"Terrible night's sleep? Blame your mobile phone" is the advice on the Mail Online website, as "exposure to artificial light 'fools' the brain into staying awake."

This – and similar headlines in the Daily Express, The Guardian and Metro newspapers – is based on a recent opinion piece in the journal Nature, which has published a dedicated supplement on the science of sleep.

The opinion piece suggests that the invention of electric light has altered our sleep patterns over the last century. In particular, the widespread use of LED lights, which we rely on to view smartphones, tablets, televisions and laptops screens, is disrupting our sleep.

This, the author suggests, could have potentially serious health consequences, as poorly controlled insomnia can cause both physical and mental health problems.

As an opinion piece, this should not be taken as evidence that light exposure hampers our ability to sleep. However, it does suggest several ways the two may be linked. The piece offers the theory that one causes the other, but these associations have not been directly tested. But given that the author is a specialist in sleep medicine, his opinion cannot simply be dismissed out of hand.

Who wrote the opinion piece?

The editorial was written by Charles Czeisler, a professor of sleep medicine at Harvard Medical School and chief of the division of sleep medicine at Brigham and Women's Hospital in Boston, US.

Over the past 35 years Dr Czeisler has published widely on sleep, the impact of light on sleep, and the effect of restricted sleep on human behaviour and performance.

What arguments are made?

Dr Czeisler suggests that since the invention of electric light, there has been a fundamental shift in our sleep patterns. He argues that light has enabled us to evolve into a "24/7 society", and that many of the features of this transformation – early starting times at work and school, long commutes, high doses of caffeine – lead to us getting insufficient amounts of sleep.

Dr Czeisler's arguments for the link between the increasing use of electric light and disrupted sleep have highlighted several issues.

The biological effect of artificial light

Dr Czeisler argues that exposure to artificial light during the evening and at night could block the effects of brain cells that help promote feelings of sleepiness, as well the "sleep hormone" melatonin.

At the same time, artificial light could also stimulate brain cells associated with alertness.

The combination of these effects could result in many of us feeling much less sleepy in the evening than we would normally.

Time-trends in light use, cost and sleep

Dr Czeisler reports that the cost of generating light dropped dramatically over the last 50 years, which was associated with an increase in the use of artificial light.

At the same time that the use of artificial light increased, reported levels of sleep deficiency also went up. A recent study looking at data in England from 1993 to 2007 found a continual increase in people seeking treatment for sleep disorders.

However, it is important to note that, as with any observational time-trend data, this argument only outlines associations between light consumption and sleep deficiency, and should not be interpreted as there being a causal relationship based on this editorial alone.

Increased use of LEDs

Dr Czeisler suggests that the recent move from traditional incandescent light bulbs to more energy efficient solid-state light-emitting diodes (LEDs) could further disrupt our sleep.

LEDs are commonly used in TVs, computer screens and handheld electronic devices such as tablets. These LEDs are typically rich in shortwave length (blue and blue-green) light, which the cells in our retina are more sensitive to.

He offers the theory that time in front of these blue light-rich screens at night will be more disruptive to our sleep than incandescent lighting.

Interestingly, one of the final discussion points in the editorial is about our ability to control the wavelengths emitted by LEDs. Dr Czeisler suggests that any adverse effect of exposure to these lights at night could be mitigated by replacing blue heavy light with red or orange heavy light in the evenings.

This editorial offers interesting discussion points surrounding the relationship between light – especially evening or nighttime exposure to light – and difficulty sleeping.

What evidence is cited?

Dr Czeisler's article makes reference to several publications, mainly centred around trends in the average number of hours adults and children sleep each night, and the prevalence of the adverse effects of sleep deprivation. As an opinion piece, the overall discussion points are narrative in nature and are not based on any individual piece of research or evidence.

This specific article on its own cannot provide evidence of a direct link between light exposure and sleep deprivation. However, it is not intended to do so. It offers a broad introduction to a series of articles on the topic, and suggests we consider the ways in which technological changes may impact our ability to get a good night's sleep.

Conclusion

It is certainly possible to reduce your exposure to artificial lights. For example, you could dump your smartphone, give away your iPad, banish television from your home, and refuse to work in any job that involves using a computer. But adopting this kind of luddite lifestyle is probably not to most people's tastes.

One proven method of improving your sleep is what is known as "sleep hygiene". This is where you control both physical and environmental factors in order to promote sleep.

Examples of good sleep hygiene include:

• not drinking tea and coffee four hours before bedtime
• avoiding drinking alcohol or smoking before bed
• using thick blinds or curtains, or wearing an eye mask if the early morning sunlight or bright streetlamps affect your sleep
• wearing ear plugs if noise is a problem

Read more advice about sleep hygiene.

If you have persistent insomnia (more than four weeks), contact your GP for advice. You may require more in-depth "sleep training" counselling, often done using cognitive behavioural therapy (CBT) techniques. Alternatively, there may be an underlying condition contributing towards your insomnia.

Read more about the treatment of insomnia.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Peering at bright screens after dark could harm health, doctor claims. The Guardian, May 22 2013

Terrible night's sleep? Blame your mobile phone: How exposure to artificial light 'fools' the brain into staying awake. Mail Online, May 22 2013

How your iPad tablet could mess with a good night's sleep. Metro, May 23 2013

Links To Science

Czeisler C. Perspective: Casting light on sleep deficiency. Nature. Published online May 23 2013

'Bad weather could raise your blood pressure and even kill you,' is the unnecessarily alarmist headline in the Daily Mail. It reports on a large, complex study that looked for any association between changes in weather and blood pressure rates.

The research focused on patients at a blood pressure clinic in Glasgow and looked at two consecutive visits the patients made within a 12-month period. The researchers combined these findings with Met Office weather data from the time of these visits to assess whether changes in patients' blood pressure were related to changes in the weather.

They found that decreases in temperature and sunshine, or increases in rainfall and frost, were associated with a slight increase in blood pressure.

In the longer term, individuals whose blood pressure seemed sensitive to decreases in temperature and sunshine had slight increases in blood pressure. They also seemed to have overall shorter survival than people insensitive to weather changes.

We know that our bodies respond to temperature changes, so it is plausible that temperature could influence blood pressure. But factors other than the weather may have had a role to play in the blood pressure results seen.

It is also important to point out that the minor increases in blood pressure detected by the study could in many cases be compensated for by taking more exercise or improving your diet.

Where did the story come from?

The study was carried out by researchers from the University of Glasgow. One of the study authors was supported by a Wellcome Trust Capacity Strengthening Strategic Award to the Public Health Foundation of India and a consortium of UK universities.

It was published in the peer-reviewed Journal of the American Heart Association.

The quality of the Daily Mail's reporting of this study is mixed. On the negative side, it presents an over-simplistic conclusion that cannot be drawn from the complex analysis used in this study. The claim made in the headline that 'bad weather...can kill you' is needlessly sensationalised.

On the plus side, its story does contain useful advice from a spokesperson from Blood Pressure UK: "Until we can control the weather, we can still rely on more traditional ways of controlling our blood pressure, such as eating more fruit and vegetables, less salt and alcohol, and taking more exercise."

What kind of research was this?

The researchers say that there is growing evidence that outdoor temperature has an influence on blood pressure, with blood pressure being higher in winter and lower in summer.

This is believed to be because the constriction of blood vessels at colder temperatures increases blood pressure. However, it is unclear whether the temperature-related response differs among individuals.

The current study aimed to examine people's individual changes in blood pressure in response to a range of weather patterns. The researchers also wanted to see whether this was predictive of longer term blood pressure control and mortality.

What did the research involve?

The study included 16,010 people from the Glasgow Blood Pressure Clinic (47% male) who had been referred by their GP in order to control their high blood pressure.

Information on the monthly average weather for the west of Scotland was obtained from the UK Met Office. The Met Office has used a consistent method to analyse climate patterns since 1961, and can provide weather for square kilometre grid points across the UK. Information on four aspects of weather was used in the study:

• air frost
• air temperature
• rainfall
• sunshine

Each visit every person made to the Blood Pressure Clinic was mapped to the mean monthly weather of the west of Scotland. Mean monthly measurements for each of the four aspects of weather were ranked from the lowest to the highest measurement, and then split into four equal groups called quartiles. The lowest quartile (Q1) contained the lowest 25% of measurements and the highest quartile (Q4) contained the highest 25% of measurements.

For each person, the researchers looked at pairs of consecutive clinic visits that were at least one month apart but within the same 12-month period. They were interested in pairs of visits where weather either remained constant (both visits in the same weather quartile) or where weather was very different (one visit in the lowest quartile and one visit in the highest quartile). They categorised the weather for these clinic visits as:

• Q1 to Q4, where weather for the first clinic visit was in the lowest quartile and the subsequent visit was in the highest quartile
• Q4 to Q1, where weather for the first clinic visit was in the highest quartile and the subsequent visit was in the lowest quartile
• Qn to Qn, where both the first and the second clinic visits were in the same weather quartile – there was no change in weather patterns

For each individual, the researchers examined changes in their blood pressure and heart rate between the two visits, and looked at how the size and direction of this change (up or down) related to the change in weather.

The researchers used the General Register Office for Scotland to obtain information on deaths among the participants and causes of death. Mortality information was available up to 2011, allowing up to 35 years of follow-up.

Analyses were adjusted for factors known to influence blood pressure (confounders), including:

• age
• smoking
• alcohol
• high body mass index (BMI)
• kidney disease

What were the basic results?

The average age of individuals at their first clinic visit was 51 years, and most were overweight (mean BMI was 28). The average length of follow-up for each person was 6.5 years.

The researchers found that when there was consistent weather between the two clinic visits (Qn to Qn), there was:

• an average 2.1% decrease in systolic blood pressure (the upper figure of a blood pressure measurement) with consistent air frost
• a 2.2% decrease with consistent temperature
• a 1.7% decrease with consistent rainfall
• a 2.2% decrease with consistent sunshine

For change from high to low weather extremes, there was:

• about a 2% increase in systolic blood pressure with a decrease in temperature and sunshine
• no significant change in systolic blood pressure with a decrease in air frost and rainfall

For change from low to high weather extremes, there was:

• a 1.4% increase in systolic blood pressure with an increase in air frost
• a 0.8% increase in blood pressure for an increase in rainfall
• there was no consistent pattern in blood pressure with a change in temperature from low to high 

When the researchers compared the blood pressure changes seen with consistent weather patterns, a change in the weather from the highest to lowest quartile was associated with about a 6% increase in systolic blood pressure when there was a decline in temperature and sunshine, and about a 4% increase in systolic blood pressure when there was a decline in air frost.

Compared with consistent weather, a change from the lowest to highest quartile was associated with 2-6.6% increases in systolic blood pressure for all four weather characteristics assessed.

Looking at longer term changes over five or more years, people whose blood pressure changed when there was a decline in temperature experienced a 2.68mmHg increase in their systolic blood pressure, and a 1.84mmHg increase in their diastolic blood pressure (the lower figure in a blood pressure measurement), compared with people whose blood pressure seemed insensitive to temperature change. 

A similar 1.31mmHg increase in systolic blood pressure and a 1.22mmHg increase in diastolic blood pressure was seen for people who were sensitive to a decline in sunshine.

Looking at survival data, people who were insensitive to temperature or sunlight change seemed to have longer survival than people who were sensitive to a decline in temperature or sunlight.

There were no significant longer term differences in blood pressure or survival between people insensitive to temperature or sunlight change, or in people sensitive to an increase in weather extremes.

How did the researchers interpret the results?

The researchers have concluded that for the first time they have demonstrated the extent of alterations in blood pressure between consecutive clinic visits associated with changes in weather in people with high blood pressure.

They have extrapolated that knowing a person's blood pressure response to weather could help prevent doctors making unnecessary changes to blood pressure medication.

Conclusion

This study has used a complex method of analysis in order to look at how individuals' blood pressure at consecutive visits within a one-year period varied according to changes in the weather.

The study benefits from its large population sample and long follow-up. The blood pressure measurements taken at this specialist clinic are also likely to be reliable.

Our bodies do respond to changes in temperature and it is biologically plausible that temperature can affect our blood pressure. The researchers have adjusted for many factors known to influence blood pressure, such as age, high BMI and kidney disease.

However, it is still difficult to say with certainty that all blood pressure changes seen in people between clinic visits were solely down to changes in the weather. For example, the researchers did not have complete information about the blood pressure medications being used by the patients, or their levels of physical activity. These factors could also be influencing the findings.

Another limitation is that blood pressure would have been recorded inside the clinics and may not be representative of what blood pressure would have been if it had been taken outside, with full exposure to the weather.

The research was conducted in individuals from the Glasgow area and it is difficult to say whether similar responses would be seen in people in other locations, particularly people living in vastly different climates.

Similarly, the study only looked at people with high blood pressure. It is not clear whether people with normal blood pressure also experience similar changes in their blood pressure in response to weather changes.

The individuals in the study seem to have been variably sensitive to different changes in the weather. It is not yet clear exactly how a person's blood pressure treatment could be individualised according to their sensitivity to weather change, and whether this would successfully reduce blood pressure variability.

One final important point to make is that although we have no control over the weather, we can control a wide range of factors that contribute towards high blood pressure, such as:

• the amount of exercise you take
• diet – if your blood pressure is high, you should cut down on salt, saturated fat and sugar, and eat plenty of fruit and vegetables
• quitting smoking, if you smoke
• the amount of alcohol you drink

Read more about proven lifestyle changes you can make to reduce your blood pressure risk.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Bad weather could raise your blood pressure and even kill you. Daily Mail, May 21 2013

Chilly days can kill by raising blood pressure. Daily Express, May 22 2013

Links To Science

Aubinière-Robb L, Jeemon P, Hastie CE, et al. Blood Pressure Response to Patterns of Weather Fluctuations and Effect on Mortality. Hypertension. Published online May 6 2013

'A stressful job really can kill you – by raising your cholesterol,' reports the Mail Online website. This headline is based on Spanish research that looked at the relationship between job stress and lipid (fat) levels in the blood of more than 90,000 people.

The research found that people who reported difficulties coping with their job had higher levels of what has been dubbed "bad cholesterol" (LDL cholesterol) and lower levels of "good cholesterol" (HDL cholesterol). High levels of LDL cholesterol can clog up the arteries, increasing an individual's risk of developing cardiovascular diseases such as coronary heart disease.

A significant strength of this study is its size – an impressive 90,000 people participated. But the study did not look at diet, which can also affect cholesterol levels. It could well be the case that people in stressful jobs tend to have unhealthy diets and it is this, rather than stress itself, that is to blame for their higher "bad" cholesterol rates.

While increased LDL levels are a risk factor for cardiovascular diseases, this study did not explore the effect this would have on people's long-term health. The Mail Online's claim that a stressful job will kill you is therefore not supported by this study.

Where did the story come from?

The study was carried out by researchers from Ibermutuamur – a mutual insurance company dealing with work-related accidents and occupational illnesses – and two universities in Spain. There were no external sources of funding for the study.

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

The Mail Online's headline over-interprets the research, as the study did not assess whether people in stressful jobs were more likely to die. The body of the story was reasonably accurate, but it did not highlight that this type of study cannot prove that one factor is definitely causing another.

What kind of research was this?

This was a cross-sectional study that explored whether there is a link between job stress and abnormal levels of fats (lipids) in the blood.

Some studies have found a link between job stress and an increased risk of coronary disease. There are various theories about how this link might come about – for example, by stress increasing the likelihood of unhealthy habits such as smoking.

Some studies have also suggested that stress could directly influence levels of lipids in the blood by possibly adversely affecting the body's metabolism. However, these studies have been small and in selected populations, and have had mixed results.

In the current study, researchers wanted to assess stress and lipid levels in a large representative sample of workers. As this study is cross-sectional, both stress and lipid levels were assessed at the same time. This means the study cannot establish whether participants' lipid levels were directly influenced by their stress levels.

What did the research involve?

The study involved workers covered by the Ibermutuamur insurance company who had yearly medical check-ups. More than 430,000 participants were recruited between 2005 and 2007, and a study questionnaire was sent out to more than 100,000 randomly selected individuals. Completed questionnaires were returned by 91,593 of these people.

The questionnaire included the question, "During the last year, have you frequently felt that you cannot cope with your usual job?". Participants who answered "yes" were considered to have job stress.

The questionnaire also included 11 questions relating to anxiety and depression symptoms, such as "Have you felt keyed up, on edge?" and "Have you had difficulty relaxing?".

The researchers took fasting blood samples from participants and measured levels of total cholesterol, HDL cholesterol (so-called "good" cholesterol), and levels of a type of lipid called triglycerides. The levels of so-called "bad" cholesterol were calculated based on these measurements.

Participants were classed as having abnormal lipid levels based on pre-specified levels if they reported taking lipid-lowering medication or had been diagnosed as having abnormal lipid levels.

The researchers then looked at whether abnormal lipid levels are linked to job stress. They took into account the following confounders:

• age
• gender
• smoking
• basic measures of alcohol consumption and physical leisure activity
• obesity 
• type of job ("blue collar" or "white collar")

What were the basic results?

Job stress was reported by 8.7% of participants. Participants reporting job stress also had higher levels of anxiety and depression symptoms.

After the researchers took into account factors that could affect the results and adjusted them accordingly, people who reported job stress were found to have 10% higher odds of having abnormal lipid levels (odds ratio [OR] 1.1, 95% confidence interval [CI] 1.04 to 1.17).

They also had increased odds of:

• high levels of "bad" cholesterol (LDL)
• low levels of "good" cholesterol (HDL)
• a high total cholesterol to "good" cholesterol ratio
• a high "bad" cholesterol to "good" cholesterol ratio
   

How did the researchers interpret the results?

The researchers concluded that their results support an association between job stress and abnormal lipid levels in the blood.

Conclusion

This study has found an association between job stress and abnormal lipid levels in the blood. Its strengths include the large number of workers assessed (more than 40,000) and the use of the same methods to assess all of the participants.

However, the fact that both job stress and lipid levels were assessed at the same time means it is not possible to say for certain whether job stress might have directly caused changes in blood lipid levels.

There are also other limitations and points to note:

• The study did not assess diet. People with job stress may have less healthy diets, which could account for the differences seen in the blood lipid levels, rather than these differences being a direct impact of job stress.
• Job stress was assessed by a single question, which may not fully capture all aspects of job stress. Also, different people may consider different things stressful, and the question did not disentangle the exact stressful workplace situations and an individual's ability to cope with them.
• Workers who were off sick would not have had the routine medical check-up. This means the sample may have missed some people with more serious health problems with stress.
• The authors acknowledge that the effect of job stress seen is relatively small – a 10% increase in the odds of having abnormal lipid levels.

Overall, it is not clear from this study whether stress is a direct cause of the increased lipid levels seen. Studies looking at whether interventions to reduce work stress can reduce lipid levels in the blood would provide an indication if this is in fact the case.

Despite these limitations, there is a wide range of good quality evidence that workplace stress can have a harmful effect on your physical and mental health.

While some people may thrive on pressure, persistent high levels of stress are likely to be harmful.

Read more about what you can do to reduce your levels of workplace stress.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

A stressful job really CAN kill you - by raising your cholesterol. Mail Online, May 17 2013

Links To Science

Catalina-Romero C, Calvo E, Sánchez-Chaparro MA, et al. The relationship between job stress and dyslipidemia. The Scandinavian Journal of Public Health. Published online January 2 2013 

”Sunshine vitamin 'may treat asthma'”, BBC News informs us, as a new lab-based study suggests vitamin D could help control symptoms of severe asthma.

Asthma is caused by inflammation of the airways, related to malfunctioning of the body’s immune system. In theory, the immune system mistakes harmless substances, such as dust mites, as a threat and triggers inflammation of the lungs and airways (which causes the symptoms of asthma).

The study in question looked at IL-17A, which is one of the molecules thought to be associated with the malfunctioning immune response seen in asthma. Researchers examined whether vitamin D had an effect on the levels of the molecule produced by white blood cells in a laboratory experiment.

Researchers found that vitamin D reduced the levels of IL-17A produced by cells from people with asthma. This included cells from people who had previously failed to respond to the treatment of choice for severe asthma – oral corticosteroids – often referred to as steroids.

While this study suggests that vitamin D can have an effect on IL-17A levels in the laboratory, it is certainly too early to hail vitamin D as a potential “cure” for asthma. A positive effect on cells in the lab does not guarantee vitamin D supplements will improve symptoms for people with asthma. Clinical trials in people with asthma are ongoing to test whether this will be the case.

Where did the story come from?

The study was carried out by researchers from King’s College London; Queen Mary, University of London, and the Homerton University NHS Foundation Trust. It was funded by Asthma UK and the National Institute for Health Research, and some researchers received Medical Research Council Funding. The study was published in the peer-reviewed Journal of Allergy and Clinical Immunology.

This study was reported by the BBC, Daily Mail, and the Daily Express. The BBC correctly points out that treating asthma patients with vitamin D “has not yet been tested”. The main text of the Mail’s coverage is generally accurate, although their headline suggests that “Vitamin D ‘helps beat the symptoms of asthma’”, when this was not assessed by the study. The Express’s coverage over-interprets the results by suggesting that “Soaking up sun could be a cure for asthma” or could be “the best way of treating asthma”.

What kind of research was this?

This was a laboratory study looking at the effect of vitamin D on one type of white blood cell (T helper cells called TH17 cells) from people with asthma.

One type of T helper cell called TH2 is known to be involved in inflammation of the airways in asthma. However, some evidence suggests that other T cells may also play a role.

TH17 cells are involved in defending the body against bacterial and fungal infections. There is some evidence that these cells may be involved in severe asthma. Also, one of the inflammatory substances produced by these cells, called IL-17A, may exacerbate asthma and reduce patients’ ability to respond to standard treatment for severe asthma – oral corticosteroids (steroids).

Previously, studies had shown that vitamin D could influence the T cells from patients with severe asthma, and also affect TH17 cells. The researchers in the current study wanted to see if vitamin D affected IL-17A production by TH17 cells collected from asthma patients. They also wanted to see whether this effect was different in people who were resistant to steroid treatments.

What did the research involve?

The researchers took blood from 10 healthy adults and 28 patients with moderate to severe asthma and extracted white blood cells, including T cells. The patients had to have had diagnosed asthma for at least six months. Of the patients, 18 had asthma that did not respond as well to oral steroid treatment (steroid resistant asthma), and 10 had asthma that responded to steroids.

The researchers grew the white blood cells in the laboratory, either with or without vitamin D and the steroid dexamethasone, and looked at how much IL-17A was being produced. They assessed whether this varied between people with and without asthma, or in people with steroid resistant asthma.

What were the basic results?

White blood cells from people with asthma produced higher levels of IL-17A than those from non-asthmatic patients. Furthermore, white blood cells from people with steroid resistant asthma produced the highest levels of IL-17A.

Treating the white blood cells with vitamin D reduced the production of IL-17A. This reduction occurred in cells from people with steroid-resistant asthma and steroid-sensitive asthma, and was not affected by adding the steroid dexamethasone.

How did the researchers interpret the results?

The researchers concluded that their results support the hypothesis that vitamin D could improve disease control in people with asthma by reducing IL-17A levels, regardless of whether the person’s asthma is steroid-resistant.

Conclusion

The current laboratory study suggests that vitamin D can reduce white blood cell production of an inflammatory molecule implicated in asthma.

These results were obtained from cells in the laboratory, and further research will be needed to determine whether this effect will also be seen if people with asthma are given vitamin D.

While the results perhaps give a reason to investigate vitamin D further, not all treatments showing initially positive results in laboratory studies go on to have a positive effect on real-world clinical outcomes.

The good news is, as the Daily Mail reports, the results of this study are being followed up with a randomised controlled trial in participants with steroid resistant asthma.

Randomised controlled trials are the best way of testing if treatments are effective. This trial, and others, will tell us if vitamin D works as a treatment for asthma and if so, who it might be effective at treating. 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Sunshine vitamin 'may treat asthma'. BBC News, May 20 2013

Vitamin D 'helps beat symptoms of asthma’. Daily Mail, May 20 2013

Soaking up sun could be a cure for asthma. Daily Express, May 20 2013

Links To Science

Nanzer AM, Chambers ES, Ryanna K, et al. Enhanced production of IL-17A in patients with severe asthma is inhibited by 1α,25-dihydroxyvitamin D3 in a glucocorticoid-independent fashion. The Journal of Allergy and Clinical Immunology.

“Study shows girls with absent fathers more likely to develop depression," the Mail Online has revealed.

It reports on a large UK study that found that girls whose biological fathers were absent during the first five years of their childhood had an increased risk of symptoms of depression. No increase in risk was found for girls whose fathers were absent later in childhood, and no increase in risk was found for boys with absent fathers.

Researchers collected information regarding the physical absence of the biological father during childhood, as well as information on depression symptoms when the child was 14. They assessed whether there was any association between these factors.

During their analysis, the researchers took into account several factors that may influence the link, such as family characteristics. However, despite the researchers' efforts to take these variables into account, the reasons why a father may be absent from the family home can be incredibly complicated. This means we can’t be sure whether other factors have produced the association between absent fathers and depression in girls.

Where did the story come from?

The study was carried out by researchers from the University of Bristol and was funded by the UK Medical Research Council, the Wellcome Trust and the University of Bristol.

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

Media coverage of this research was broadly accurate, though neither ITV nor Mail Online outlined any of the study’s limitations.

What kind of research was this?

This was an analysis of data from a prospective cohort study called the Avon Longitudinal Study of Parents and Children. This is a study that has been ongoing since the 1990s that assesses influences on the health and development of children.

The researchers were interested in the potential link between the absence of the biological father in early childhood and the risk of mental health problems. They were specifically interested in symptoms of depression that were not necessarily severe enough to be considered clinical depression.

As a prospective cohort study, this research is less likely to be affected by certain types of bias, especially recall bias. It was important that the researchers collected data on the effect of family factors on the children’s mental health at the time, rather than at a later date, to help ensure the information was accurate. Prospective studies allow for this.

What did the research involve?

The researchers measured two main factors:

• absence of the biological father during childhood
• experience of depressive symptoms during the teenage years

To measure parental absence, the researchers used questionnaires, filled out by the children’s mothers regularly throughout the children’s lives. These questionnaires asked whether the ‘present live-in father-figure is the natural father of the child and, if not, how old the child was when the natural father stopped living with the family’. This information was used to divide the children into three groups:

• biological father present
• biological father not present during the first five years of life (during early childhood)
• biological father not present from age 5 to 10 (during middle childhood)

To assess the teenagers’ experiences of depressive symptoms, the researchers asked the study participants to complete a 13-item questionnaire when they were approximately 14 years old. This asked about the presence of certain symptoms over the previous two weeks. The questionnaire is reported to be a reliable and valid measure of depression in children. Children scoring 11 or higher on this questionnaire were considered to have high levels of depressive symptoms. This is not the same as being diagnosed with depression, however.

The researchers then analysed the data, comparing the risk of having high levels of depressive symptoms among children whose biological father left during early or middle childhood to the risk in children whose fathers were still living with them. These analyses were adjusted for several factors (confounders) that could be linked to both the absence of the father and depressive symptoms, including:

• socioeconomic status (including home or car ownership, major financial problems, family size and parents’ jobs)
• mother’s characteristics (including having a child before the age of 20, experiencing depression during pregnancy), and
• any parental conflict between the mother and her current partner

Separate analyses were carried out for boys and girls, to determine whether the child’s gender had any impact on the relationship between father’s absence and depressive risk.

What were the basic results?

There were approximately 14,500 children in the original cohort study, approximately 11,000 of whom had data available on the presence or absence of their biological father. Among these children, approximately 6,000 had available data regarding depressive symptoms at age 14.

Overall, girls reported higher levels of depressive symptoms than boys, regardless of whether their father lived with them or not – a trend that has also been found in previous studies.

Girls

The study included:

• 374 girls whose father left during early childhood, 87 (23.3%) of whom had high depressive symptoms at age 14
• 193 girls whose father left during middle childhood, 27 (14.0%) of whom had high depressive symptoms at age 14
• 2,295 girls whose father was present throughout childhood, 332 (14.5%) of whom had high depressive symptoms at age 14

Boys

The study included:

• 357 boys whose father left during early childhood, 30 (8.4%) of whom had high depressive symptoms at age 14
• 185 boys whose father left during middle childhood, 17 (9.2%) of whom had high depressive symptoms at age 14
• 2,227 boys whose father was present throughout childhood, 166 (7.4%) of whom had high depressive symptoms at age 14

When assessing the association between the absence of the father in early childhood and teenage depressive symptoms, researchers found that:

• Girls with absent fathers during early childhood had a 53% greater chance of experiencing high levels of depressive symptoms compared with girls with fathers present during this time (odds ratio  [OR] 1.53, 95% confidence interval [CI] 1.07 to 2.21).
• Boys with absent fathers were no more likely to report high levels of depressive symptoms at age 14 than boys whose fathers were present during early childhood (OR 1.08, 95% CI 0.65 to 1.79).

There was no significant association between middle childhood father absence and teenage depressive symptoms.

How did the researchers interpret the results?

The researchers concluded that “father absence in early childhood increases risk for adolescent depressive symptoms, particularly in girls”.

Conclusion

This large prospective cohort study suggests that there is a link between a father’s absence during the first few years of life and a girl’s risk of experiencing depressive symptoms.

This study has several strengths, including its large sample size, its long-term follow-up and prospective collection of data for the analyses. It also attempted to consider confounding variables during the analysis and was based in the UK, which helps to ensure that the results are applicable here.

There are some limitations, however, that should be taken into account, including the following.

• Only a third of the original cohort was analysed due to missing data on key factors. It is unclear to what extent those included differed from the entire population-based cohort. The researchers report that drop-outs were more likely among participants in lower socioeconomic groups. This factor is linked to both parental absence and depressive symptoms, so it could reduce the validity of the results and how much we can infer from them.
• The adjusted analyses further reduced the available sample size due to missing data on confounding factors, and the researchers suggest that this may have resulted in loss of statistical power to detect an effect.
• Several potential confounders were not included in the analysis, and could have influenced the results. The study authors report some of these potential confounders (quality of parent-child relationship, the father’s involvement in the child’s life regardless of whether he lived in the same house).
• The questionnaire used to assess depressive symptoms is not a measure of clinical depression. A high score on this questionnaire does not indicate that the child has or will develop a diagnosable depressive disorder.

Overall, this study suggests that early childhood family environments may play an important role in the mental health of children. At this stage we don’t know what accounts for the study’s results, and the researchers say that this should inspire future research into the possible biological and psychological mechanisms underpinning this relationship.

Depression is one of the most common mental health conditions, yet there is very little good quality evidence about how to prevent people developing depression. Research that gives us insight into the factors that increase children’s likelihood of developing depression would be invaluable.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

A quarter of young girls with absent fathers 'grow into depressed teenagers': Researchers say boys cope better with parental separation. Mail Online, May 15 2013

Study shows girls with absent fathers more likely to develop depression. ITV News, May 15 2013

Links To Science

Culpin I, Heron J, Araya R, et al. Father absence and depressive symptoms in adolescence: findings from a UK cohort. Psychological Medicine. Published online May 14 2013

"Depressed people are out of sync with the rest of the world because their body clocks are broken," reports the Mail Online website, while The Independent claims that depressed people live in a "different time zone".

The story comes from a study that looked at the activity of genes thought to be involved in regulating the body's internal clock – the innate sense that most people have of the changes over a 24-hour day to night cycle (circadian rhythms).

Researchers did a detailed study of gene expression, the effect that certain proteins contained inside individual genes have on genetic activities inside the body.

The study involved examining brain tissue taken from people who donated their brains to science after their deaths. Of the sample, 55 people had no history of psychiatric illness, while 34 patients had a history of severe depression (major depressive disorder, or MDD).

Researchers found that the gene activity associated with regulating circadian rhythms was much weaker, and often disrupted, in the brains of patients who had MDD.

These results possibly present, as philosophers put it, a "causality dilemma" (a chicken and egg problem) – does depression lead to a disrupted body clock, or does a disrupted body clock make people vulnerable to depression?

It is too early to say what help these findings may be in the understanding and treatment of MDD.

Where did the story come from?

The study was carried out by researchers from the University of Michigan, the University of California, Weill Cornell Medical College, Stanford University and the HudsonAlpha Institute for Biotechnology, and was supported by the Pritzker Neuropsychiatric Disorders Research Fund.

It was published in the peer-reviewed Proceedings of the National Academy of Sciences.

Both the Mail Online and The Independent covered the research uncritically. Given the specialised nature of this research, it's not surprising that both of the news stories appeared to be strongly based on an accompanying press release and were not a critical appraisal of the study itself.

What kind of research was this?

This was laboratory research using donated post-mortem brains. In it, researchers analysed in detail the gene expression of certain genes thought to be associated with circadian rhythm regulation at the time of death.

The authors point out that a common symptom of major depressive disorder is the disruption of circadian patterns, which can trigger symptoms of insomnia as well as excessive daytime sleepiness and fatigue (feeling tired all the time). However, to date there is no direct evidence of "circadian clock dysregulation" in the brains of patients with major depressive disorder.

What did the research involve?

Researchers used human brain tissue taken from a US donor programme with the consent of next of kin. They also took information from medical records, medical examiners and interviews with relatives to record the donors' previous physical health, medication use, psychiatric problems, substance use and details of death.

This was done in order to assess whether donors had a major depressive disorder, a severe form of depression that has a significant impact on day-to-day living.

They also assessed whether physiological stress at the time of death would have had an effect on gene expression, and took account of this potential confounding factor.

Researchers analysed the brain tissue of 55 donors with no history of psychiatric or neurological illness and 34 patients with major depressive disorder. Using specialist techniques called DNA microarray, they measured the expression of genes thought to be associated with regulating circadian rhythms in different areas of the brain.

They used the control group to build a detailed picture of circadian gene expression in brain tissue and compared the results with those found in the brains of people with MDD. They also used the rise and fall of the top 100 "cyclic" genes in 60 of the donors to predict the time of death in all the others, both cases and controls. 

What were the basic results?

In the brain tissue from donors without major depressive disorder, they found that the activity of "circadian" genes at certain times of the day and night was consistent with data derived from other diurnal (day-active) mammals. More than 100 genes showed "consistent cyclic patterns" over six brain regions.

However, in the brains of patients with MDD gene expression of cyclic patterns was far weaker and more disrupted, with the patients' day pattern of gene activity often resembling a night pattern.

They found that predictions of time of death were more accurate among controls than for those with MDD.

How did the researchers interpret the results?

The researchers say the results provide convincing evidence that there is a "rhythmic rise and fall" in the activity of hundreds of genes in the human brain associated with regulating the day/night cycle. There is also evidence that the activity of genes associated with circadian rhythms is abnormal in people with MDD.

The study identifies hundreds of genes in the human brain that are likely to be involved in the sleep/wake cycle. The researchers conclude that daily rhythms in these genes are "profoundly dysregulated" in MDD. They say the results pave the way for the identification of new biomarkers and treatments for mood disorders.

Conclusion

This study is of interest, but at the moment it has little bearing on our understanding and treatment of depression. It could lead to new insights and treatments in the future, but there is no guarantee that this will be the case.

Also, as the authors point out, gene activity can result from many factors, including disease and drug history. In particular, it should be pointed out that:

• the researchers relied on only 55 patients to build a "normal" picture of genetic expression associated with the sleep/wake cycle
• it is not clear whether those in the MDD group had all been formally diagnosed with MDD or how long they had had depression, and it is possible there were errors in the classification of patients either with or without MDD

In conclusion, it is too early to say whether this study's findings might help in the understanding and treatment of major depressive disorders.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

New forensic technique for estimating time of death by checking internal clock of the human brain. The Independent, May 13 2013

Out of sync with the world: Depressed people suffer with 'broken body clocks'. Mail Online, May 14 2013

Links To Science

Zi JZ, Bunney BG, Meng F, et al. Circadian patterns of gene expression in the human brain and disruption in major depressive disorder. PNAS. Published online May 13 2013

‘Research has found emotional eaters tend to eat more when happy’, reports the Mail Online website.

The news is based on a small study looking at whether experimentally altering mood has an effect on the amount of calories a person eats.

The researchers examined the effects on what they describe as ‘emotional eaters’ – people who reported using food as a coping mechanism for emotions.

A group of 86 students, who said they were either emotional or non-emotional eaters, were shown TV and movie clips to evoke either a positive, negative or neutral mood. The researchers then assessed how much the students ate when provided with bowls of crisps and chocolate, as well as assessing their change in mood.

Emotional eaters who were shown the positive mood-inducing scenes significantly increased their food intake compared to emotional eaters shown the neutral mood-inducing scenes. However, the negative mood-inducing scenes had no effect on food intake of emotional or non-emotional students.

The common assumption is that emotional eaters eat more when in a negative mood, but this study provides very limited evidence to suggest that this may not always be the case.

However, because this experiment was based in a laboratory and researchers did not measure how hungry people were, even this finding should be viewed with caution. As ever, more and better research is needed if people with eating disorders or weight problems are to be helped effectively.

Where did the story come from?

The study was carried out by researchers from Maastricht University in The Netherlands and was funded by the Netherlands Organisation for Scientific Research. It was published in the peer-reviewed journal, Appetite.

The story was picked up by the Mail Online website and it was covered appropriately, although the limitations of the study could have been described in more detail.

What kind of research was this?

This was a laboratory study looking at the effect of experimentally influencing mood changes in a group of students reported to be emotional or non-emotional eaters, and then looking at the effect on their food and calorie intake.

The researchers say emotional eaters are thought to increase their food intake in response to negative emotions, but little is known about the effect of positive emotions on their food intake. Meanwhile, non-emotional eaters are not believed to change their intake levels in response to emotions, and they might even restrict food intake in response.

The main limitation of this research is that a study of a small, select population sample under experimental conditions can only provide very limited indications about the possible influence emotions may have upon the eating patterns of different people in daily life.

For example, if you thought that researchers could be measuring how much you were eating it could make you, perhaps unconsciously, reluctant to eat as much as you normally would. Alternatively, being in this type of study could make you nervous, leading you to eat more than you normally would.

What did the research involve?

The researchers recruited 86 psychology students in their second year at Maastricht University in the Netherlands who received credit points for their participation. The students were predominantly female (75%) and had an average age of 21.6 years (range 19 to 43).

The students answered a series of questionnaires to assess their mental health and eating behaviours. Emotional eating was assessed using a questionnaire called the Dutch Eating Behaviour Questionnaire (DEBQ). Students were asked, ‘Do you have a desire to eat when you’re feeling lonely?’ and provided answers on a five-point Likert scale that ranged from ‘never’ to ‘very often’.

The researchers then carried out a series of experiments in a laboratory setting that aimed to change the student’s mood. Students were randomly allocated to view clips from television or films that aimed to evoke either a positive, negative or neutral mood:

• 28 students were shown two clips to evoke a positive mood. Firstly, they were shown a scene from the television series Mr Bean (which showed Mr Bean struggling to copy answers from his neighbour during an exam). The second clip was taken from the movie ‘When Harry Met Sally’ which showed the famous scene where Meg Ryan’s character simulates an orgasm in front of other diners in a restaurant.
• 28 students were shown one negative clip from the film ‘The Green Mile’, which showed an innocent man being executed.
• 30 students were shown part of a documentary about fishing to evoke a neutral mood.

The students were told to give in to the emotions the clips evoked, and were presented with bowls containing 191g of chocolate (white, milk and dark, equivalent to 1,000 kcal), 225g of salted crisps (1,229 kcal) and 225g of ketchup crisps (1,217 kcal). The bowls were weighed before and after the experiment to determine the amount of food eaten and calorie intake. 

The students were asked to assess their mood using a visual analogue scale (this is essentially a straight line – where the far left of the line represents poor mood and the far right represents very good mood) at five points during the experiment:

• before the experiment began
• immediately after watching the television or movie scenes
• 5 minutes after the experiment
• 10 minutes after the experiment
• 15 minutes after the experiment

The students were told when entering the laboratory that they were taking part in an experiment on the effect of movie clips on taste perception.

The researchers analysed their results using validated methods and adjusted the results for gender, body mass index (BMI), external eating and dietary restraint as assessed by the DEBQ, and negative mood as assessed by the Positive and Negative Affect Schedule (PANAS).

What were the basic results?

Overall, there was no significant difference between emotional eaters eating more than non-emotional eaters who were shown positive, negative or neutral clips.

When looking specifically at only the emotional eaters:

• those shown the positive mood-inducing scenes significantly increased their intake of food compared to those shown the neutral mood-inducing scenes
• there was no difference in food intake between students shown negative mood-inducing scenes and those shown neutral or positive mood-inducing scenes

How did the researchers interpret the results?

The researchers concluded that self-reported emotional eaters respond in a different way to emotions than non-emotional eaters. They say that emotional eaters ate more in a positive mood compared to a neutral mood, whereas non-emotional eaters ate about the same amount in both conditions.

In discussing the results, the researchers say the findings could be of value for the treatment of obesity.

Conclusion

Overall, this small study provides very limited evidence to suggest emotional eaters eat more when feeling in a positive mood. There are several limitations to this study, some of which are noted by the researchers. These include the facts that:

• the laboratory setting may not be an appropriate setting to test emotional eating with different mood feelings. It is possible that students felt uncomfortable in this setting and limited their food intake as they were being watched
• the students were told they were partaking in an experiment of taste perceptions, so may have been inclined to eat more than they normally would have because of what they were told the study was looking at
• no hunger measurements were taken during the study and how hungry each student was could have greatly affected the results
• there was no group included in the study that did not eat, so it is not possible to say from the findings that the changes in mood were due to food intake
• all of the participants were students, so findings may not be the same as if the same experiments were carried out in different groups who report being emotional eaters

To draw firmer conclusions about the effects of mood on emotional eating, larger studies of different groups are required that carry out experiments in more natural environments. 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Forget comfort eating - could happiness be the reason you're piling on the pounds? Mail Online, May 13 2013

Links To Science

Bongers P, Jansen A, Havvermans R, et al. Happy eating: The underestimated role of overeating in a positive mood. Appetite. Published online April 10 2013

'Redheads are at increased risk of skin cancer even if they don't spend time in the sun,' is the headline on the Mail Online website.

The story refers to a discussion piece in a journal that outlines theories about the results of some animal experiments. This research involved mice genetically engineered to have red fur and predisposed to develop melanoma.

Although exposure to ultraviolet (UV) light is known to be a major risk factor for melanomas, the researchers found that genetically engineered mice with red fur still had a high risk of developing melanomas even without UV exposure.

The article discusses potential explanations for why this could be the case, and these theories now need to be tested to see if they are correct.

It is not yet clear how well these animal studies represent what happens in people with red hair. It would be very difficult to test this directly, as keeping people completely away from sunlight would be impractical and potentially unethical.

UV light exposure is known to increase the risk of melanoma in redheads and non-redheads alike. It is important that people with red hair should continue to use sensible precautions to avoid excessive UV exposure and sunburn, despite this news.

Where did the story come from?

The article was written by researchers from the Cutaneous Biology Research Center at Massachusetts General Hospital in the US.

No sources of funding for the article were reported. It was published as an "Ideas and Speculations" article in the journal BioEssays. These pieces are described as "creative thinking and predictions on open questions and recent developments in biology".

The article has been peer-reviewed.

The news is based on an article by researchers that presents possible explanations for their previous finding that genetically engineered mice with red fur and a predisposition to melanoma develop this cancer even without UV exposure.

Some of the Mail Online reporting suggests that the findings of this research are more conclusive than is possible to say at this stage: "Scientists have discovered that the production of red hair pigment causes an increased risk of melanoma".

However, the BioEssays article was only presenting possible explanations for observations from animal experiments. It was not claiming to have definitive proof that these findings apply to humans.

What kind of article was this?

This was an article discussing the potential link between the red pigment in red hair and skin cancer.

People with red hair and fair skin are known to be at greater risk of getting melanoma, the least common but most serious form of skin cancer, which is responsible for around two thousand deaths a year in the UK.

In general, it is thought that redheads' pale skin makes them more susceptible to UV damage from the sun's rays.

However, the authors of the article say that a recent study from their lab suggests that the pigment that causes hair to turn red (pheomelanin) could itself be linked to the increased risk of cancer, even without UV exposure.

In their article, the authors discuss two possible ways in which the red pigment in red hair might increase the risk of cancer. These preliminary ideas – or hypotheses – are based on previous research and a general understanding of human and cancer biology.

A hypothesis is a possible explanation of why something that researchers have observed might happen. Researchers design experiments to test whether their hypothesis is correct. This process is fundamental to the scientific method.

What did the article say?

The researchers first describe how the red colour in red hair is made, and discuss the results of their recent study before going on to present their hypotheses.

Specific cells in the skin called melanocytes make two kinds of pigment – a brown pigment called eumelanin and a red-orange pigment called pheomelanin. A biochemical process within cells determines how much of each pigment is made.

This process involves a protein called MC1R, which influences the switch between the production of these pigments based on the strength of the signal it sends to the cell and whether the cell has enough of the amino acid cysteine.

In redheads, variations in the gene for the MC1R protein means that it sends weak signals. This means that the cells' stores of cysteine are usually enough for it to favour producing the red/orange pigment pheomelanin.

The researchers recently carried out a study where they introduced a genetic mutation commonly found in melanoma cells into the melanocytes of mice. When they also introduced a genetic mutation into these mice that inactivated the MC1R protein, the mice had red fur and developed melanoma, even without UV exposure. If they introduced another genetic mutation that stopped pigment being made altogether, the mice were albino but they did not develop melanoma.

This led the researchers to suspect that the red pigment pheomelanin could be itself increasing the risk of melanoma. Their research also found that the mice with red fur had more damage to their skin cell DNA caused by very reactive chemicals called free radicals. Free radicals can cause damage to cells at a molecular level.

The researchers do not yet know how the red pigment might be linked with the free radical DNA damage that can increase the risk of melanoma. However, they have presented two hypotheses:

The first hypothesis

The researchers' first hypothesis was that the red pigment itself might generate more free radicals, and that these cause DNA damage that could lead to melanoma. They say that the red pigment is already known to make free radicals when it is exposed to UVA light, but it may be able to do this without UVA light. These free radicals could potentially:

• damage DNA directly
• damage its building blocks, or
• use up the cell's stores of antioxidants, making it more vulnerable to damage by other free radicals

The researchers also discuss in detail the biochemical ways in which the red pigment might generate free radicals.

The second hypothesis

The second hypothesis was that the process of making the red pigment might use up the cell's stores of antioxidants, rather than the red pigment itself. This might make the cells more vulnerable to damage by other free radicals.

They say that the amino acid cysteine used in making the red pigment is also found in the most important antioxidant in the cell, glutathione. If cysteine is used to make the red pigment, this might reduce the cell's ability to make this antioxidant.

The researchers report that red-haired wild boars have been found to have less glutathione in their muscles. However, they acknowledge that it is not possible to say from this whether there is less glutathione due to free radicals from the red pigment itself or the making of the red pigment.

What were the researchers' conclusions?

The researchers presented two hypotheses that could explain how the red skin and hair pigment pheomelanin could increase the risk of the skin cancer melanoma.

They say that their two proposed methods could both be occurring, and that more research could help identify how redheads can reduce their risk of melanoma.

Conclusion

The researchers' article discusses potential ways in which the red pigment found in the cells of people with red hair might increase the risk of melanoma, the most serious form of skin cancer. It is not a standard report of a research study, but the authors put forward potential explanations for their previous research findings. These now need to be tested to see if they are correct.

The researchers' previous research found that mice genetically engineered to be predisposed to melanoma and red fur developed melanomas even without UV exposure. It is not clear to what extent these genetically engineered mice represent what happens in humans.

It would be very challenging to test this – keeping people completely away from UV light would not be feasible or ethical, as we need some sun exposure to make vitamin D, which is needed to make and maintain strong bones. For this reason, research in mice can be very helpful.

It is important that redheads do not take this news as a reason not to protect themselves from the effects of the sun. We already know that UV light exposure increases the risk of melanoma in people regardless of hair colour. People with red hair should continue to use sensible precautions to avoid excessive UV exposure and sunburn.

Read more about reducing your melanoma risk. 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Redheads are at increased risk of skin cancer even if they don't spend time in the sun. Mail Online, May 10 2013

Links To Science

Morgan AM, Lo J, Fisher DE. How does pheomelanin synthesis contribute to melanomagenesis? BioEssays. Published online May 7 2013

‘Children's exposure to traffic pollution could…lead to diabetes' BBC News explains, reporting on a German study.

The study included around 400 children aged 10. Researchers looked at measures of air pollution and proximity to the nearest road at the address each child had lived as a baby.

They also measured each child’s blood sugar and insulin levels.

The second measurement allowed them to calculate each child’s level of insulin resistance – to what extent the cells of the body fail to respond to the hormone insulin (which the body uses to convert blood sugar into energy).

Once insulin resistance reaches a certain level, the symptoms of type 2 diabetes can develop.

The researchers found an association between exposure to air pollution and increased levels of insulin resistance.

However, an association is not the same as proof of a direct causal effect. Living near a busy road would usually imply that a child lives in an urban environment. So there could be a range of environmental factors, other than air pollution, affecting levels of insulin resistance (as well as a wide-range of other possible individual genetic and health-related factors).

The study also does not tell us whether any insulin resistance measured in the child actually had any clinical significance and would lead to a child developing diabetes in later life.

Due to these limitations, further studies in other population samples would be useful.

Where did the story come from?

The study was carried out by researchers from German Center for Diabetes Research and other institutions in Germany, and was funded by German Federal Ministry of Education and Research, and The European Community’s Seventh Framework Programme.

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

The quality of the reporting on the study in the UK media is mixed. The BBC News headline gives an accurate representation of the current study as it includes the all-important word ‘may’. However, the Mail Online’s headline linking air pollution to a child’s risk of developing diabetes may be misleading.

This study has many limitations, not least, that increased levels of insulin resistance in childhood, while a risk factor, is not a guarantee that a child will grow up to develop type 2 diabetes.

Also, the association between childhood and diabetes may confuse some readers into thinking that the study was looking at type 1 diabetes – the form of the condition that normally begins in childhood and where the body’s own immune system destroys the insulin-producing cells, so the person is not able to produce any insulin at all.

What kind of research was this?

This was a cohort study looking at whether there was an association between air pollution and insulin resistance.

The researchers say that previous research has shown that traffic and air pollution may increase the risk of diseases affecting the lungs and cardiovascular system.

This is speculated to be due to exposure to pollution that may trigger oxidative stress (a disruption in the body’s ability to repair cellular damage). Pollution could also lead to low levels of inflammation in certain cells of the immune system and those lining the blood vessels.

Animal studies have also suggested that pollution may make cells of the body more resistant to the action of insulin – the hormone released from the pancreas that helps the body to make use of the glucose in the blood.

The researchers say that no study has yet looked at whether traffic-related air pollution can lead to insulin resistance in school-aged children. This German cohort study aimed to look at the relationship between particulate matter in the air and proximity to the nearest road at the child’s birth address, and the child’s insulin resistance when they reached the age of 10.

The limitations of such a study include it being difficult to conclude that the air pollution at the birth address has directly caused the child’s insulin resistance at age 10.

There may be many other genetic, environmental and health-related factors involved.

The study also does not tell us whether any insulin resistance measured in the child has any clinical significance, and whether it is related to later development of type 2 diabetes in adult life.

What did the research involve?

The researchers included sub-groups of 10-year-old children taking part in two separate birth cohorts in Munich, South Germany and Wesel, West Germany:

• The German Infant Study enrolled almost 6,000 healthy newborns and was a trial looking at the effect of a hypoallergenic infant formulae on a child’s risk of allergy (in addition to looking at other environmental and genetic influences).
• The Lifestyle-Related Factors study included just over 3,000 healthy newborns and was an observational study looking at the effect of lifestyle factors on the child’s immune system and risk of allergies.

The present study included 397 children randomly sampled from these two cohorts (though 82% came from the Munich cohort) who had blood samples taken for insulin and glucose measurement at age 10, and who had information available for air pollution exposure at the time they were born.

To measure pollution exposure at the birth address, the researchers used models to estimate levels of:

• nitrogen dioxide (N02)
• particulate matter of less than 2.5 micrometres in diameter
• particulate matter of less than 10 micrometres in diameter

Particulate matter is the term for a mixture of solid particles and liquid droplets found in the air.

Measurements were taken at selected monitoring sites on three occasions over 14 consecutive days, and in different seasons.

When conducting their analyses, factors taken into account at each monitoring site were location, surrounding land use, population density and traffic patterns.

Other factors taken into account that could have an influence on the results (confounders) related to the individual child included:

• parental education (used as an indicator of socioeconomic status)
• exposure to second-hand smoke
• height and weight at age 10
• whether they had started to go through puberty

What were the basic results?

There were no differences between children in the two cohorts, except that those from Wesel were more likely to have been exposed to second-hand smoke and to be of lower socioeconomic status. Pollutant levels were also higher in Wesel than Munich.

After adjustment for all potential study-centre and child-related confounding factors, each two-point standard deviation increase in nitrogen dioxide levels was associated with a 15.8% increase in insulin resistance (95% confidence interval (CI) 3.8 to 29.1).

Each two-point standard deviation increase in particulate matter of less than 10 micrometres in diameter, was associated with a 17.5% increase in insulin resistance (95% CI 1.9 to 35.6). There was no significant association with particulate matter of less than 2.5 micrometres in diameter.

Distance to the nearest road, as would be expected, was significantly associated with pollutant levels (shorter distance equalled higher levels of nitrogen dioxide and particulate matter). Shorter distance to the road was also associated with increased insulin resistance (each 500 metre decrease in distance to road increased insulin resistance by 6.7%, 95% CI 0.3 to 13.5).

The researchers found that the link between pollution levels and insulin resistance was stronger in children who had not moved from their birth address by age 10.

How did the researchers interpret the results?

The researchers conclude that traffic-related air pollution may increase the risk of insulin resistance in children. They say that the associations observed may have important public health implications despite the small effect seen.

Conclusion

This German study looked at the relationship between air pollution and proximity to the nearest road at the child’s birth address, and the child’s insulin resistance when they were aged 10. Though links were found between increasing levels of nitrogen dioxide and levels of particles less than 10 micrometres in diameter and increasing insulin levels at age 10, there are important limitations to bear in mind:

• Though the researchers have attempted to adjust for many potential confounders, it is difficult to conclude that the air pollution at the birth address has directly caused the child’s insulin resistance at age 10, when there may be many other genetic, environmental and health-related factors involved.
• The confidence intervals around the increase in insulin resistance with each incremental increase in pollutant levels are very wide. For example, each increase in particles of less than 10 micrometres was associated with a 17.5% increase in insulin resistance, but the actual increase could lie anywhere between 1.9% and 35.6%. This means we can have less confidence in the reliability of these estimates.
• The study does not tell us whether any insulin resistance measured in the child has any clinical significance, and whether it will be related to higher risk of developing type 2 diabetes in adult life.
• Also, as mentioned above, the news headlines should not be wrongly interpreted to mean that a child has increased risk of developing type 1 diabetes – the type that readers may associate with start in childhood.  
• Lastly, the results are based on only a relatively small sample of children from two regions in Germany. Studies of much larger samples from different countries would give more weight to any observations.

Overall, this study cannot prove that air pollution increases a child’s risk of developing diabetes, only that there may be an association with insulin resistance.

As it is unlikely that we are going to live in a world free from air pollution anytime soon, the most effective way of reducing your child’s diabetes risk is to encourage them to take plenty of exercise and eat a healthy diet. These types of good habits in childhood often carry on into adulthood meaning that your child is more likely to maintain a healthy weight – a proven method of reducing type 2 diabetes risk.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Diabetes: dirty air 'may raise' insulin resistance risk. BBC News, May 10 2013

Why living near a busy road could be dangerous for your child's health: Traffic pollution linked to diabetes risk in children. Mail Online, May 10 2013

Air pollution could raise diabetes risk. The Daily Telegraph, May 10 2013

Links To Science

Thiering E, Cyrys J, Kratzsch J, et al.  Long-term exposure to traffic-related air pollution and insulin resistance in children: results from the GINIplus and LISAplus birth cohorts (PDF, 278KB). Published online May 9 2013

"Middle class professionals… are the country’s biggest problem drinkers," is the stark and somewhat misleading claim in The Daily Telegraph, with similar claims appearing across the UK media.

The story is based on a study looking at just 49 ‘white collar’ people’s attitudes towards alcohol consumption. The study involved interviewing five small groups in a ‘focus group’ setting.

Researchers found that among these small groups:

• problem drinking was something that was seen to happen to other people – such as teenagers in city centres or binge drinkers in pubs
• if regular alcohol consumption did not significantly disrupt day-to-day functioning (such as in work or parenting skills) or lower social standards, then it was acceptable and harm-free
• regular ‘controlled’ drinking at home (for example as a way to relax), was also acceptable and harm-free 

It is important to note the study was very small and these findings may not be applicable to other countries or cultures. However, the attitudes reported suggest that key messages of some public health campaigns about reducing harm from alcohol are going unheard or being ignored.

It is not just binge drinking that can damage your body; regularly drinking above the recommended limits – whatever the social context – can also be harmful.

Where did the story come from?

The study was carried out by researchers from Newcastle University and the University of Sunderland, UK and was funded by the Public Health NHS Directorate Stockton-on-Tees.

It was published in the peer-reviewed journal, BMC Public Health and made freely available to read on an open-access basis.

The story was picked up widely in the media. While the findings of the study were reported accurately, the tone of some of the reporting was slightly confusing.

It appears that some of the media fail to understand the nature and implication of this method of qualitative research. Such studies can provide useful insights into people’s attitudes and behaviours; however, they cannot provide hard statistical evidence. So headlines such as the Daily Express’s “Middle class ‘drink more than teens’” are misleading, as are sweeping statements like the Telegraph’s “Middle class professionals who drink at home are the country’s biggest problem drinkers”.

What kind of research was this?

This was a qualitative study looking at the drinking habits of a small number of adult ‘white collar workers’ in the UK. The study explored their views on alcohol use, how public health messages about alcohol are perceived, and the role alcohol plays in the workers' personal and professional lives.

The researchers say that little is known about white collar workers’ views on drinking alcohol.

Qualitative research uses individual in-depth interviews, focus groups or questionnaires to collect, analyse and interpret data on people’s behaviours and the reasons behind them. Typically, the number of participants is relatively small, but the transcripts from interviews and focus groups provide a large amount of data. Such studies report on meanings, concepts, definitions, metaphors, characteristics, symbols, and descriptions. As such, their conclusions can be more subjective than quantitative research, as questions are often exploratory and open-ended.

What did the research involve?

The researchers carried out interviews with 49 volunteers (17 male, 32 female) from five workplaces in the UK. The participants were aged between 21 and 55 years and were all working full time (at least 35 hours per week). To be included, participants had to be working in managerial, supervisory, clerical or other professional roles, referred to by the researchers as ‘white collar workers’.

Group interviews (focus groups) were carried out by the researchers at each of the five workplaces during lunch breaks. The five focus groups were made up of workers from:

• local government offices (focus groups one and two)
• a private sector chemical storage company (focus group three)
• a prison (focus group four)
• a tax office (focus group five)

The group interviews lasted between 45 and 75 minutes and were led by two researchers. The researchers used open-ended questions loosely based around four main themes related to drinking alcohol:

• lifestyle behaviours
• drinking at home
• variations in drinking during the week
• the effect of drinking on work

The researchers say areas of agreement and disagreement were explored with the participants, and that questions were continually adapted depending on the flow of conversation. The participants were informed that the purpose of the research was not to find out the quantity or frequency of alcohol consumption of the volunteers. The volunteers were given a £5 voucher and lunch for their time.

The researchers then used a particular technique called ‘constant comparison’ to analyse their results and grouped findings into themes relating to views of alcohol.

What were the basic results?

After analysing the focus group findings, the researchers reported three main themes.

Unacceptable or problem drinking

Unacceptable or problem drinking was perceived by the volunteers as being associated with long-term, heavy or binge drinking of ‘others’. The researchers reported that the participants highlighted ‘others’ as including young people, people with complex needs, and other stereotypes. The perception of excessive drinking was associated with looks and behaviour, rather than how much they have drunk. Personal drinking was viewed as a controlled choice rather than something they ‘need to do’.

Drinking at home

Drinking at home was considered normal, convenient and a socially acceptable form of relaxation from the responsibilities of work or parenting. Volunteers reported less drinking at ‘leisure premises’ such as a bar or pub, and driving was identified as the greatest factor influencing drinking behaviours. Drinking alcohol was considered part of everyday life and not something that interferes with other parts of life or causes harm.

Effect of drinking on functioning

Ability to function at work and act responsibly were key indicators of whether drinking was within acceptable limits. So, if a person was able to maintain employment in skilled jobs, they were therefore perceived to be drinking in a way that was not considered harmful. Despite awareness of guidelines for drinking, little notice was taken by participants and there was confusion about what a ‘unit’ was, the researchers report. Public health messages were also considered to have little or no personal relevance.

The researchers say that discussions indicated that the volunteers' reported alcohol use exceeded recommended guidelines for both the amount and how often drinking occurred. Interestingly, when the ill effects of alcohol were discussed, they were reported as only in relation to coping with a hangover and the loss of valuable time while feeling unwell. More subtle, insidious adverse effects such as gradual loss of liver function did not appear to occur to the volunteers.

Finally, lunchtime drinking at work was considered a 'thing of the past' and very much taboo.

How did the researchers interpret the results?

The researchers say that this study helps reveal the meanings attached to alcohol use by white collar workers and identifies resistance to public health messages. They say, "these findings suggest that current public health interventions have not been effective in engaging this group who are likely to drink at unhealthy levels but be highly resistant to reducing their alcohol consumption – especially as they do not consider their use to be problematic unless it impairs their capacity to fulfil responsibilities or function at work".

They conclude by saying, "future public health messages around alcohol should be less focused upon the crime and personal safety implications of irresponsible drinking and be more sensitive to the lifestyles and long-term health of the populations they target".

They add that further research is needed to identify which factors (other than driving) would engage white collar workers to change their views and drinking behaviours.

Conclusion

Overall, this research provides some early findings of so-called ‘white collar’ workers' views of drinking behaviours in the UK.

Although the study was very small, with only 49 volunteers' views analysed, it is useful in determining emerging themes, and the researchers do state that there was relative consistency across the five groups. The researchers also note that ‘strong personalities’ within the group may have influenced how the other participants responded.

Research among larger groups of white collar workers is needed to draw firmer conclusions about the drinking culture in the UK. It is worth noting that these findings may not be applicable to other countries or cultures. Ethnicity, cultural identity and religious beliefs of the participants were not reported, which may have influenced how participants responded to the questions.

One important final message to stress – and one that seems to have not been grasped by the volunteers in the study – is that it is not where you drink, why you drink, or who you drink with that matters. It is how much you drink.

Regularly exceeding the recommended daily amounts for alcohol can harm your health, regardless of whether it is with three litres of strong white cider on a park bench, or a bottle of Californian merlot in front of a DVD box set. 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Middle class wine drinkers 'think they know better than health experts'. The Daily Telegraph, May 8 2013

Middle classes are 'ignoring the dangers of using casual drinking to combat stress'. Daily Mail, May 9 2013

Alcohol abuse: Concern over middle-aged middle classes using booze to relieve stress. Daily Mirror, May 8 2013

Middle class ‘drink more than teens’. Daily Express, May 9 2013

Links To Science

Ling J, Smith KE, Wilson GB, et al. The ‘other’ in patterns of drinking: A qualitative study of attitudes towards alcohol use among professional, managerial and clerical workers. BMC Public Health. Published online October 23 2012