role" in this increased immune activity. They say this "could explain why the seasonal effect was weaker in people from Iceland, where the extremely long summer days and short, dark winter days may upset the process". But this seems contradictory – if daylight plays a role, you would expect a greater seasonal effect in Iceland. 

What kind of research was this?

This research combined several observational studies that looked at the level of immune system activity at different times of the year in people from around the world.

It aimed to see if there was seasonal variation in the:

• gene expression of inflammatory proteins and receptors such as interleukin-6 (IL-6) and C-reactive protein (these proteins are associated with autoimmune conditions such as rheumatoid arthritis)
• number of each type of white cell in the blood (white cells fight different types of infections)

As these were observational studies, they can only show an association between the different seasons and the immune system. They cannot prove that the season causes the immune system to become more or less active, as there could be other factors (confounders) causing any results seen.

What did the research involve?

The researchers looked at the gene expression of nearly 23,000 genes in one type of white blood cell in samples of blood taken from children and adults at different times of the year.

They measured the number of each type of white cell in blood samples from healthy adults from the UK and The Gambia taken during different months. They then looked at gene expression in samples of fat tissue from women in the UK.

Gene expression of 22,822 genes was analysed in samples from 109 children genetically at risk of developing type 1 diabetes. The samples came from the German BABYDIET study, where babies had a blood test taken every three months until the age of three.

Gene expression was measured from blood samples taken at different times of the year from:

• 236 adults with type 1 diabetes from the UK
• adults with asthma but no reported current infection from Australia (26 people), the UK/Ireland (26 people), the US (37 people) and Iceland (29 people)

The researchers then measured the number of each type of white cell in blood samples taken from 7,343 healthy adults from the UK and 4,200 healthy children and adults from The Gambia. They wanted to see if there were seasonal changes in the types of white cells in the blood.

Finally, they looked at gene expression in fat tissue samples taken from 856 women from the UK. They did this to see whether only cells in the immune system showed variation in gene expression with the seasons. 

What were the basic results?

In the first group of children and adults from Germany, the researchers found almost a quarter of all genes (23%, about 5,000 genes) showed seasonal variation in the white blood cells assessed. Some genes were more active in the summer and others in winter.

When looking at all of the population groups they tested, 147 genes were found to show the same seasonal variation in the blood samples taken from the children and adults from the UK/Ireland, Australia and the US.

Again, some genes were more active in the summer and others in the winter. The genes included one encoding protein, which controls the production of anti-inflammatory proteins and was found to be more active in the summer months.

Other genes involved in promoting inflammation were more active in the winter. Seasonal genes from the samples of Icelandic people did not show the same pattern.

The numbers of different types of white blood cells from the UK samples also showed seasonal variation. Lymphocytes, which mostly fight viral infections, were highest in October and lowest in March. Eosinophils, which have many immune functions, including allergic reactions, were highest in the summer.

There were also seasonal patterns in the numbers of different types of white blood cell from people in The Gambia, but these were different from those in the UK. All white cell types increased during the rainy season.

The researchers also found some genes showed seasonal variation in their activity in fat cells.  

How did the researchers interpret the results?

The researchers say their results indicate gene expression and the composition of blood varies with seasons and geographical locations.

They say the increased gene expression of inflammatory proteins in the European winter may help explain why some autoimmune conditions are more likely to start in the winter, such as type 1 diabetes.

Conclusion

This research found seasonal variations in gene expression in one type of white blood cell. Some genes became more active in the summer months, while others became more active in the winter.

For example, one gene involved in the body's anti-inflammation response was increased during the summer, while some involved in inflammation were increased in the winter.

The researchers also found seasonal variation in the numbers of each type of white cell. These patterns were different in samples taken from people in the UK, compared with people from The Gambia.

Because of the observational nature of each study, it is not possible to say for certain that the time of year caused the results seen. The immune system is affected by a variety of factors, such as current and past infections, stress and exposure to allergens.

For example, it is not surprising that the number of eosinophils was highest in the UK during the summer months, when the allergen pollen (linked to hay fever) is most abundant.

Concurrent illness may have confounded the results of the gene expression studies, as they were performed on adults with either type 1 diabetes or asthma and children at increased risk of type 1 diabetes.

The immune system is extremely intricate, involving a wide range of different genes, proteins and cells that have complex interactions, as shown in this study. Further research into this area is required before any practical application of these results can be found.

The most season-specific health advice we can offer at this point is to wrap up warm in winter, avoid getting sunburnt during the summer, and take the opportunity to safely top up your vitamin D throughout the year.

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

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Texting may help relieve pain during minor surgery

Friday May 1 2015

Social support may distract people from any pain during surgery

"Need pain relief for surgery? Try a text," the Daily Mail reports. The advice was prompted by a small study that found people who used a mobile phone during minor surgery were less likely to require additional pain medication.

During surgery, participants in this study were allocated to texting a close friend or family member, texting a research assistant they did not know, playing Angry Birds, or receiving usual care.

Researchers found patients who used a mobile phone to text someone were less likely to need additional painkillers during surgery. Interestingly, people who texted a research assistant tended to need slightly less painkillers than those who texted somebody that they knew.

The researchers speculate this could be because the conversations with the research assistant were not about their surgery, so this may have helped take their mind off the experience.

While the study was well designed, it was relatively small and may not be representative of all people having this type of surgery, or be able to detect small effects.

Larger studies assessing a wider variety of pain-related outcomes, such as the patient's own rating of their pain, are needed to confirm the findings.

Distraction techniques and social support can be useful self-help methods for coping with pain. 

Where did the story come from?

The study was carried out by researchers from Cornell University in the US and McGill University and LaSalle Hospital in Canada, and was funded by Cornell University. It was published in the peer-reviewed journal, Pain Medicine.

The Daily Mail covered the story reasonably, but does not highlight any of the study's limitations. The Daily Telegraph's headline, "Angry Birds could reduce pain during surgery, study finds", is misleading. There was no statistically significant difference between the "Angry Birds" group and the "no special activities" group in terms of their need for the painkiller.

It would be a shame if the paper just included the term to create an eye-catching headline rather than trying to report the study accurately.  

What kind of research was this?

This was a randomised controlled trial (RCT) looking at whether text messaging or playing a mobile phone game during minor surgical procedures could reduce patients' need for a strong painkiller.

Having social support has been reported to have a number of benefits, including reducing a person's pain sensation and making them able to bear pain for longer (in childbirth, for instance).

Distraction techniques, such as listening to music or using virtual reality simulations, have also been reported to help reduce anxiety and people's need for anaesthesia.

The researchers were interested in whether social support (in the form of text messaging) would have a greater effect than just being distracted (in the form of a game).

They also tested whether there was a difference between texting a friend or family member, who might be anxious about the person's surgery, and texting a stranger. An RCT is the best way to compare the effects of different interventions.  

What did the research involve?

The researchers recruited 98 adults scheduled to undergo minor surgery with regional, rather than general, anaesthesia. They allocated them at random to perform one of four things just before and during their surgery:

• texting a close friend or family member
• texting a research assistant they did not know about their hobbies and interests, for example
• playing Angry Birds on a phone
• no special activities (usual care)

The participants had the normal pre-surgery procedures, including being given their anaesthesia and initial dose of painkillers.

All except one of the anaesthetists (the doctors who give anaesthetic during surgery) did not know the aim of the study or what it was measuring. They knew whether the patient had a phone with them, but were not told what the patient had been asked to do with it.

The anaesthetists asked patients if they were in pain after the first surgical incision was made, then again within the first 5-10 minutes of surgery and throughout the procedure. If the patient reported pain, the anaesthetist could give them the painkiller fentanyl or sedation as they judged appropriate.

The researchers then compared the groups to see if they differed in terms of how much fentanyl was needed during the surgery.

What were the basic results?

The patients in the four groups did not differ in their anxiety levels before surgery, or the type of surgery or how long they were in the operating room. Only about a quarter of the patients (27.6%) needed extra fentanyl during the surgery.

The researchers found that:

• patients who texted a close friend or family member during their surgery needed less fentanyl than those who did not do any of the activities
• patients who texted the research assistant needed less fentanyl than those playing the game and those who did not do any of the activities
• patients in the two texting groups did not differ significantly in their need for fentanyl
• patients in the game group and those who did not do any of the activities did not differ significantly in the amount of fentanyl they needed

The researchers also analysed the odds of needing additional fentanyl during surgery. They report that those doing nothing were four times more likely to need more fentanyl than those texting friends or family, and six times more likely than those texting the research assistant.

Looking at the text conversations, those who texted the research assistants tended to be more positive, while the texts with a friend or family member tended to use more biological terms, so seemed to focus on the surgery itself. 

How did the researchers interpret the results?

The researchers concluded that their study "provides the first evidence of the analgesic-sparing benefits of social support from text messaging in a surgical setting". 

Conclusion

This relatively small study suggests text message conversations during minor surgery may reduce the need for painkillers, and are more effective than playing the game Angry Birds.

The study was an RCT, the best design for comparing different interventions, which should ensure the groups were well balanced. This means any differences in the patients' outcomes should be the result of the interventions.

But this study does have some limitations:

• It was relatively small and may not be representative of all people having this type of surgery. The authors suggest the study's small size may also be why they did not find an effect for the Angry Birds intervention.
• The anaesthetists could not be completely blinded to which group patients were in, as they knew whether the person had a phone with them. They may also have been able to guess what a person was doing (texting or playing a game) based on their hand movements or expression. This might influence their perception of the participants' pain.
• Being engaged with the phone might affect the frequency anaesthetists asked the participants about their pain. The researchers say they tried to make sure this wasn't the case, but acknowledge this was down to the discretion of the anaesthetists.
• It only assessed one outcome. Ideally, comparison of the patients' own assessment of pain and satisfaction with the procedure would be an important outcome to assess.

There is interest in developing non-drug-related methods to reduce people's pain and discomfort during surgery or other procedures.

The researchers suggest that texting could be a good approach, as it is simple and doesn't need specialised equipment or input from healthcare staff. However, whether this would be considered acceptable from an infection control perspective is unclear.

Overall, this study suggests that using a mobile phone during surgery has some effect, but larger studies assessing a wider variety of outcomes are needed.

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

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http://ift.tt/1zxHbcB Feed for NHS Choices News pagesFri, 01 May 2015 09:43:56 GMTNHS Choices SharePoint RSS Feed Generator60http://www.nhs.uk/News/Pages/NewsArticles.aspxhttp://www.nhs.uk/news/2015/04April/Pages/UK-life-expectancy-expected-to-rise-to-late-80s-by-2030.aspx

"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.

Links To The Headlines

Life expectancy increases but gap widens between rich and poor. The Guardian, April 30 2015

Men near equality with women in life expectancy. The Times, April 30 2015

Men 'catching up' on life expectancy. BBC News, April 30 2015

Britain is facing a life expectancy timebomb: By 2030, the average man will live to 85... and women will reach 87. Daily Mail, April 30 2015

Richest one per cent will live over eight years longer on average than those living in poorest parts of UK by 2030, say experts. The Independent, April 30 2015

Britons to live up to four years longer than official estimates by 2030. The Daily Telegraph, April 30 2015

Why we are all living longer: Life expectancy set to soar for Britons. Daily Express, April 30 2015

Links To Science

Bennett JE, Li G, Foreman K, et al. The future of life expectancy and life expectancy inequalities in England and Wales: Bayesian spatiotemporal forecasting. The Lancet. Published online April 29 2015

]]> NHS ChoicesThu, 30 Apr 2015 11:50:00 GMThttp://www.nhs.uk/news/2015/04April/Pages/UK-life-expectancy-expected-to-rise-to-late-80s-by-2030.aspxLifestyle/exerciseMedical practiceOlder peoplehttp://www.nhs.uk/news/2015/04April/Pages/Having-a-spine-similar-to-a-chimp-could-lead-to-back-pain.aspx

"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.

Links To The Headlines

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

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

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

Links To Science

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

]]> NHS ChoicesMon, 27 Apr 2015 12:00:00 GMThttp://www.nhs.uk/news/2015/04April/Pages/Having-a-spine-similar-to-a-chimp-could-lead-to-back-pain.aspxMedical practiceLifestyle/exercisehttp://www.nhs.uk/news/2015/04April/Pages/Parents-may-pass-anxiety-on-to-their-children.aspx

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.

Links To The Headlines

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

Links To Science

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

]]> NHS ChoicesMon, 27 Apr 2015 12:00:00 GMThttp://www.nhs.uk/news/2015/04April/Pages/Parents-may-pass-anxiety-on-to-their-children.aspxLifestyle/exerciseMental healthPregnancy/childhttp://www.nhs.uk/news/2015/04April/Pages/Air-pollution-linked-to-shrunken-brains-and-silent-strokes.aspx

"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.

Links To The Headlines

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

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

Links To Science

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

]]> NHS ChoicesFri, 24 Apr 2015 12:00:00 GMThttp://www.nhs.uk/news/2015/04April/Pages/Air-pollution-linked-to-shrunken-brains-and-silent-strokes.aspxLifestyle/exerciseNeurologyhttp://www.nhs.uk/news/2015/04April/Pages/A-magnet-for-mosquitoes-Could-be-your-genes-fault.aspx

"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.

Links To The Headlines

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

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

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

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

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

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

Links To Science

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

]]> NHS ChoicesThu, 23 Apr 2015 10:30:00 GMThttp://www.nhs.uk/news/2015/04April/Pages/A-magnet-for-mosquitoes-Could-be-your-genes-fault.aspxLifestyle/exerciseGenetics/stem cellshttp://www.nhs.uk/news/2015/04April/Pages/Why-you-should-drink-water-before-you-drive.aspx

"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.

Links To The Headlines

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

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

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

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

Links To Science

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

]]> NHS ChoicesMon, 20 Apr 2015 12:30:00 GMThttp://www.nhs.uk/news/2015/04April/Pages/Why-you-should-drink-water-before-you-drive.aspxFood/dietLifestyle/exerciseMental healthhttp://www.nhs.uk/news/2015/04April/Pages/study-doesnt-prove-e-cigs-make-quitting-smoking-harder.aspx

"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."

Conclusion

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

]]> NHS ChoicesFri, 17 Apr 2015 08:46:00 GMThttp://www.nhs.uk/news/2015/04April/Pages/study-doesnt-prove-e-cigs-make-quitting-smoking-harder.aspxLifestyle/exercisehttp://www.nhs.uk/news/2015/04April/Pages/Does-happiness-have-a-smell-and-is-it-contagious.aspx

"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)".

Conclusion

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

]]> NHS ChoicesThu, 16 Apr 2015 14:00:00 GMThttp://www.nhs.uk/news/2015/04April/Pages/Does-happiness-have-a-smell-and-is-it-contagious.aspxLifestyle/exerciseMental healthhttp://www.nhs.uk/news/2015/04April/Pages/60-the-new-40-claims-media.aspx

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