Medical News

Could a 30-minute 'power nap' make up for a bad night's sleep?

Medical News - Thu, 02/12/2015 - 18:05

"Indulging in a power nap can repair the damage caused by a lack of sleep," the Daily Mail reports. But the study that prompted the headline is very small – involving just 11 healthy young men.

It has long been known that a lack of sleep at night can have a negative impact on the immune system and stress levels.

Researchers wanted to see if two short naps during the day, each lasting 30 minutes, could repair some of the damage caused by a poor night's sleep of just two hours.

They measured biological indicators (biomarkers) such as stress hormones, and then compared them to controls in an attempt to gauge the effects of the short nap.

One of the three stress hormones measured was increased the day after the men were sleep-deprived, but not if they were allowed to take naps. The level of a protein involved in immune responses (Interleukin-6, or IL-6) was reduced after little sleep, but not if the men had naps.

The implications of these findings are unclear. Measuring one immune biomarker, such as IL-6, does not provide any insight into whether the immune system has "recovered", as it is involved in both activating and dampening the immune system.

Nor does this study show that naps relieve stress. The level of one stress-related hormone, noradrenaline, was increased after sleep deprivation, but this may have been affected by other factors.

So the results of this small study do not show whether naps improve the immune system or the body's response to stress.

If you are struggling with daytime sleepiness, you may need to improve the quality and duration of your sleep during the night.

 

Where did the story come from?

The study was carried out by researchers from the University of Paris Descartes and the Institut de recherche biomédicale des armées.

It was funded by the insurance company RÉUNICA and the Societé Française de Recherche et Médecine du Sommeil.

The study was published in the peer-reviewed Journal of Clinical Endocrinology and Metabolism on an open access basis, so it is free to read online.

The Daily Express informed readers that, "Even if you only get two hours of proper sleep, a half-hour snooze will relieve stress and bolster the immune system by restoring hormones and proteins."

But we can't say conclusively that a nap can do either of these things based on the results of this small, short-term study.

Only one of the three stress-related hormones tested was raised if the men did not take a nap. There are other reasons this could occur, and it was not clear if the study ruled these out.

The Express also failed to point out that this study was conducted on just 11 healthy young men over three days.

The Mail Online reported the study more accurately, but did not point out any of the limitations of this kind of research.

 

What kind of research was this?

This was a randomised cross-over study that aimed to look at whether naps could counteract the effect of restricted sleep on specific markers of stress and immune system response.

A group of healthy male volunteers were studied after their sleep was restricted to two hours. In one session they were allowed naps afterwards, but naps were not allowed in the other session.

The researchers measured various stress hormone levels and one immune system protein called IL-6, looking at whether the restricted sleep and naps had any effect on these levels.

The study design allows comparison of the same group of people under different conditions. This type of study needs to be careful to make sure the effects of one set of conditions do not carry over on to the other period, which is why the researchers need to allow a period of "washout" time between the two sessions.

A study of this nature does not have a separate control group – participants are compared to themselves under different conditions; in a sense they serve as their own controls. This can make it easier to detect differences that result from the conditions, as the groups being compared are essentially the same.

 

What did the research involve?

Eleven young men were recruited to the study through advertisements in the hospital and university campus. They were aged between 25 and 32, had a body mass index (BMI) within the healthy range of 19 to 25, and were non-smokers.

All were considered to be healthy and none had depression, anxiety or emotional distress according to a commonly used measurement tool (the Hospital Anxiety and Depression Scale). The men normally slept seven to nine hours a night on average and did not report any sleeping problems.

The men had two admissions to the sleep laboratory in random order. In the "sleep-restricted" admission, the volunteers slept from midnight to 8am on the first night, were restricted to sleeping from 2am to 4am on the second night, and were then allowed to sleep from 8pm until they woke up on the final night.

They were not allowed to sleep at any other time and were kept awake by staff with films and games.

The same night-time sleep protocol was used for the "sleep restriction plus nap" admission, but the volunteers were allowed to have a 30-minute nap at 9.30am after the restricted night's sleep, and again at 3.30pm.

The men were asked to try to be asleep from midnight to 8am for a week before the admissions, and to record their sleep in a daily diary.

During each three-day stay, their activity levels were monitored and they were provided with meals up to a maximum of 2,500 calories a day. They were not allowed to have any:

  • medication
  • alcohol
  • coffee
  • tea
  • cola
  • chocolate

A monitor that records brain electrical activity (an EEG) was attached to each participant for the duration of each admission to record whether they were awake or asleep.

Urine samples were taken every three hours between 10am and 7pm to test for three hormones that help regulate the body's response to stress: noradrenaline, adrenaline and dopamine.

Salivary samples were taken every two hours while the men were awake, and tested for Interleukin-6 (IL-6) levels. IL-6 is a protein that is part of the immune system. It plays a complex role – it stimulates the body's immune system to react, but also reduces inflammation, depending on the circumstances.

 

What were the basic results?

After the sleep-restricted night, the level of noradrenaline in the men's urine was 2.5 times higher in the afternoon than at the same time of day after a night of eight hours' sleep. There was no increase in noradrenaline if they had been allowed the naps.

There was no significant difference between the sleep-restricted and non-restricted days, or with and without naps, in terms of the levels of adrenaline, dopamine or testosterone in the men's urine samples.

Levels of IL-6 were significantly lower at 10am and 7pm after the restricted sleep night compared with after eight hours' sleep. The levels were not lower if the men had napped.

After the recovery night's sleep, adrenaline and dopamine levels were increased in the afternoon in the "sleep-restricted" session, but not in the "sleep-restricted plus nap" session. IL-6 salivary levels were the same as after the eight hours' sleep in both sessions.

 

How did the researchers interpret the results?

The researchers concluded that: "Napping as a countermeasure to sleep restriction could, in addition to benefits on alertness, improve neuroendocrine stress and immune recovery with a potential prophylactic long-term effect on cardiovascular health."

They acknowledge that interpretation of the varying levels of the immune system marker IL-6 is complex as it can be a sign of inflammation, but it may also be involved in preventing inflammation.

 

Conclusion

This was a small study that is interesting on an intellectual level, but has little real-world practical applications or implications.

This study found the levels of one stress-related hormone (noradrenaline) increased after restricted sleep, but not if the men had naps. However, this does not prove that naps "relieve stress", as the media has indicated.

Noradrenaline is just one of several hormones that fluctuate during the day in response to a variety of bodily functions. Although it is known as one of the stress hormones, this refers to stress on the body, which can include exercise and excitement.

In this study, we do not know what the men were doing when these higher levels were recorded and whether this differed from the time when the lower levels were recorded. They could have been exercising, watching films, or playing games, therefore affecting their results.

Although activity was reported to be "controlled" by monitoring, it was not clear whether this meant that activity was restricted in all periods, and the results were not adjusted to take activity into account.

Also, the other two stress-related hormones measured were not affected by sleep restriction or naps.

This study has not proven that naps improve the immune system, which has been reported in the media. IL-6 has a complex role in both stimulating and dampening the immune response in different circumstances.

Therefore, a one-off reading of IL-6 like this, without any other markers of the immune system, is difficult to interpret accurately.

What may have been a more relevant outcome is what effect a nap might have on concentration and the ability to think clearly and reason after a night of poor sleep.

This could have been achieved through psychometric testing, although the numbers would still have been small, limiting the power of the study to detect an effect.

Further limitations include the fact the study conditions did not mimic normal life – the participants had to stay in the sleep laboratory for three days at a time and were not allowed to drink tea, coffee or alcohol. They were also only sleep-deprived on one night. This means the results may not reflect what would happen in normal circumstances.

It is not clear what the men's normal daily schedules were like and whether having a break for three days from hectic life would have been less stressful, or conversely if being cooped up in a laboratory would have felt claustrophobic.

In conclusion, this study of just 11 men does not prove that naps successfully counteract the negative effects of losing a night's sleep on the immune system or symptoms of stress.

Many adults fall into bad habits when it comes to sleep, such as drinking alcohol before bedtime or overstimulating the mind late in the evening. You may need to improve your sleep hygiene – adopting better habits that will help promote better sleep. Read more about sleep hygiene

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

Links To The Headlines

Power napping really IS good for you: A 30-minute snooze can repair the damage caused by a lack of sleep. Daily Mail, February 10 2015

Power naps can counter lost sleep, new study reveals. Daily Express, February 11 2015

Links To Science

Faraut B, Nakib S, Drogou C, et al. Napping Reverses the Salivary Interleukin-6 and Urinary Norepinephrine Changes Induced by Sleep Restriction. The Journal of Clinical Endocrinology & Metabolism. Published online February 10 2015

Categories: Medical News

Long-term smoking 'may cause' brain shrinkage

Medical News - Thu, 02/12/2015 - 14:00

“Smokers have thinner brain cortex and could have impaired thinking,” The Independent reports. MRI scans of long-term smokers show signs that the cerebral cortex – the grey matter of the brain – which plays a key role in thinking and memory, was thinner than expected.

The study looked at brain scans of more than 500 people aged 73 to see if there were any noticeable differences between smokers, ex-smokers and people who never smoked.

Smokers had the thinnest cortex on the MRI scans. However, despite some media reports, none of the participants had dementia or memory loss, and the researchers did not reveal any differences between the groups in terms of cognitive ability. The smoking group was limited in size to 36 participants (possibly because smokers are less likely to live until they are 73).

Thinning was also seen in ex-smokers compared to never smokers (these groups both had more than 200 participants). However as the study only took one measurement at one point in time, it cannot tell us either if this thinning in ex-smokers is due to smoking or if it partially recovers once a person quits smoking.

The authors acknowledge that this study doesn’t prove that smoking caused the cortex to thin as the measurement was only taken once. However, we already know that smoking is unhealthy and it is always a good idea to quit however long you have been smoking.

 

Where did the story come from?

The study was carried out by researchers from Edinburgh University, McGill University in Montreal, and Harvard Medical Schools in Massachusetts. It was funded by a Research Ageing Program grant, the Age UK-funded Disconnected Mind project, the UK Medical Research Council, the Scottish Funding Council, the UK Biotechnology and the Biological Sciences Research Council.

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

The media has implied that there are direct links between having a thinner cortex and experiencing memory and cognitive problems, but this was not a result presented by this research.

 

What kind of research was this?

This was a cross sectional study comparing the thickness of the cortex of the brain between people who currently smoked, ex-smokers and non-smokers. The people are part of an ongoing, longstanding cohort study of people born in 1936.

This type of study can show associations, but it is not able to prove that one factor (smoking in this case) causes the other (thinning cortex). Ideally the study would assess people’s brain and smoking habits over time to see whether the changes come after a person takes up smoking and not before.

However, such a study is likely to be expensive to do and take a long time, so often researchers start with a cross sectional study. (And for this cohort, such a study would have been impossible, as MRI scanners weren’t invented until the 1970s).

randomised controlled trial would not be ethical for this type of research, so an observational study like this is appropriate.

 

What did the research involve?

The researchers compared the thickness of the cortex of people aged 73 who were current smokers, ex-smokers and non-smokers. The cortex thins naturally as we age, but researchers wanted to see if this process was accelerated in smokers.

A group of 504 people from a longstanding study called the Lothian Birth Cohort 1936 (LBC 1936) was recruited into the study. This original study had started collecting data on people born in the Lothian region of Scotland in 1936 including mental ability and intelligence, which was tested when they were 11 years old.

The 504 participants (260 women and 244 men) were invited to have a brain MRI scan to measure the thickness of their cerebral cortex – the grey matter of the brain. None of them had any evidence of dementia, according to self-report and scoring more than 24 out of 30 on Mini Mental State Examination (MMSE) – a test commonly used to look for cognitive problems.

The participants were assessed on a range of factors, including:

  • smoking status, including age starting, age stopping (if they stopped) and average number smoked per day
  • recent alcohol consumption
  • socioeconomic status
  • cognitive testing and other psychological assessments
  • history of any medical conditions
  • physical examination, including blood pressure and lung function
  • blood tests

The researchers then analysed the results to look for any association between the thickness of the cortex and smoking history. They adjusted their results for gender and exact age.

 

What were the basic results?

There were 36 current smokers, 223 ex-smokers and 245 non-smokers. There was no significant difference between the groups in terms of gender, intelligence or socioeconomic status aged 11. However, those who never smoked were less likely to have a history of cardiovascular disease, had better lung function and drank fewer units of alcohol per week.

Current smokers had a significantly:

  • thinner cortex over most of the brain than people who had never smoked
  • thinner cortex than ex-smokers, but the difference was less than compared to never smokers

Ex-smokers had a significantly thinner cortex than non-smokers, but the difference was not as large as for current smokers compared to non-smokers. Those ex-smokers who had stopped smoking a longer time ago tended to have less difference in cortex thickness than those who stopped more recently.

 

How did the researchers interpret the results?

The researchers concluded that “smokers need to be informed that cigarettes are associated with accelerated cortical thinning, a biomarker of cognitive aging”. They also say that “the potential to at least partially recover from smoking-related thinning might serve as a strong motivational argument to encourage smoking cessation”.

 

Conclusion

This study has shown an association between smoking and a thinner cortex, though it cannot prove that smoking caused the cortex to thin. The study was cross sectional, so cannot say which came first – the smoking or the cortex differences. Also, confounding factors other than smoking may be contributing.

Strengths of the study include:

  • Having access to measurements of cognitive ability when the participants were 11 years old, before most of them would have started smoking, as a potential indicator of cortex thickness.
  • The radiologists were blinded to which MRIs came from each group, reducing the risk of them introducing bias based on interpreting scans differently for people they knew to be smokers.
  • All participants were the same age when they had the MRI scan, so age did not need to be adjusted for in the results. This is important because the cortical thickness naturally decreases with age.
  • The fact that those who gave up smoking seemed to have less difference to the non-smokers than those who continued to smoke fits with the idea that the two factors might be related to each other rather than arising just by chance.

Limitations acknowledged by the authors include:

  • The number of current smokers was small, only 36.
  • It is possible there were differences in cortex thickness before a person started smoking. They say that structural changes in the frontal part of the brain related to impulse control may have made it more likely for people to start smoking in the first place.

All this considered, it has long been known that smoking is bad for you.

Aside from the risk of cancerheart disease and stroke, smoking may also increase the risk of dementia type conditions, such as vascular dementia and Alzheimer’s disease.

So, if smoking by itself does not directly cause cortical thinning, it is a good idea to quit if you smoke, whatever your age. Quitting, however long you have smoked, should lead to an increase in life expectancy and quality of life. Help and advice on quitting can be found here.

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

Links To The Headlines

Smokers have thinner brain cortex and could have impaired thinking. The Independent, February 11 2015

Smoking shrinks your brain and may damage your memory, study finds. Metro, February 11 2015

Smoking shrinks critical part of the brain – leading to memory loss. Daily Mirror, February 10 2015

Links To Science

Karama S, Ducharme S, Corely J, et al. Cigarette smoking and thinning of the brain’s cortex. Molecular Psychiatry. Published online February 10 2015

Categories: Medical News

Obesity damage to eggs may be reversible

Medical News - Wed, 02/11/2015 - 15:00

“Damaging effect of obesity on a woman’s eggs can now be reversed,” is the potentially misleading headline from the Mail Online today.

The over-egged headline refers to a mouse study showing that signs of lower fertility due to obesity could be reversed using experimental drugs. This was not tested in humans, however.

Maternal obesity is known to lower the chance of successful conception, as well as increasing the risk of miscarriage.

The study compared the fertility of mice before and after they became obese due to a genetic condition that makes them overeat. When given IVF drugs, their fertility at the start was similar to mice of a healthy weight, but as the mice became obese, their fertility reduced. They became less able to develop eggs, and any eggs produced were less likely to be fertilised. The researchers also found that once obese, there was reduced activity of mitochondria (the part of the cell that converts food to energy) in the eggs.

All of these effects were reversed if the obese mice were given either a drug called Salubrinal or BGP-15. BGP-15 is an experimental, unlicensed drug that is being trialled for use in people with type 2 diabetes.

The study does not prove that the reduced mitochondrial activity causes obesity in the offspring, but it is a plausible explanation that will require further research.

The immediate impact of this research to women is minimal, as this is very early stage research. However, the study does reinforce the message that women should maintain a healthy weight before pregnancy.

Where did the story come from?

The study was carried out by researchers from the University of Adelaide, Monash University, and the Baker IDI Heart and Diabetes Institute in Melbourne. It was funded by the National Health and Medical Research Council of Australia, the Operational Infrastructure Support Program of the Government of Victoria, and the Women’s and Children’s Hospital Foundation. 

The study was published in the peer-reviewed journal Development.

In general, the media headlines implied that these drugs have been tested on women, when this is not the case. For example, the Mail Online’s article did not mention that the research was carried out on mice, and had not actually been tested for this use in humans. This means we don’t know if the drug would have the same effect in people as it does in mice.

The Independent’s coverage was more balanced. It acknowledged the mouse origins of the research, but could have done more to spell out why this was a limitation. The article usefully included a quote from Professor Adam Balen, “a leading expert in reproductive medicine at the University of Leeds, and chair of the British Fertility Society” who said: “while any drug treatment was a long way off, the findings were ‘very interesting’”. He added that the important message to take away from this study is that: “women [need] to be nutritionally healthy before they get pregnant”.

 

What kind of research was this?

This was an animal study looking at the effect of obesity on fertility in mice.

Previous animal studies have indicated that obesity affects the metabolism and growth of offspring, and rat studies have shown that obesity alters the egg before fertilisation. The authors also highlight that overweight women are more likely to require assisted reproduction, and the success rates are lower.

The researchers had already done studies using obese female mice to investigate what biological changes obesity might be causing. They found that mice fed high-fat diets had eggs with signs of intracellular stress. This included higher fat content, increased reactive oxygen species and altered mitochondria. Mitochondria are the parts of the cell that convert food to energy and feature heavily in the debate on whether three-parent fertility technology can or should be used in the UK.

In this study, they wanted to see whether this alteration in mitochondria was associated with reduced fertility, whether it is passed on to the offspring, and whether it affected the weight of the growing foetus. They also wanted to find out if the use of two experimental drugs that reduce intracellular stress could reverse these changes.

 

What did the research involve?

The researchers compared the fertility of obese mice with healthy-weight mice in a variety of experiments.

Mice with a genetic disorder similar to Alstrom syndrome in humans were used, and compared to mice of a healthy weight. This syndrome causes overeating that leads to severe obesity, increased insulin and diabetes, despite eating a low-fat diet.

The mice were given IVF drugs to stimulate their eggs to become ready for fertilisation. The following aspects were measured, comparing mice before and after they had become obese with healthy-weight mice:

  • the number of eggs stimulated by IVF drugs
  • the level of mitochondria activity in the eggs
  • the number of eggs able to be fertilised
  • weight of the growing foetus when implanted into mice of a healthy weight

The researchers then repeated the experiments after giving obese mice an experimental drug once per day for four days, to see if this could reverse the effects of obesity on the eggs and their development. The drug was either:

  • Salubrinal – an experimental drug that reduces cell stress responses
  • BGP-15 – an experimental drug that has been shown to protect against obesity-induced insulin resistance in mice. It is currently undergoing human trials for type 2 diabetes

 

What were the basic results?

Before the mice were obese, the same number of eggs developed after stimulation with IVF drugs as in healthy-weight mice. After they were obese, a reduced number of eggs were produced. This indicated that the fertility of the mice was affected by obesity, rather than the syndrome.

When obese mice were given either Salubrinal or BGP-15 for four days before the IVF drugs, the number of eggs developed more than doubled and was almost the same as for the healthy-weight mice. The number of eggs also increased when these drugs were given to healthy-weight mice.

The eggs of obese mice had indications of higher levels of intracellular stress and decreased mitochondrial activity. Obese mice given either drug did not have reduced mitochondrial activity.

Fewer fertilised eggs from obese mice survived compared to healthy-weight mice by four hours after fertilisation, or two days later. The same numbers survived if they were given IVF before they had become obese, or if obese mice had been given either Salubrinal or BGP-15.

When they implanted the fertilised eggs into normal-weight mice, compared to foetuses from healthy-weight mice:

  • foetuses from obese mice were significantly heavier
  • foetuses from obese mice given Salubrinal or BGP-15 were the same weight

 

How did the researchers interpret the results?

The researchers concluded that eggs from obese mice give rise to foetuses that are heavier and have reduced mitochondrial activity. They say that obesity causes intracellular stress in the eggs. They found that if either of two experimental drugs were given before fertilisation, this could reverse the following effects of obesity:

  • reduced response to IVF drugs
  • reduced mitochondrial activity
  • reduced fertilisation rate
  • developing foetus of increased weight

 

Conclusion

This mouse study has shown that obesity reduces fertility, but the exact mechanism remains unclear. It found that eggs from obese mice had reduced mitochondrial activity compared to when the mice were of a healthy weight, and this reduced mitochondrial activity is evident in the growing foetus. The researchers give a plausible explanation that it is the damaged mitochondria that causes the reduced fertility and increased weight; however, this is just a theory. The study does not prove that obesity causes reduced mitochondrial activity or that this would cause the offspring to be obese. The weight of the growing foetuses of obese mice was greater, but none were born.

Strengths of the study include the type of obese mice used (which are known as “Blobby mice” in Australia). Mice with this syndrome become obese regardless of the type of food they eat, because of the volume they consume. In this experiment, the researchers did not want to compare healthy-weight mice with obese mice that had become so because of just eating a high-fat diet, as this could confound the results.

While studies of other mammals such as mice are useful, they cannot tell us exactly what happens in humans. It is known that fertility rates improve when women who are overweight or obese lose weight, and this can be achieved through small changes such as increasing your activity levels and reducing your intake of calories.

The drugs in this trial are not yet available for humans, other than BGP-15 in a trial for type 2 diabetes. Neither of them have been tested in any fertility trials on humans. For further tips on improving your fertility, see our fertility pages.

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

Links To The Headlines

Damaging effect of obesity on a woman's eggs can now be reversed: Drug can 'restore egg quality to original level'. Mail Online, February 10 2015

Health risks for obese mothers and their babies can be reversed. The Independent, February 10 2015

Links To Science

Wu LL, Russell DL, Wong SL, et al. Mitochondrial dysfunction in oocytes of obese mothers: transmission to offspring and reversal by pharmacological endoplasmic reticulum stress inhibitors. Development. Published online February 2015

Categories: Medical News

Unemployment and job insecurity linked to increased risk of suicide

Medical News - Wed, 02/11/2015 - 14:00

“Unemployment causes 45,000 suicides a year worldwide,” The Guardian reports. The story comes from a study that looked at the association between suicide rates and unemployment in 63 countries across the world.

It found that between 2000 and 2011, one in five of an estimated 233,000 annual suicides were linked to unemployment.

The study cannot prove that unemployment causes suicide, although it certainly suggests a strong association.

The research is useful because it looks at the possible link between suicide and unemployment in the long term and not just during times of economic crisis. It estimates that unemployment between 2000 and 2011 was associated with nine times as many suicides annually as those that were attributable to the 2008 economic recession.

Interestingly, it also found that in countries where being out of work is uncommon the link between suicide risk and a rise in unemployment is stronger.

This could be due to a sense of being stigmatised. In the UK, there are regular media stories about people perceived as abusing the benefit system, but these are likely to be the exception, not the rule. Such distorted coverage may increase the sense of stigmatisation.

The researchers make the suggestion that professionals such as social workers and human resource officers who deal with people who are unemployed or at risk of redundancy, should be given advice to spot possible warning signs, as this may help prevent potential suicides.

 

Where did the story come from?

The study was carried out by researchers from the University of Zurich in Switzerland. There is no information about external funding.

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

While The Guardian and the Mail Online’s coverage was generally accurate, they both fell into the trap of assuming correlation equals causation – wrongly stating that a direct cause and effect relationship has been proven between unemployment and suicide rates.

Unemployment may have an influence on suicide rates, though other factors such as depression and poor health could also play a part.

So a headline such as The Guardian’s “Unemployment causes 45,000 suicides a year worldwide, finds study” is incorrect.

 

What kind of research was this?

This was an observational study that looked at the association between suicide and unemployment in 63 countries between 2000 and 2011. Importantly this was a period that included times of economic stability as well as the 2008 global economic recession and its aftermath.

The researchers say that previous research suggests an association between the 2008 economic crisis, rising unemployment and increased suicide rates, with men and those of working age particularly affected.

Unemployment may increase the risk of suicide through mechanisms such as an increased risk of depression, financial strain and reduced affordability of mental health care.

However, they say a specific effect of unemployment on suicide rates has not been clearly shown.

 

What did the research involve?

The researchers extracted data on suicide rates from 2000 to 2011 by age and sex, from the mortality database of the World Health Organization. They looked at the number of suicides per 100,000 population for the following four age categories, by sex: 15-24 years, 25-44 years, 45-64 years and 65 years and older.

They extracted four economic indicators from 2000 to 2011 from the world economic database of the International Monetary Fund. These were the unemployment rate, Gross Domestic Product (GDP), growth rate and inflation.

For their analysis they selected 63 countries drawn from the four world geographic regions – the Americas, northern and western Europe, southern and eastern Europe, and non-Americas and non-Europe. The countries were chosen based on completeness of data available and sample size.

Using statistical methods they analysed the link between unemployment rates, suicide and other economic factors.

 

What were the basic results?

The study found that the link between unemployment and suicide was similar in all four world regions. It estimates that in the 63 countries studied between 2000 and 2011:

  • there were about 233,000 suicides annually
  • suicides associated with unemployment totalled about 45,000 annually, making up about 20% of all suicides
  • suicide associated with unemployment rose by 4,983 from 2007 to 2009 (the period of the recent economic downturn)
  • men and women of all ages were equally vulnerable to suicide associated with unemployment
  • overall, the relative risk of suicide decreased by 1.1% (95% confidence interval (CI) 0.8-1.4%) annually, during this period

Researchers also found a six-month time lag between higher suicide rate and a rise in unemployment, There was also a stronger association between suicide and unemployment in countries where baseline unemployment was low.

 

How did the researchers interpret the results?

The researchers say that in countries where unemployment is uncommon, a rise in job losses might trigger greater fears and insecurity than in countries with higher previous unemployment rates. They also comment on the time lag between suicide and the rise in unemployment, suggesting that downsizing and labour market restructuring may create additional stress and a sense of job insecurity.

Suicide associated with unemployment might be severely underestimated if studies focus only on times of economic crisis they argue. “There is a continuous need to focus on preventing suicides, even more so in economically prosperous, stable time periods than in times of lower prosperity, when resources are scarcer,” they say, with prevention efforts needed in countries with both low and high unemployment rates.

 

Conclusion

This large study suggests there is a strong association between suicide and unemployment in times of economic stability as well as in times of economic recession. 

However, analysis at world regional level is unable to take account of clinical and psychosocial factors associated with suicide and further research into individuals at risk in times of high unemployment would be useful. In addition, there is missing information from large countries such as China, India and most of Africa, which may affect the reliability of their estimates.

As an accompanying paper in The Lancet Psychiatry notes, fluctuating unemployment is only one effect of economic recession that may affect mental health. Other economic strains include falling income, zero hour contracts, job insecurity and debt.

Read more advice about coping in times of job and economic uncertainty.

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

Links To The Headlines

Unemployment causes 45,000 suicides a year worldwide, finds study. The Guardian, February 11 2015

Unemployment is linked to 45,000 suicides a year. Mail Online, February 11 2015

Links To Science

Nordt C, Warnke I, Kawohl W. Modelling suicide and unemployment: a longitudinal analysis covering 63 countries, 2000–11. The Lancet Psychiatry. Published online February 11 2015

Categories: Medical News

'Smart insulin' could be used to treat type 1 diabetes

Medical News - Tue, 02/10/2015 - 15:30

The Guardian today reports that “smart insulin” may ease the burden on type 1 diabetes – a condition that means the body cannot produce insulin.

This means that those with the condition require frequent insulin shots to stabilise their blood glucose levels. However, this can be a difficult balancing act, as glucose levels can fluctuate throughout the day. Fluctuations can also be potentially dangerous, as they can lead to complications such as hypoglycaemia (low blood glucose).

This was an animal study looking into the development of a new type of “smart insulin” that contains a “molecular switch”, allowing it to directly respond to blood glucose levels, to bring them under control.

When injected into diabetic mice, it was able to normalise their blood glucose levels when they were given glucose challenges (where mice are given a sugary drink) even as long as 13 hours after the initial injection. This suggested that the modified insulin could help with blood glucose control and have a long duration.

Though promising, this research is in the very early stages. This modified insulin has so far only been tested in mice. It is far too early to know whether there could be a new insulin treatment available for type 1 diabetes.   

 

Where did the story come from?

The study was carried out by researchers from Massachusetts Institute of Technology in the US, and was funded by donations from the Leona M. and Harry B. Helmsley Charitable trust and the Tayebati Family Foundation. The study was published in the peer-reviewed journal PNAS.

The Guardian put a generally positive spin on the results, outlining the potential benefits the new insulin might bring to people with diabetes. It did well in mentioning that the research was done on mice. However, it didn’t really say or discuss why this was an important limitation of the research. While mice share many of our biological traits, we can never be sure that a drug that works in mice will work in humans (or be safe).

Only at the end of the piece was a note of caution introduced. This came from Dr Richard Elliott, of Diabetes UK, who said: “Years of further research and clinical trials will be needed to find out if a similar drug could be used safely and effectively by people with diabetes”.

BBC News’ reporting of the study was less optimistic, as they were quick to mention that “it will take years of testing before treatments could become a reality for patients”.

 

What kind of research was this?

This was an animal study that looked at developing a type of insulin that is tailored to the individual.

Type 1 diabetes is a condition where the body’s immune system destroys the insulin-producing cells of the pancreas, making the person reliant on life-long insulin injections. There are currently various types of insulin, ranging from some that act quickly and have a short-lasting effect, to those that have a much slower onset and last for longer periods. The type or combination of insulin preparations used will vary considerably from one individual with type 1 diabetes to another.

However, most people will experience difficulty at some point in their insulin treatment, such as problems controlling their blood glucose levels. This means they are potentially at risk of complications such as glucose becoming dangerously low (hypoglycaemia) or high (hyperglycaemia).

In this study, the researchers aimed to prepare a type of insulin that has a “molecular switch” that switches it on or off, depending on glucose levels. They tested it in mice. It is hoped that this treatment could one day give more targeted insulin therapy with better glucose control.

 

What did the research involve?

The research team prepared their modified insulin, which contains two small chemical molecules bound to insulin. One of the molecules (phenylboronic acid, PBA) is a “glucose sensor”, while the other molecule (an aliphatic domain) helps to give it a long “half-life” so it has similar duration in terms of action to long-acting insulin.

The researchers then tested this new insulin treatment in a mouse model of type 1 diabetes (mice that had been given a treatment to destroy their insulin-producing cells). The mice fasted overnight and were then given injections of the modified insulin at different doses, combined with glucose challenges (given a sugary solution to simulate eating a meal). Blood glucose levels were continuously monitored throughout the tests.

The main analysis compared the glucose control achieved with the new insulin to that achieved using standard insulin injections, all using diabetic mice. They also compared the effects of their insulin with glucose challenges given to healthy, non-diabetic mice.

 

What were the basic results?

Briefly, the researchers found that their treatment was successful when given to mice with type 1 diabetes. It rapidly normalised their blood glucose levels following the glucose challenge and also demonstrated longer-term effects. In some tests, the modified insulin was able to normalise blood glucose levels in glucose challenges given up to 13 hours after the initial injection.

Their “best-performing” insulin was also demonstrated to give better blood glucose control than standard long-acting insulins. When given a glucose challenge, the diabetic mice given the modified insulin were also able to normalise their blood glucose levels in a similar way to healthy non-diabetic mice.

 

How did the researchers interpret the results?

The researchers say their study is the first of their knowledge to have demonstrated the effects of a modified insulin molecule in a live animal model. They say that this approach to insulin modification “could afford both long-term and glucose-mediated insulin activity, thereby reducing the number of administrations and improving the fidelity of [blood glucose] control”.

 

Conclusion

This animal study has demonstrated promise for a modified insulin molecule that contains a “molecular switch”, allowing it to respond to blood glucose levels. When injected into diabetic mice, it was able to normalise their blood glucose levels in response to glucose challenges, sometimes many hours after the initial injection.

This suggested, as the researchers hoped, that the modified insulin could give targeted blood glucose control, and also have a long duration of action, similar to current long-acting insulins.

The researchers hope that this could one day lead to the development of an insulin treatment for people with type 1 diabetes that would give better blood glucose and reduce the risk of complications such as hypoglycaemia.

Though promising, this research is in the very early stages, having only been tested in mice. There are many more developmental hurdles to pass before this innovation could be a new treatment for people. The first stage would be seeing whether the treatment could be developed for testing in humans, then seeing whether it is safe, then gradually conducting trials in successively larger numbers of people. This will determine whether it is safe and effective compared with other insulins used by people with type 1 diabetes.

While it is perfectly fine to be optimistic, there are no guarantees. Promising research in mice does not necessarily lead to effective treatments for humans.

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

Links To The Headlines

'Smart' insulin may ease burden of type 1 diabetes patients, research suggests. The Guardian, February 9 2015

'Smart' insulin hope for diabetes. BBC News, February 10 2015

Links To Science

Chou D, Webber MJ, Tang DC, et al. Glucose-responsive insulin activity by covalent modification with aliphatic phenylboronic acid conjugates. PNAS. Published online February 9 2015

Categories: Medical News

1980s fat guidelines 'lacked evidence,' study argues

Medical News - Tue, 02/10/2015 - 15:00

"Butter isn't bad for you after all: Major study says 80s advice on dairy fats was flawed," is the headline on the front of the Daily Mail as a new study argues dietary fat guidelines introduced in the 1980s lacked a rigorous evidence base.

The study in question looked at guideline advice on saturated fat published in 1983 in the UK and in 1977 in the US. The researchers wanted to see if the evidence available at the time – specifically, the results of randomised controlled trials (RCTs) – supported the recommendations made.

The researchers identified six RCTs available at the time. The pooled results showed that specific advice to control saturated fat intake did not have a significant effect on deaths from heart disease or other causes.

But it is very important that these findings are interpreted in the correct context – this means we cannot conclude the recommendations were "incorrect".

We do not know what evidence was used to back up the official guidelines in the late 70s and early 80s. They could have looked at studies other than RCTs, such as observational studies (where health outcomes are studied over time).

This new review considered just six RCTs published before 1983, and all of them were conducted in men, most of whom already had heart disease.

Current dietary advice is not stuck in the 1980s, wearing shoulder pads and sporting a bubble perm. It has evolved as new evidence has emerged. In fact, a small amount of saturated fat is recommended as part of a balanced, Mediterranean-style diet.

But it would be a mistake to conclude from this evidence that you can eat as much saturated fat as you like without damaging your health.

 

Where did the story come from?

The study was carried out by researchers from the University of the West of Scotland, Cardiff Metropolitan University, and the University of South Wales in the UK, and Saint Luke's Mid America Heart Institute in the US.

No sources of funding are reported and the authors declare no conflicts of interest. But the lead author of the study, Zoë Harcombe, does run a commercial diet plan called The Harcombe Diet®, which promotes "eating real food", including dairy products.

The study was published in the peer-reviewed medical journal, Open Heart. This is an open-access journal, so the study can be read online for free or downloaded as a PDF.

Overall, the media reporting was poor and potentially quite dangerous for several reasons. Much of the reporting gives the impression that the claim "saturated fats are not bad for you" represents a change in official dietary advice. This is not the case. The claim is the opinion of a small group of researchers.

The headline writing was particularly sensationalist. Journalists took the findings at face value, writing potentially scaremongering headlines, and may leave their readers questioning the evidence base for the current guidelines. Debate on national guidelines is always welcome, but much of the debate in the media was ill-informed.

Even if you did accept the claim that saturated fat is not especially harmful, it certainly does not follow that eating more of it would be good for you, as the Daily Express bizarrely claimed: "Fat is key to living longer". A diet high in saturated fat could in fact lead to obesity.

A more balanced account of the relevance of this study was given in the accompanying Open Heart editorial, which is also open access.

Various dietary experts have considered this research in a broader context. The consensus from the experts is that only focusing on evidence from RCTs for dietary guidelines is somewhat unrealistic and narrow, and missed useful evidence of other types.

Some went a lot further. Professor Christine Williams, professor of human nutrition at the University of Reading, said: "The claim that guidelines on dietary fat introduced in the 1970s and 80s were not based on good scientific evidence is misguided and potentially dangerous."

 

What kind of research was this?

This was a systematic review and meta-analysis of research published 30 or more years ago.

It aimed to investigate whether national dietary advice introduced in the 1970s and 80s in the US and the UK to reduce coronary heart disease (CHD) by reducing saturated fat intake was backed up by contemporaneous evidence from randomised controlled trials (RCT), which are seen as the "gold standard" in evidence-based medicine.

In the US, public health dietary advice was issued by the Select Committee on Nutrition and Human Needs in 1977. This was followed in 1983 by UK public health dietary advice from the National Advisory Committee on Nutritional Education.

The authors state these recommendations advised that people reduce their overall fat consumption to 30% of their total energy intake, and reduce their saturated fat consumption to 10% of their total energy intake.

The researchers discuss several possible limitations of these publications, saying they included wording that was far from conclusive, such as "tended to be related", and how neither publication made reference to any RCTs available at the time.

The authors of this review therefore aimed to look for RCTs available when the dietary guidance was published to see whether the available evidence supported the recommendations.

 

What did the research involve?

The authors searched the literature databases Medline and the Cochrane Library to identify studies published up to 1983. They restricted their search to these two databases because others did not provide adequate coverage of the early publications this review was interested in.

They looked for RCTs in adults of at least one year's duration where:

  • people were randomised to a dietary intervention (a programme that attempted to control or modify specific elements of their diet)
  • the aim of the study was to look at whether a reduction or modification in dietary fat or cholesterol had an effect
  • health outcome data on all-cause mortality, CHD mortality and cholesterol measurements was available

Six RCTs met their inclusion criteria:

  1. Rose Corn Oil Trial
  2. Research Committee Low-fat Diet
  3. MRC Soya-bean Oil
  4. LA Veterans Study
  5. Oslo Diet Heart Study
  6. The Sydney Diet Heart Study

The researchers extracted data from these studies and considered their quality and risk of bias. They pooled the results of these trials in a meta-analysis.

 

What were the basic results?

The six RCTs included a total of 2,467 men, and all but one of the studies looked at secondary prevention. This means the participants already had cardiovascular disease.

The researchers involved in these RCTs looked at whether dietary intervention could reduce the risk of further disease events, such as a heart attack. The average study duration was five to six years.

Of the six studies, four looked at giving vegetable oil (three of which assessed it as a replacement for saturated fat), one looked at a roughly 20% fat diet, and one looked at a 10% saturated fat diet.

As this new study points out, five of the six RCTs did not look at either a total fat consumption of 30% or saturated fat as 10% of energy intake, as given in the offical recommendations made in the 70s and 80s.

Across the studies, 30.2% of the intervention groups and 29.8% of the control groups died. The pooled results of all the studies found no statistically significant effect of the dietary interventions on deaths from all causes (relative risk [RR] 0.996, 95% confidence interval [CI] 0.865 to 1.147).

The pooled results did not find that the dietary interventions had any significant effect on coronary heart disease mortality specifically (RR 0.989, 95% CI 0.784 to 1.247).

Cholesterol levels fell in both intervention and control groups, though there was a greater reduction in the intervention groups. The pooled reduction in the intervention groups was a reduction of 12.6% (give or take 6.7%), while the reduction in the control groups was 6.5% (give or take 5.1%).

 

How did the researchers interpret the results?

The researchers say that: "No randomised controlled trial had tested government dietary fat recommendations before their introduction.

"Dietary recommendations were introduced for US and UK citizens by 1983, in the absence of supporting evidence from RCTs."

They state that: "The present review concludes that dietary advice not merely needs review; it should not have been introduced."

 

Conclusion

This research found the pooled results of six RCTs available prior to 1983, which all looked at interventions to moderate saturated fat intake, did not find this had an effect on deaths from heart disease or any other cause.

But it is very important that the specific purpose of this review is considered, and the findings are interpreted in the right context.

This review specifically looked at nutrition guidance given in the US in 1977 and in 1983 in the UK. In particular, the researchers looked at two recommendations:

  • reduce overall fat consumption to 30% of total energy intake
  • reduce saturated fat consumption to 10% of total energy intake

The researchers specifically wanted to see whether RCTs available at that time supported those recommendations. But there are some specific points to consider from the results of this analysis.

Evidence considered by the 1977 and 1983 guidelines

We are not able to review the methods used by the US and UK government bodies in forming their nutrition recommendations. We also do not know what evidence they considered.

The authors of the current review state that: "Both documents acknowledged that the evidence was not conclusive ... the Dietary Goals for the US noted 'there will undoubtedly be many people who will say we have not proven our point.' The UK publication referred to 'a strong consensus of opinion'."

We cannot comment further on how this nutrition guidance may have been produced, or how they may have considered their evidence and formed their recommendations.

It is possible the methods used by these organisations more than 30 years ago may have differed from those used in producing the most robust evidence-based guidelines today.

But we cannot conclude that the recommendations were unreasonable, or not backed by any supporting evidence, just by looking at the information included in this systematic review.

It is likely the guidance from more than 30 years ago may have considered observational evidence looking at how saturated fat intake was related to mortality and heart disease.

While the lack of RCTs at the time may potentially be of concern, it is also not particularly surprising. RCTs involving diet are notoriously difficult to run because of compliance issues: researchers can never be sure that participants are sticking to their recommended diet plans. Also, exposing participants to an intervention you think may be harmful is unethical.

It is also not fair to say observational study designs are of no value. In fact, when looking at issues such as dietary patterns, there is often more information available from observational studies. These types of studies can review a person's longer-term lifetime dietary patterns and see how this is related to health outcomes.

We therefore cannot conclude that the recommendations made over 30 years ago were "incorrect". This review has kept a narrow focus, only looking at RCTs available at the time.

Other types of study, such as long-term population-based studies, can provide rich and useful information, and may have been considered when the guideline recommendations were being formed.

Issues with the RCTs included in the review

The finding there is no link between saturated fat intake and deaths from heart disease and other causes is based on six very specific RCTs. These studies are all likely to have differences in terms of their design, the methods used, their duration, and their quality.

The studies only included men, so the results may not be applicable to women, for a start. And five out of six included men who already had heart disease.

The studies also looked at the relatively short-term effects of specific interventions (such as substituting vegetable oil) and whether this influenced outcomes. They did not look at lifetime dietary patterns. Overall, they found the interventions did not affect outcomes.

This review's findings do not mean that current government nutritional advice and recommendations (the eatwell plate) are wrong.

National dietary guidance is based on all the relevant evidence that has accumulated to date, and is updated regularly to consider important new evidence. Current guidance will have considered a much larger body of research than the guidance issued in 1983. 

There's nothing wrong with the occasional buttered scone. But, based on the current body of evidence, it would be potentially dangerous to think you can eat as much saturated fat as you want without it having an effect on your health.

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

Links To The Headlines

Butter ISN'T bad for you after all: Major study says 80s advice on dairy fats was flawed. Daily Mail, February 9 2015

Fat guidelines lacked any solid scientific evidence, study concludes. The Guardian, February 10 2015

Dietary advice from the 1970s found to be a big fat mistake. The Independent, February 10 2015

Food fat warnings 'should not have been introduced'. The Daily Telegraph, February 9 2015

Fat Guidelines 'Shouldn't Have Been Introduced'. Sky News, February 10 2015

FAT is the key to living longer: Previous diet advice was WRONG, say experts. Daily Express, February 10 2015

Links To Science

Harcombe Z, Baker JS, Cooper SM, et al. Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart. Published online February 9 2015

Categories: Medical News

Do men have greater chewing power than women?

Medical News - Mon, 02/09/2015 - 18:55

"Why men wolf down their meals while women take their time: The sexes have different chewing patterns," the Mail Online reports, after a Korean study found men had "greater eating power" than women.

This small study compared the chewing behaviours of 48 young Korean men and women in controlled laboratory conditions.

It found men took bigger bites, had greater chewing power, and ate faster than women. Women chewed more and took longer to finish their food.

But this study has considerable limitations – mainly, that its results may not apply to wider populations, such as people of different ages or from different countries.

This highly controlled experiment, where participants ate plain boiled rice while monitors were attached to their jaws, may not even be representative of how the volunteers would chew in a real-life situation.

Overall, this research is not sufficient to conclusively say that men and women have different chewing patterns, or what the implications of this might be.

It is probably better to concern yourself with what and how much you are eating rather than how long you take to chew and swallow your food.

 

Where did the story come from?

The study was carried out by researchers from Semyung and Hanyang Universities in the Republic of Korea. It was funded by the Korean Ministry of Food, Agriculture, Forestry and Fisheries.

The study was published in the peer-reviewed journal Physiology and Behavior, and is available to read online or download as a PDF on an open-access basis.

The Mail Online's reporting was generally accurate, but did not point out the relatively limited applicability and implications of this study.

 

What kind of research was this?

This was an experiment comparing eating behaviours and chewing in men and women. It also looked at whether obesity influenced these behaviours.

The researchers say some previous studies found that obese individuals chew faster and take bigger bites than those who are not obese, while other studies have reached different conclusions.

They say there have been similar findings looking at the different ways men and women eat.

This study design is reasonable for assessing eating behaviours, but the highly controlled setting of the experiment may not be representative of people's behaviours in everyday life.

 

What did the research involve?

The researchers recruited 24 male and 24 female volunteers to eat portions of rice. They compared the volunteers' reported eating behaviours, and also measured their chewing under controlled conditions in the lab.

They then looked at whether there were differences between men and women, or between those who were heading towards being obese (pre-obese) and those who were not.

To be eligible to take part, the volunteers had to be aged 20 to 29 years, have a full set of healthy teeth, and no eating disorders. The researchers recruited people who were:

  • non-obese – body mass index (BMI) between 18.5 and 23, and a waist circumference less than 80cm for women and 90cm for men
  • pre-obese – BMI 25 or over, and a waist circumference of 80cm or more for women, and 90cm or more for men

The volunteers filled out a standard questionnaire assessing their subjective views about their control of three dietary behaviours:

  • restraint – ability to cognitively control eating behaviour
  • disinhibition – susceptibility to eating in response to emotional factors and sensory cues, such as smells
  • hunger – susceptibility to eating in response to hunger

They then took part in the eating experiment in the lab. They fasted for 12 hours overnight and had not exercised for 24 hours. They were then all given 152g of boiled rice to eat served with 200ml of water.

The researchers asked the volunteers to rate their hunger and fullness before and after eating the rice. While the volunteers were eating the rice, the researchers measured their chewing using sensors attached to the jaw.

 

What were the basic results?

The researchers found that:

  • pre-obese volunteers reported greater susceptibility to eating in response to emotional factors and sensory cues than non-obese volunteers
  • women and men differed in their chewing, but pre-obese and non-obese individuals did not
  • men took bigger bites than women
  • men's chewing power (the muscle pressure exerted by their jaws) was greater than women's
  • men ate faster than women
  • women chewed more than men
  • women took longer to finish their rice than men

The researchers found men who reported greater susceptibility to eating in response to emotional factors and sensory cues tended to eat faster.

Both men and women who reported greater susceptibility to eating in response to emotional factors and sensory cues tended to have a smaller bite size and less chewing power.

 

How did the researchers interpret the results?

The researchers concluded that, "The results suggest that the effects of gender, and, in part, obesity, on eating responses may be explained as chewing performance."

They say this means that, "Gender-specific interventions and counselling aimed at slowing the rate of ingestion could be promising behavioural treatments for obese persons."

 

Conclusion

This small study suggests that chewing behaviours in controlled laboratory conditions differ between young Korean men and women.

But this study of just 48 people has considerable limitations. Its results may not apply to wider populations, such as people of different ages or from different countries.

This highly controlled experiment, where participants ate plain boiled rice while monitors were attached to their jaws, may not even be representative of how the volunteers would chew in a real-life situation.

The many statistical tests carried out also mean that some may be statistically significant by chance.

Although the researchers found some differences between men and women in chewing, they did not find any between those who were considered pre-obese and those who were not obese.

It is not possible to say from this study whether the "gender-specific interventions and counselling aimed at slowing the rate of ingestion" would indeed "be promising behavioural treatments for obese persons", as suggested by the authors.

This study does not provide compelling evidence of differences between men and women in "masticatory performance", or whether these can lead to increased fitness, better health, or weight loss.

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

Links To The Headlines

Why men wolf down their meals while women take their time: The sexes have different chewing patterns. Mail Online, February 9 2015

Links To Science

Park S, Weon-Sun S. Differences in eating behaviors and masticatory performances by gender and obesity status. Physiology & Behavior. Published online October 18 2014

Categories: Medical News

Type 1 diabetes 'more dangerous' in women

Medical News - Mon, 02/09/2015 - 14:00

"Type 1 diabetes is more dangerous for women than men, study finds,” The Daily Telegraph reports. A large review found gender inequality in overall deaths among people with type 1 diabetes, and also deaths due to heart disease.

These results come from a systematic review of studies looking at how risk of death in men and women with type 1 diabetes differs from their counterparts without the disease. It pooled results from 26 studies, and found that type 1 diabetes was associated with a greater increase in risk of death from any cause, or death from heart disease, over a given period in women than it is in men.

The researchers suggest it may be because diabetes is less well controlled among girls and women than among boys and men. If this proves to be the case, then greater efforts may be targeted towards to improving diabetes management in women.

Type 1 diabetes is, at the moment, an incurable condition, so it is important to stay informed about the best way to live with diabetes, whatever your gender.

 

Where did the story come from?

The study was carried out by researchers from the Universities of Queensland and other universities in Australia, the Netherlands, UK and US. The researchers were funded by a Niels Stensen Fellowship, an Australian National Health and Medical Research Council Fellowship, and an Australian Research Council Future Fellowship. The study was published in the peer-reviewed medical journal The Lancet.

The Daily Telegraph covers this study reasonably well; however, the results are expressed in a way that could be misleading. It says, for example, that “female patients are twice as likely to die from heart disease than men with [type 1 diabetes]”. It is not quite as simple as this. As men do not generally live as long as women, researchers needed to take this into account in their analyses – otherwise, the figures would not be showing them the potential impact of diabetes, but the effect of gender.

So, to get a fair idea of the potential impact of diabetes, the researchers did not directly compare rates of death in men and women. Instead, they first compared the risk of death over a given period in women with type 1 diabetes to that of women in the general population, to see what effect diabetes had in women. The equivalent comparison was then made for men.

These figures were then compared to see whether type 1 diabetes had a greater or lesser effect on risk of death in women than in men.

 

What kind of research was this?

This was a systematic review that aimed to determine whether there was any difference between men and women with type 1 diabetes and their likelihood of dying within any given period.

The researchers say that although management of type 1 diabetes has improved, the condition is still associated with an increased risk of death over a given period, compared to the general population. They say that some studies have suggested that men and women may differ in how much type 1 diabetes affects their risk of death, but no review has ever pooled the results of these studies.

A systematic review is the best way to identify and summarise the best-quality studies available to answer a given question. This review statistically pooled (meta-analysed) the results of the studies it identified. The meta-analysis includes more people than each individual study alone, and this means it is better able to detect differences between groups, if they exist.

 

What did the research involve?

The researchers systematically searched one major research literature database (PubMed) to identify studies that identified risk of death in men and women with diabetes over time. They selected those studies which had data that would allow them to compare the effect of type 1 diabetes in terms of risk in men and women. They then extracted and pooled the results of these studies to see if there was a difference overall.

The researchers only included studies that provided information on deaths in a form that they could use. This meant either hazard ratios (HR), comparing deaths among people with and without type 1 diabetes, or standardised mortality ratios (SMR), comparing deaths among people with type 1 diabetes against what would be expected among people with similar characteristics in the general population.

As men and women have different expected lifespans, researchers were looking for studies which compared deaths among women with type 1 diabetes versus women without the disease, and did the same for men. This meant they could compare the likelihood of a person of each gender dying to someone of the same gender without the disease. They then compared these figures.

The researchers were mainly interested in deaths from any cause, but also looked at deaths from specific causes separately. They also looked at new diagnoses of various conditions, including coronary heart disease (where a build-up of fatty substances causes blockage in the arteries providing blood to the heart muscle) and cardiovascular disease (coronary heart disease, stroke, or other cardiovascular disease). They also looked at various factors which might affect the outcome, such as how long the studies followed people for, or the quality of the study.

The researchers complied with accepted standards for pooling of this study type and for reporting their systematic review.

 

What were the basic results?

The researchers identified 26 studies that provided the data they wanted. These studies included 214,114 people, although not all of them were included in all of the analyses.

It found that during follow up, women with type 1 diabetes were 5.8 times more likely to die than women in the general population, and men with type 1 diabetes were 3.8 times more likely to die than men in the general population. Overall this equated to a 37% greater relative increase in likelihood of death than men with the condition (ratio of SMRs for women versus men: 1.37, 95% confidence interval [CI] 1.21 to 1.56). There was statistical evidence that different studies in this analysis had varying results. Some of this variability seemed to be due to differences between the studies in exactly how likely men and women were to die.

Women with type 1 diabetes also had a greater relative increase than men with the condition in terms of risk of:

  • a new diagnosis of coronary heart disease (ratio 2.54, 95% confidence interval (CI) 1.80 to 3.60)
  • a new diagnosis of stroke (ratio 1.37, 95% CI 1.03 to 1.81)
  • dying from kidney disease (ratio 1.44, 95% CI 1.02 to 2.05)
  • dying from cardiovascular disease (ratio 1.86, 95% CI 1.62 to 2.15)

There was no difference between men and women in how type 1 diabetes affected their risk of cancer or accident and suicide.

 

How did the researchers interpret the results?

Researchers concluded that “women with type 1 diabetes have a roughly 40% greater excess risk of all-cause mortality, and twice the excess risk of fatal and nonfatal vascular events, compared with men with type 1 diabetes”. They say that greater understanding of this issue “is likely to have profound clinical implications for how women with type 1 diabetes are treated and managed throughout their life course”.

 

Conclusion

This systematic review suggests that type 1 diabetes is associated with a greater increase in risk of death in women than men.

A systematic review is the best way to identify and summarise the best-quality studies available to answer a given question. The pooling (meta-analysis) of the studies' results means the review includes more people than the individual studies, and is therefore better able to detect differences between groups.

The figures presented are comparisons of the relative increases in risk of death associated with type 1 diabetes within each gender. As women generally live longer than men, even though the relative increase in risk in women with type 1 diabetes may be greater than in men, the women’s actual (absolute) risks of death in a given period may not differ as much, and could still be less than men’s risks.

There are some other limitations and points to note:

  • This study is only about type 1 diabetes, so results may not apply to those with type 2 diabetes.
  • The review only searched one literature database, and also looked for relevant studies mentioned in the studies they identified. Ideally, systematic reviews search more than one literature database to increase their chances of finding all relevant studies.
  • The pooled studies did have differences in their designs and methods, and this may influence the results. There was statistical evidence that there were differences in the results of the individual studies, which the researchers were not entirely able to explain. In part, it related to different risks of death in the populations being studied. This may mean that the pooled results are not representative of each different study population. The researchers also say it means their results “remain speculative until confirmed by future studies”.
  • The review pooled observational studies. Factors other than type 1 diabetes (confounders) could be influencing the results seen. The individual studies differed in the extent to which they took these factors into account, so they could still be having an effect. The researchers think that this is unlikely to be a big issue, as the same confounders should be affecting men and women, and therefore effectively cancelling each other out.

It is likely that more research will go into exploring why this difference might exist. The researchers suggest it may be because girls’ and women’s diabetes is less well controlled, or due to hormonal differences. The researchers were not able to look at diabetes control in men and women in the included studies to see if there was a difference. If the difference does prove to be due to poorer diabetes control, then greater efforts could be targeted towards improving diabetes management in women.

Whatever the reason for these findings, they do not take away from the fact that good diabetes control is important for both genders, to maintain a person’s health and reduce the risk of complications from the disease.

The NHS offers information and support services for people living with all forms of diabetes.

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

Links To The Headlines

Type 1 diabetes is more dangerous for women than men, study finds. The Daily Telegraph, February 7 2015

Links To Science

Huxley RR, Peters SAE, Mishra GD, Woodward M. Risk of all-cause mortality and vascular events in women versus men with type 1 diabetes: a systematic review and meta-analysis. The Lancet – Diabetes and Endocrinology. Published online February 5 2015

Categories: Medical News

Finger length 'not a pointer' for future sexual behaviour

Medical News - Fri, 02/06/2015 - 19:00

"How to work out if your partner is cheating on you? Check their fingers," the Daily Mirror advises. The news comes from research founded on the theory that humans are believed to display two types of mating pattern – one more promiscuous, and the other more monogamous.

Previous animal and human studies have already suggested higher testosterone exposure is associated with longer ring to index finger ratios. And high testosterone has been linked to sexual promiscuity.

To look into this further, the researchers studied two separate samples. One sample of just over 500 people completed an online survey of their sexual behaviour. A completely separate sample had their finger lengths measured.

The results from the first sample found more men tended towards the promiscuous side, and more women towards the monogamous.

The second sample's results found more men have longer ring fingers than index fingers, while roughly equal proportions of women have either similar length fingers or longer ring fingers.

From this, the researchers inferred that – contrary to the findings of the survey – a more promiscuous pattern seems to be found in both sexes. Had women been more monogamous, as the survey suggested, they apparently should have had longer index fingers.

Whatever interpretation you could reasonably take, the study proves nothing about any association between sexual behaviour and the ratio of finger length.

Comparing two entirely different data sets takes you into "oranges and apples" territory – trying to find connections between two entirely different objects.

You also have to consider how representative people who chose to complete an online survey of sexual behaviour are of the general population.

 

Where did the story come from?

The study was carried out by psychology researchers at the University of Oxford and Northumbria University, and received funding from the European Research Council.

It was published in the peer-reviewed journal, Biology Letters, which is a publication of The Royal Society.

The article is open access, so it can be read online for free.

The UK media appear to have taken the study at face value, choosing not to report its important limitations. Namely, this study separately analysed sexual behaviour in one group and finger length in another group, and then drew links between the two.

But from the tone of the reporting, we suspect the journalists themselves were taking the findings of the study with a pinch of salt and with their tongues firmly in their cheeks.

If the suggestion that finger length can be used as a reliable predictive method for something as complex as human sexual behaviour sounds ridiculous, then it probably is ridiculous.

 

What kind of research was this?

This was a study looking at sexual behaviour patterns in one study sample, and the ratio of index and ring finger length in another study sample.

It aimed to look at the patterns of distribution of the two separate factors in these two separate samples, and from this see whether there may be an association between sexual behaviour and finger length.

The researchers say, in animal terms, humans are believed to fall midway between a monogamous and polygamous species, respectively a mix of longer-term and short-term mating patterns.

They say the extent to which any individual primarily pursues a "restricted" mating strategy, favouring exclusive pair-bonds, or an "unrestricted" strategy of promiscuity, is called "sociosexual orientation".

As a broad generalisation, males are usually considered more likely to favour promiscuous patterns than females as a way of getting more mating opportunities. 

The researchers say previous studies have shown that index to ring finger ratio is influenced by the amount of testosterone the growing foetus is exposed to in the womb, as well as the density of testosterone receptors.

Other studies in primates are also said to have shown finger length is associated with mating patterns.

This research tested the theory that there are two restricted and unrestricted types of people by looking at two large data sets – one sample completed a sociosexual orientation survey, and one sample had their index to ring finger ratio measured.

 

What did the research involve?

A total of 595 North American and British men and women (average age 25 years) completed the online sociosexual orientation survey (SOI-R).

Preferred mating strategy was said to be assessed using the "attitude" and "desire" subscales of the SOI-R, but this was not explained further.

A separate study collected data on index to ring finger ratios on the right hand of 1,314 British men and women.

The researchers then carried out analyses looking at the modelled distribution of sexual behaviours in the North American and British sample, and the distribution of finger length ratios in the other British sample.

 

What were the basic results? Sociosexual orientation survey

The researchers plotted distribution curves, where SOI-R score is plotted against density (the number of people who had that score). They did this for four separate groups: British men and women, and North American men and women.

All the groups of men and women showed what is called a "bimodal" distribution – two normal patterns of distribution. For all four groups, there was one pattern with a peak of normality at a lower SOI score (a more monogamous pattern), and a second pattern with a peak of normality at a higher SOI score (a more promiscuous pattern).   

There was a slight difference for men and women, though. For both North American and British men, the higher peak was at the higher SOI score, corresponding with slightly more men with a more promiscuous pattern.

Meanwhile, for both North American and British women, the opposite was seen – the higher peak was at a lower SOI score and corresponded with slightly more women following the monogamous pattern.

Finger length ratios

When similarly looking at the distribution of index to ring finger ratios for the other British sample, the researchers also found two normal distributions, but this time there was more of an overlap between the two curves.

For the sample of British men, the much higher peak was at a ratio of around 0.94 (ring finger slightly longer than index). There was a second much lower peak at a ratio of around 1 (similar length fingers).

For women, there was one common peak at around 0.94 and another equally common peak at a ratio of around 1.

Interpreted crudely, this means in men it is more common to have a longer ring finger than index finger, while in women equal numbers have fingers of the same length, or a ring finger longer than an index finger.

 

How did the researchers interpret the results?

The researchers concluded that: "This study is the first, to the best of our knowledge, to show statistically that both men and women exhibit two reproductive phenotypes of varying proportions."

But they go on to say that: "The proportional split in males slightly favours an unrestricted (short-term) mating strategy, with a 57:43 split on average, whereas females have a reversed split (47:53)."

The researchers then said that: "However, the mixing proportions in the [index to ring finger] ratio data set suggest that a slightly higher proportion of the unrestricted phenotype is present in both sexes (males approx. 62%, females approx. 50%)."

Presumably, this is based on previous research, which suggested testosterone levels are associated with finger ratios.

 

Conclusion

This research was founded on the theory that, as a species, humans are believed to display two types of mating pattern – one more promiscuous pattern made up of shorter-term attachments, and the other more monogamous pattern favouring longer term pair-bonds.

Traditionally, the male of a species is considered to favour the more promiscuous pattern to create more mating opportunities.

The research also centres on the other observation from previous human and animal studies, which found finger length is associated with mating patterns, and that index to ring finger ratio is influenced by testosterone levels.

The researchers used two separate samples for their study:

  • The first sample suggested there does seem to be two normal mating patterns for both men and women – one more promiscuous, and the other more monogamous. However, a higher proportion of men tend towards the more promiscuous side, while a higher proportion of women tend towards the more monogamous side.
  • The second sample, which assessed index to ring finger ratio, suggested more men have longer ring fingers than index fingers, while roughly equal proportions of women have either similar length fingers or their ring fingers are longer.

The researchers seem to imply from this that finger ratios actually show a more promiscuous pattern seems to be found in both sexes. This is because men tend to have longer ring fingers, which presumably ties up with higher testosterone levels and more promiscuous patterns.

However, women were found to have two equal distributions of finger length ratios. But if women were indeed more monogamous, as the other survey suggested, the researchers should have expected them to have longer index fingers.

Overall, this paints a rather unclear picture and it is hard to draw any reliable conclusions from this study.

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

Links To The Headlines

How to work out if your partner is cheating on you? Check their fingers. Daily Mirror, January 4 2015

Are you faithful or promiscuous? The answer could lie in your index finger. The Independent, January 5 2015

Are you promiscuous or faithful? Measure your index finger to find out. The Daily Telegraph, January 4 2015

Links To Science

Wlodarski R, Manning J, Dunbar RIM. Stay or stray? Evidence for alternative mating strategy phenotypes in both men and women. Biology Letters. Published online February 4 2015

Categories: Medical News

Flu jab is not a 'waste of time'

Medical News - Fri, 02/06/2015 - 13:10

“Flu jab given to millions is 'useless',” and "Flu jab is a waste of time," are the irresponsible headlines in The Daily Telegraph and the Daily Mail.

While recent research shows that the current seasonal flu vaccine only has 3% protection against the main circulating strain – A(H3N2) – in adults, it can still protect against other strains.

Both papers also ignore the fact that another version of the flu vaccine, in the form of a nasal spray designed for vulnerable children, is also available.

Discouraging parents of vulnerable children from getting vaccinated could increase the risk of serious childhood illnesses and possible hospitalisation.

 

Why is the flu vaccine not working?

There are many strains of the influenza virus and each one can mutate. It takes time to develop and produce vaccines against them. Global surveillance is used to predict which strains are likely to be circulating the following winter, and in February the World Health Organization (WHO) announces which strains the flu vaccine should cover. Last year, it decided to cover three flu varieties:

  • Influenza A (H1N1), also known as “swine flu"
  • Influenza A (H3N2)
  • Influenza B

In March, the WHO Global Influenza Surveillance and Response System detected a new strain of influenza A (H3N2), but this was too late to change the production of the vaccine.

It was also not known whether this particular strain would be the predominant strain this winter, which it has been, and so the vaccine is not effective against it.

How effective is it?

The vaccine is effective against the other strains of influenza, but not the new strain of influenza A (H3N2). The mid-season vaccine effectiveness rate is just 3.4%. Vaccination against this new strain and other possible mutations will be considered at the WHO meeting this February for next winter.

 

Reactions to the news

Dr Michael Skinner, Reader in Virology, Imperial College London said: “The current type of seasonal influenza vaccine is, at the moment, the best we have. Annually it saves tens of thousands of lives. Unusually, but not uniquely, this year one (H3N2) of the four targeted viruses ‘drifted’ (mutated) in an unanticipated direction after the vaccine was formulated for production, so that the vaccine offers little protection against the drifted H3N2.

"Even so, the vaccine still protects against the other three components (pre- and post-2009 H1N1 and B). And it does at least stop the virus drifting back along the path that had been predicted. To describe it as ‘useless’ would be misguided.”

 

Should you still get the jab?

The other strains can still cause infection so the vaccine is still recommended for pregnant women, people aged over 65 and those with any of the following conditions:

 

When to visit your GP

If you are otherwise fit and healthy, there is usually no need to visit your GP if you have flu-like symptoms.

The best remedy is to rest at home, keep warm and drink plenty of water to avoid dehydration.

You can take paracetamol or ibuprofen to lower a high temperature and relieve aches.

If you are in any of the high risk groups listed above then you should visit your GP.

Depending on your circumstances, your GP may recommend a short course of antiviral medication, such as Tamiflu (oseltamivir). 

Antivirals are not used for everyone with flu because this would lead to further mutations in the viruses and drug resistance, making them ineffective.

If you suspect you have the flu it is important to take steps to prevent it spreading; especially to one or more of the vulnerable groups listed above.

Always:

  • make sure you wash your hands regularly with soap and water
  • clean surfaces such as your keyboard, telephone and door handles regularly to get rid of germs
  • use tissues to cover your mouth and nose when you cough or sneeze
  • put used tissues in a bin as soon as possible

 

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

Links To The Headlines

Flu jab given to millions is 'useless'. The Daily Telegraph, February 6 2015

Flu jab is a waste of time for 97% of patients: Vaccine developed only a year ago no longer 'matches' because the virus has mutated so much. Daily Mail, February 6 2015

Flu vaccine 'barely effective' against main viral strain. BBC News, February 5 2015

Useless flu jab blamed for surge in death toll. Daily Express, February 6 2015

Current winter flu jab works in only 3% of cases. ITV News, February 6 2015

Flu vaccine gives only ‘low protection’ in UK this winter, experts warn. The Guardian, February 5 2015

Flu jab given to millions offers almost no protection. The Times, February 6 2015

Flu Jab Found To Work In Just 3% Of Cases. Sky News, February 6 2015

Links To Science

Pebody RG, Warburton F, Ellis J, et al. Low effectiveness of seasonal influenza vaccine in preventing laboratory-confirmed influenza in primary care in the United Kingdom: 2014/15 mid-season results. Eurosurveillance. Published online February 5 2014

Categories: Medical News

'Facebook envy' associated with symptoms of depression

Medical News - Thu, 02/05/2015 - 15:00

"Facebook can cause depression in people who compare themselves with others," The Independent reports. A new study has examined the relationships between Facebook use, feelings of envy, and feelings of depression.

Researchers surveyed more than 700 US university students, aiming to look at the relationships between the extent of Facebook use and feelings of envy and depression.

Importantly, it found the extent of Facebook use in itself was not associated with depression symptoms.

However, increased Facebook use was associated with feelings of "Facebook envy", such as feeling envious when seeing photos of old friends on luxury holidays.

Increased feelings of envy were then associated with increased symptoms of depression.

The relationship between feelings of envy, Facebook usage, and symptoms of depression is likely to be a complex one, and overall the study does not prove a cause and effect relationship.

The idea that spending increased time looking at the posts of Facebook friends could contribute to feelings of envy, which could in turn lead to feelings of low mood, seems plausible.

But there are likely to be many other unmeasured factors that are also having an influence. These could include personal characteristics, lifestyle and physical and mental health.

If you are prone to envy, Facebook may not be the social network for you. Why not try Twitter, where, as we discussed last month, people often post "angry tweets" unlikely to provoke any feelings of envy.

Where did the story come from?

The study was carried out by researchers from Nanyang Technological University in Singapore, and Bradley University and the University of Missouri in the United States. No sources of financial support were reported.

It was published in the peer-reviewed journal, Computers in Human Behavior.

Overall, the UK media's reporting was generally accurate, though many of the headlines failed to make it clear that Facebook itself did not cause depression.

In fact, "Facebook envy" was the main mediator of any link – but many other unmeasured factors are likely to be having an influence.

What kind of research was this?

This was a cross-sectional study based on a survey of US college students, which aimed to investigate the association between Facebook use, envy and depression.

In it, the researchers discuss the various traumas surrounding the transition to college life for young adults, including moving away from home, gaining new freedom and forming new relationships.

They report how a previous study found US adults aged 18 to 24 are likely to suffer from symptoms of depression and anxiety, particularly college students.

As the researchers say, multiple factors are likely to contribute to this, but they state that, "policy makers and scholars have hypothesized that heavy use of online social networks such as Facebook and mobile technologies may contribute to the phenomenon".

The researchers aimed to look at whether or not heavy Facebook use among college students could lead to depression, and the factors that may influence this relationship.

What did the research involve?

In the background to their survey, the researchers first of all present a literature review, where they discuss studies that have examined various theories.

This review does not appear to be systematic in that no methodology is provided, so we can't be sure that all relevant research into these issues has been considered.

The researchers first of all discuss various studies that have examined what is called "social rank theory" – a theory that depression is a result of competition, where humans, like other animals, compete for food, mates, and resources.

They also discuss research covering the evolution of Facebook, "the most popular social networking site". 

They then discuss studies that have looked at the mental health of college students, and introduce the theory of "Facebook envy" as a lead-up to their questions:

  • What is the relationship between frequency of Facebook use and depression among college students?
  • What specific uses of Facebook predict Facebook envy?
  • Does Facebook envy mediate the relationship between Facebook use and depression among college students?

The study is based on an online survey of 736 college students from a large mid-western university. All participants were taking journalism courses. The majority (68%) were female, identified themselves as White American (78%), and the average age was 19 years.

The researchers asked participants to report the average number of hours a day they spend using Facebook. They also asked them to rate how often they did the following, using a five-point scale from (5) very frequently, to (1) never:

  • write a status update
  • post photos
  • comment on a friend's post
  • read the newsfeed
  • read a friend's status update
  • view a friend's photo
  • browse a friend's timeline

They then assessed envy by asking people to rate on a similar five-point scale how much they agreed with the following statements:

  • "I generally feel inferior to others."
  • "It is so frustrating to see some people always having a good time."
  • "It somehow doesn't seem fair that some people seem to have all the fun."
  • "I wish I could travel as much as some of my friends do."
  • "Many of my friends have a better life than me."
  • "Many of my friends are happier than me."
  • "My life is more fun than those of my friends."

The researchers assessed depression symptoms using the Center for Epidemiologic Studies Depression (CES-D) scale, reported to be one of the most commonly used measures of depression. The responses were analysed using statistical software.

What were the basic results?

The researchers found the following:

  • There was no significant direct relationship between Facebook use and depression symptoms.
  • There was a significant relationship between Facebook use and feelings of envy – those reporting heavier use reported stronger feelings of envy than those with lighter use.
  • Relationships between Facebook use and feelings of envy were not influenced by the number of Facebook friends a person had.
  • There was a significant relationship between Facebook envy and depression symptoms. In analyses adjusted for age, gender, time spent on Facebook, and number of friends, increased feelings of envy were significantly associated with increased depression symptoms. Envy was said to account for around a quarter of the variance in depression symptoms.
How did the researchers interpret the results?

Addressing their question of whether Facebook use is depressing, the researchers say: "It is not – unless it triggers feelings of envy."

The effect of depression when using Facebook is mediated by feelings of envy. When envy is controlled for, Facebook use actually lessens depression.

Conclusion

Overall, the results of this survey of US college students show Facebook use in itself is not associated with depression. However, increased Facebook use was found to be associated with "Facebook envy", and envy was then associated with depression symptoms.

The study does have various strengths. The researchers carried out statistical tests to ensure their sample size was adequate to address their questions, and also assessed depression symptoms using a validated scale.

With regard to the study design, they researchers say that,: "Since this study explores relationships among Facebook use, envy and depression, the survey method is appropriate."

While it is true the survey design can explore relationships between these factors, this is all it can do. The study still cannot prove direct cause and effect relationships.

There are likely to be many other unmeasured factors also having an influence on the extent of Facebook use and feelings of envy and depression, including personal characteristics, lifestyle, and physical and mental health.

There are also some further limitations to the strength of the findings. For example, questions on frequency of Facebook use and feelings of envy were all rated on five-point scales.

Though this is likely to be the only available (and most appropriate) method to assess these factors, it can still introduce error, as frequency can mean different things to different people.

For example, one person could reply they use Facebook "very frequently" when they look at it every 10 minutes, while another person could consider very frequent use to be looking once a day. Similarly, the questions about envy will also lead to a highly subjective response.

It is also worth noting that although the researchers used a validated depression scale in their study, they have only carried out statistical analyses looking at relationships between frequency of symptoms, frequency of Facebook use, and frequency of envy. They have not looked at actual diagnoses of depression.

The study also includes a selective sample of young university students from the US, all of whom were taking the same courses. They may not be representative of other population groups.

Overall, the general theory that spending increased time looking at the posts of Facebook friends could contribute to feelings of envy, which could in turn lead to feelings of low mood, seems plausible.

However, many other factors are still likely to be mediating this relationship in different individuals.

This study will contribute to the growing body of literature assessing the possible health effects of social media use. 

If you find yourself troubled by envious thoughts that lead to symptoms of depression, you may benefit from cognitive behavioural therapy. Arguably, envy is an unhelpful pattern of thinking that brings you no benefits, but plenty of grief.

Our Moodzone area of the site contains podcasts and resources that may help you tackle patterns of unhelpful thinking.

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

Links To The Headlines

Facebook can cause depression in people who compare themselves with others. The Independent, February 4 2015

Facebook can lead to depression, researchers find. The Daily Telegraph, February 4 2015

Being jealous of Facebook friends 'leads to depression': Users who constantly compare their lives to others could be damaging their mental health. Daily Mail, February 4 2015

Facebook Could Make You Depressed – Study. Sky News, February 4 2015

Facebook makes you depressed: New research explains WHY social media leaves you feeling down. Daily Mirror, February 4 2015

Links To Science

Tandoc EC, Ferrucci P, Duffy M. Facebook use, envy, and depression among college students: Is facebooking depressing? Computers in Human Behavior. Published online February 2015

Categories: Medical News

E-cigarettes may make lungs vulnerable to infection

Medical News - Thu, 02/05/2015 - 13:50

“Vaping may not be as safe as smokers think, research suggests,” The Guardian reports. New research found that mice exposed to e-cigarette vapours comparable to a typical human level experienced mild lung damage and a reduced immune response to infection.

This may be due to the fact that the vapour produced by e-cigarettes contains free radicals (atoms and molecules that are toxic to cells).

Mice exposed to e-cigarettes daily for two weeks had increased levels of macrophages in their lungs. Macrophages are a type of white blood cell that remove damaged and dead cells, and are evidence of cell damage. These mice also had a worse response when infected with either a bacteria that causes pneumonia or the flu virus.

E-cigarettes vapour contains 1% of the amount of free radicals that are produced from normal cigarettes, so it is not clear from this study what effect this would have for humans.

Are e-cigarettes safer than normal cigarettes? Almost certainly. Are they 100% safe? Probably not.

If you are planning to quit smoking, especially if you have a lung condition such as chronic obstructive pulmonary disease, other types of nicotine replacement therapies (NRTs), such as patches, may be a safer option.

 

Where did the story come from?

The study was carried out by researchers from John Hopkins University in Maryland, the University of Tennessee Health Science Center and Louisiana State University. It was funded by the Flight Attendant Medical Research Institute and the US National Institutes of Health.

The study was published in the peer-reviewed medical journal PLOS ONE on an open-access basis, so the article is free to read online here.

The study was accurately reported in the UK media.

 

What kind of research was this?

This was an animal study looking at the effects of e-cigarettes on the immune system. The authors say that many people perceive e-cigarettes to be a healthy alternative to cigarettes. However, there have only been limited studies in humans and animals on their safety.

They report that on current evidence, the US Food and Drug Administration (FDA), the World Health Organization (WHO) and the European Respiratory Society do not consider them a safe alternative. This study in mice was designed to look specifically at the effect of e-cigarettes on the immune system and their ability to fight a bacterial and viral infection of the lungs after exposure to e-cigarette vapour.

 

What did the research involve?

Eight-week-old mice were randomly assigned to be either exposed to e-cigarettes or normal air, and then their response to viral and bacterial infections was compared.

The mice in the e-cigarette group were put in a chamber in which a smoke machine delivered the equivalent of a two-second puff of menthol e-cigarettes (1.8% nicotine) every 10 seconds for one-and-a-half hours. This occurred twice per day for two weeks. The researchers stated that this level of exposure was comparable to the exposure you would expect to see in an “average” e-cig user.

The vapour was analysed to see if it contained free radicals, which are toxic to cells. A subset group were exposed in the same way to traditional flavoured e-cigarettes, also containing 1.8% nicotine. This level of vapour exposure gave them an average blood level of cotinine, a breakdown product of nicotine, of 267ng/ml. In humans who smoke cigarettes and e-cigarettes, the level is usually between 200ng/ml and 800ng/ml, so this was fairly low exposure.

At the end of the last exposure, both groups of mice were infected via the nose with either a bacterial infection of Streptococcal pneumonia or the viral infection influenza. Macrophages from the lungs of some mice from each group were grown in dishes and also exposed to these infections, to study their response.

The researchers then compared the level of infection and the immune response in mice exposed and not exposed to e-cigarettes.

 

What were the basic results?

The e-cigarette vapour contained free radicals. The level was just less than 1% of that found in cigarette smoke.

Compared to the mice exposed to air, lungs from mice exposed to e-cigarettes had:

  • increased levels of oxidative stress (evidence of damage from free radicals)
  • a 58% increase in the number of macrophages, indicating that they needed to remove damaged cells

After infection with Streptococcal pneumonia:

  • mice exposed to e-cigarettes had higher levels of the bacteria in their lungs
  • the macrophages from mice exposed to both types of e-cigarettes were less able to deal with the infection when grown in dishes, which may be why there was a higher level of bacteria in the lungs

After infection with influenza, mice exposed to e-cigarettes:

  • had higher levels of the virus four days after the infection
  • lost more weight 10 to 12 days after infection, which was taken as an indicator of more severe illness
  • two out of the 10 mice died, compared to none in the air-exposed group

After infection with a higher dose of influenza, 60% of mice exposed to e-cigarettes died, compared to 30% in the air-exposed group.

 

How did the researchers interpret the results?

The researchers concluded that, “E-cig exposure is not a safe alternative to cigarette smoking”. They say that the exposure caused “airway inflammation, oxidative stress, and impaired anti-bacterial and anti-viral responses that include increased bacterial burden and viral titers in the lungs, impaired bacterial phagocytosis [removal of bacteria by immune cells], and increased virus-induced morbidity and mortality”.

 

Conclusion

This animal study has shown that the vapour from e-cigarettes contains free radicals, which are toxic to cells and are linked to cancer. Exposure to e-cigarettes caused inflammation in the lungs of mice, with increased numbers of macrophages, which mop up damaged and dead cells. Mice exposed to e-cigarette vapour also had a reduced ability to fight both bacterial and viral infections.

Taken together, this is convincing evidence suggesting that e-cigarettes are not harmless. However, the effect of e-cigarettes was not compared to normal cigarettes in this study, so it is not clear how much safer they might be. The study was also not conducted in humans. An animal study such as this can give us a good idea of the effects that a chemical could have in humans. However, mice and humans do not have identical biology, so we cannot be certain that the effects would be identical.   

The authors worryingly report that in the US, despite e-cigarettes being marketed as an aid to help people stop smoking, they are gaining popularity among people who have never smoked. This could soon be the case in the UK. Studies such as this show that they could still be bad for your health, and contribute to the growing body of research investigating e-cigarettes, both in terms of their effectiveness as aids to stop smoking, and their possible health effects.

There are many other ways to help you stop smoking that do not potentially expose the lungs to harm (though they may still have side effects). These include nicotine patches, gum and inhalers, as well as medication designed to reduce cravings for cigarettes, such as Zyban (bupropion). Read more about stop smoking treatments, as well as the NHS Stop Smoking Services that are available.

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

Links To The Headlines

Vaping may not be as safe as smokers think, research suggests. The Guardian, February 4 2015

E-cigarettes 'increase the risk of flu and pneumonia'. The Independent, February 4 2015

E-cigarettes are 'NOT a safe alternative to smoking': Toxic chemicals harm the lungs and weaken the immune system, study claims. Mail Online, February 4 2015

E-Cigarettes Are Harmful To Lungs – Study. Sky News, February 5 2015

E-cigarettes are 'not a safe alternative'. ITV News, February 5 2015

Links To Science

Sussan TE, Gajghate S, Thimmulappa RK, et al. Exposure to Electronic Cigarettes Impairs Pulmonary Anti-Bacterial and Anti-Viral Defenses in a Mouse Model. PLOS One. Published online February 4 2015

Categories: Medical News

Flu and freezing weather may be driving up winter death rates

Medical News - Wed, 02/04/2015 - 16:00

"The current death rate in England and Wales is running about one-third higher than its normal rate for this time of year," BBC News reports. A combination of flu and very cold weather may be responsible.

The BBC's story comes from the latest official statistics on deaths in England and Wales. They show that in the last three weeks of January, death rates were significantly higher than predicted for the time of year.

In addition, over the last six weeks a significantly higher than predicted death rate was reported in people aged 65 and above living in England. 

Although the cause of these spikes is uncertain, experts point out they coincide with both seasonal increases in respiratory problems – in particular the flu – and the recent cold snap.

The number of deaths always rises in winter, especially among elderly people. This is because of the colder weather and increases in respiratory problems.

While flu is a viral infection, it can make the lungs vulnerable to bacterial infections, such as pneumonia, which can be fatal in the elderly.

Who should have the seasonal flu jab?

Flu is not a serious threat for most fit and healthy adults, but the elderly and those with other illnesses, such as diabetes and asthma, are at risk of developing serious complications, including pneumonia.

See your GP about the flu jab if you're 65 or over, or if you have any of the following problems (however old you are):

Your GP may advise you to have a flu jab if you have serious liver disease, multiple sclerosis (MS), or other diseases of the nervous system.

Read more about who should have the flu jab.

Pregnancy

If you're pregnant, you should have the flu jab, regardless of the stage of pregnancy you've reached.

Pregnant women are more prone to complications from flu that can cause serious illness for both mother and baby.

If you are pregnant and catch flu, talk to your GP urgently as you may need treatment with antiviral medicine.

Read more about the flu jab in pregnancy.

Children

The flu vaccine is recommended for:

  • children over the age of six months with a long-term health condition
  • healthy children aged two, three and four

Children aged between six months and two years of age who are eligible for the flu vaccine should have the flu jab.

Children eligible for the flu vaccine aged between two and 18 will usually have the flu vaccine nasal spray.

Read about who should have the children's flu vaccine.

Where did the story come from?

The figures used in the BBC story come from the Office for National Statistics (ONS), which produces figures on issues of public importance.

It is also based on an analysis of mortality figures from Public Health England (PHE), the body responsible for maintaining the nation's health. These are both government bodies.

The BBC also included an interview with Professor John Newton, chief knowledge officer at PHE. One explanation for the higher than usual death rates is the prevalence of the H3N2 sub-type, a flu virus.

Professor Newton reportedly said that while PHE tries to anticipate which subtypes of the virus may be circulating in any year so the virus can be vaccinated against, the type this year may have mutated and might not be as well matched to vaccines at the end of the flu season as at the beginning.

What were the figures?

The ONS has published weekly figures on deaths registered in England and Wales from December 5 2014.

This shows that in the week beginning January 9 2015, there was a total of 16,237 deaths, followed by a total of 14,866 deaths in the week beginning January 16 2015, and 13,934 deaths in the week beginning January 23 2015. 

This rate is about one-third higher in the last two weeks compared with deaths over the same period in the previous five years.

The majority of these deaths were in those aged 65 or over. For example, in the week starting January 16 2015, 13,083 of the deaths were in those aged 65 and over.

According to the ONS, in the week beginning January 9 2015 and January 23 2015, 3,515 and 3,215 of all deaths were registered as caused by respiratory disease. 

The PHE surveillance report points out the estimated 16,237 deaths in week two and the 14,866 deaths in week three of January was above the upper limit predicted for the time of year.

In England, PHE says there have been excess deaths from week 50 in 2014 up to week four in 2015 among those over the age of 65 in England. They point out the excess deaths coincide with circulating influenza and recent cold snaps.

Significant excess deaths were also seen in children under five and in 15- to 64-year-olds in the first week of this year.

Similar excess deaths were seen in Scotland and Wales during this period, but not in Northern Ireland.

How did the researchers interpret the results?

PHE says there are always a higher number of deaths in winter months compared with the summer, and that some peaks in mortality above the expected level typically occur in winter.

This is most commonly the result of factors such as cold snaps and the increase in respiratory viruses, particularly the flu.

However, PHE also says "acute" weekly excess mortality rates "triggers further investigations of spikes and informs any public health responses".

Conclusion

There are always more deaths in winter than other seasons, particularly among elderly people. But why these fairly dramatic spikes in the death rate have occurred is still not understood.

It should be noted these figures are provisional, as there can be a delay in the ONS receiving the data.

Although the media has focused on the likely cause being flu, the numbers provided are for all respiratory conditions. Cold weather can exacerbate many of these conditions, such as asthma and chronic obstructive pulmonary disease.

For most fit and healthy people, flu is not a serious threat, but the elderly and those with other illnesses, such as diabetes and asthma, are at risk of developing serious complications, including pneumonia.

It's important to stay healthy in winter and protect yourself against illness.

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

Links To The Headlines

Death rate up by a third in January. BBC News, February 4 2015

Death rate rises as cold snap grips UK. The Guardian, February 4 2015

Categories: Medical News

Modified bacteria may be useful in treating diabetes

Medical News - Wed, 02/04/2015 - 14:45

“Breakthrough pill can cure diabetes,” is the completely misleading report in the Daily Express. While researchers have achieved some level of success in using bacteria to improve diabetes control in rats, this in no way amounts to a cure for humans.

The rats had an equivalent of type 1 diabetes, where the pancreas fails to produce the insulin needed by the body to regulate glucose.

The rats were given a daily pill of a genetically modified bacterium. This engineered bacterium secreted a compound that converted cells in the lining of the gut to produce insulin. 

After 90 days, these diabetic rats were able to reduce blood glucose levels in a similar way to healthy rats. While diabetic rats fed a normal type of this bacterium had 60% lower levels of insulin and were not able to reduce their blood glucose levels adequately.

Though the treated diabetic rats were able to produce more insulin, the overall level of insulin was still half that of normal rats.

This is preliminary research and there are many questions unanswered, such as how many cells might be converted over time. In addition, it should be made clear that this was not a probiotic pill. This was a genetically modified bacterium.

And, even assuming the engineered bacterium was safe to use in humans, an increase in insulin levels, while welcome, does not amount to a cure for diabetes.

Where did the story come from?

The study was carried out by researchers from Cornell University, New York and was funded by the US National Institutes of Health and the Hartwell Foundation. A conflict of interest has been declared by one of the authors as he is involved with a company that has licensed this technology.

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

The pill is not strictly a “probiotic” as reported by the media. Probiotics are live bacteria and yeasts that are usually present in the human body. The bacteria in the pill in this study has been genetically engineered to secrete a compound called GLP-1, and it is not known what effects this might have if ingested by humans.

Any talk of a cure for diabetes is highly misleading, and arguably irresponsible, as it may offer false hope to people living with diabetes.

What kind of research was this?

This was an animal study in which diabetic rats were given a daily pill of a modified bacterium to see what effect it had on their glucose and insulin levels.

Insulin regulates the level of glucose in the blood and is produced by beta cells in the pancreas. In type 1 diabetes, the pancreas no longer produces insulin as the beta cells have been destroyed by the body’s immune system, and so insulin injections are required. While people with type 2 diabetes have a reduced response to insulin, so higher levels are needed to maintain healthy blood glucose levels.

Initially the pancreas responds by making extra insulin, but over time this fails. Type 2 diabetes is managed through diet, medication and in some cases, insulin.

Previous research found that a compound called GLP-1 can convert intestinal cells into cells that produce insulin. The problem is that GLP-1 in humans breaks down quickly in the blood (it has a very short half-life) so the challenge is to find a way to move the compound into the intestine.

These experiments were conducted on cells in the laboratory setting. The researchers wanted to see if they could find a way to get GLP-1 to intestinal cells in rats and whether these cells could be reprogrammed as they were in the laboratory.

What did the research involve?

The researchers engineered Lactobacillus, a bacterium that is usually present in the human gut, to secrete a compound called GLP-1. They created a pill of these bacteria and gave it to rats with type 1 diabetes to see if it could deliver GLP-1 to the gut wall. They then investigated whether it changed the type of cells lining the intestine so that they could produce insulin.

Rats with type 1 diabetes were given two pills daily for 90 days of either:

  • engineered Lactobacillus that secrete GLP-1
  • normal Lactobacillus

Healthy rats were kept in the same conditions and given a placebo to act as a control.

To test whether the GLP-1 had converted any cells to produce insulin, after 51 days the rats were fasted for 10 hours and then given an injection of glucose. Blood glucose and insulin levels were measured after 30 minutes, one hour, one and a half hours and two hours.

At the end of the 90 days, the cells lining the intestine and the pancreas were examined and the level of gut bacteria was measured.

What were the basic results?

There was no significant difference in the blood glucose or insulin levels in diabetic rats fed engineered Lactobacillus compared with healthy control rats. Whereas diabetic rats fed normal Lactobacillus had higher blood glucose and lower blood insulin levels, as would be expected.

The level of insulin in the intestines of rats fed engineered Lactobacillus was more than five times higher than either of the other groups of rats. These rats had insulin-secreting cells in their intestines that had features of beta cells (the cells that produce insulin in the pancreas). These cells appeared to produce insulin in response to glucose. On average, 0.06% of the intestinal cells had been converted to secrete insulin.

Rats fed engineered Lactobacillus had 60% more total insulin than those fed normal Lactobacillus.

The overall level was half that of the control rats.

How did the researchers interpret the results?

The authors concluded that feeding diabetic rats the genetically engineered bacteria can cause them to produce insulin in response to eating, which significantly reduced their blood glucose levels. They say this appeared to have been produced from cells in the intestine that had been transformed from normal gut cells to insulin secreting cells. The researchers call for further work to be done to fully understand the mechanism involved.

Conclusion

This animal research has shown that a pill of genetically engineered Lactobacillus can convert cells lining the gut into cells that produce insulin in rats. This conversion was made by stimulating the cells with a compound called GLP-1 that was secreted by these modified bacteria that are usually present in the human gut.

The researchers were able to demonstrate that the cells had changed function to become more like the beta cells that usually produce insulin in the pancreas. They also showed that the insulin reduced the rats’ blood glucose levels to that of control rats.

There are a number of questions that need to be addressed before this new technique progresses to primate studies on the long road to becoming a treatment for either form of diabetes. Over the 90 days 0.06% of the intestinal cells were converted but it is unclear whether this proportion would increase over time and whether this depends on the dose of bacteria given. It is also not known whether these cells need daily bacteria to continue to behave like cells from the pancreas or whether the change is permanent and the cells can renew.

There are also unanswered questions about what effect having a reduced number of normal intestinal cells could have on the function of the gut. Finally, it will need to be determined how any such cell renewal is controlled so that it does not go into overdrive and produce too many insulin producing cells.

Overall, the results of this preliminary piece of research are encouraging in the search for a possible cure for diabetes, though this is still a long way off.

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

Links To The Headlines

Breakthrough pill can CURE diabetes: New drug fights both types of killer disease. Daily Express, February 3 2015

Both types of diabetes could be CURED by a daily probiotic pill that 'rewires' the body, scientists claim. Mail Online, February 3 2015

Links To Science

Duan FF, Liu JH, March JC. Engineered Commensal Bacteria Reprogram Intestinal Cells Into Glucose-Responsive Insulin-Secreting Cells for the Treatment of Diabetes. Diabetes. Published online January 27 2015

Categories: Medical News

MPs vote to give the go-ahead to three-parent IVF

Medical News - Wed, 02/04/2015 - 13:30

“In an historic move, MPs have voted in favour of the creation of babies with DNA from two women and one man,” BBC News reports. The UK is set to become the first country to license the technique known as three-parent IVF, which could potentially be used to prevent babies being born with mitochondrial diseases.

Many researchers welcomed the news.

Doug Turnbull, Professor of Neurology at Newcastle University, said: “I'm delighted for patients with mitochondrial disease. This is an important hurdle in the development of this new IVF technique ... and something the UK should rightly be proud of.”

The news was also welcomed by government officials. Professor Dame Sally Davies, the Department of Health’s Chief Medical Officer, said: “I’m delighted that MPs have voted to approve these regulations and hope the Lords will do the same. Mitochondrial donation will give women who carry severe mitochondrial disease the opportunity to have children without passing on devastating genetic disorders. It will also keep the UK at the forefront of scientific development in this area.”

Though other experts were not so optimistic. Dr Paul Knoepfler, associate professor at the University of California, Davis, is quoted in The Daily Telegraph as saying that the UK could be on the brink of a “historical mistake”. “Since this is uncharted territory and the children born from this technology would have heritable genetic changes, there are also significant unknown risks to future generations.”

The proposed change to the law, specifically an amendment to the Human Fertilisation and Embryology Act, will now go the House of Lords, who do have the power to delay the passage of the amendment into law.

What are mitochondrial diseases?

Almost all of the genetic material in our bodies is inside the cell nucleus that contains 23 chromosomes inherited from our mother and 23 inherited from our father. However, there is also a small amount of genetic material contained in cellular structures called mitochondria, which produce the cells’ energy. Unlike the rest of our DNA, this small amount of genetic material is passed to the child only from the mother. There are a number of rare diseases caused by gene mutations in the mitochondria. Women carrying these mutations will pass them directly to their child, with no influence from the father.

The IVF technique being considered aims to prevent these “mitochondrial diseases” by replacing the mother’s mitochondria with healthy mitochondria from a donor, thereby creating a healthy embryo.

Despite the media-friendly nickname, the techniques do not really constitute three-parent IVF. Only 1% of DNA would come from the “third parent”.

It is probably more accurate to consider the technique as a form of donation, akin to blood donation.

How many women could benefit from the technique?

modelling study published last month estimated that 2,473 women in the UK could benefit from the new IVF technique. This was based on the proportion of women known to be at risk in the north east of England, so does not take into account variations across the UK or US in terms of ethnic diversity or average maternal age.

The researchers based these estimations on data on how many women have a mitochondrial DNA (mtDNA) mutation and whether this affects their fertility.

The researchers concluded if all women in the UK estimated to have an mtDNA mutation wanted to have a child and had the new IVF procedure, this could benefit 150 births per year.

What is mitochondria replacement?

There are two IVF mitochondria replacement techniques currently at the research stage, called pronuclear transfer and spindle transfer. These are the techniques under debate.

Pronuclear transfer involves an egg during the process of fertilisation. In the laboratory, the nucleus of the egg and the nucleus of the sperm, which have not yet fused together (the pronuclei) are taken from the fertilised egg cell containing the “unhealthy” mitochondria and placed into another donor fertilised egg cell, which has had its own pronuclei removed. This early-stage embryo would then be placed into the mother’s body. The new embryo would contain the transplanted chromosomal DNA from both of its parents, but would have “donor” mitochondria from the other egg cell.

The alternative mitochondria replacement technique of spindle transfer involves egg cells prior to fertilisation. The nuclear DNA from an egg cell with “unhealthy” mitochondria is removed and placed into a donor egg cell that contains healthy mitochondria and has had its own nucleus removed. This “healthy” egg cell can then be fertilised.

Pronuclear transfer and spindle transfer are said to be potentially useful for the few couples whose child may have severe or lethal mitochondrial disease, and who would have no other option for having their own genetic child. It is estimated that in the UK, around 10-20 couples a year could benefit from these treatments. 

What ethical concerns have been raised about the techniques?

There are obvious ethical implications from creating an embryo with genetic material from three parents.

Among the questions raised are:

  • Should the details of the donor remain anonymous, or does the child have the right to know who their “third parent” is?
  • What would be the long-term psychological effects on the child knowing it was born using donated genetic tissue?

Opponents of these types of treatments cite what can be broadly summarised as the “slippery slope” argument. This suggests that once a precedent has been set for altering the genetic material of an embryo prior to implantation in the womb, it is impossible to predict how these types of techniques might be used in the future.

Similar concerns were raised, however, when IVF treatments were first used during the 1970s. Today, IVF is generally accepted.  

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

Links To The Headlines

MPs say yes to three-person babies. BBC News, February 3 2015

'Three-parent babies': Britain votes in favour of law change. The Independent, February 3 2015

Three-parent babies could be at greater risk of cancer, warn scientists. The Daily Telegraph, February 3 2015

Three-parent babies is not 'playing God', says Cameron as MPs vote to legalise IVF technique in Britain. Mail Online, February 3 2015

Babies with 3 different parents could soon be reality and benefit 2,500 women by end of year. Daily Mirror, February 3 2015

Categories: Medical News

Strenuous jogging 'as bad as doing no exercise' claim

Medical News - Tue, 02/03/2015 - 15:00

“Too much jogging 'as bad as no exercise at all',” BBC News reports. However, the results of the new Danish study on which this headline is based, are not as clear cut as the media has made out.

The study involved about 1,500 people in Denmark. It found that light to moderate jogging was associated with living longer compared with being sedentary, but strenuous jogging was not.

A major limitation to this study was that once the joggers were split into groups by duration, frequency, and pace, some individual groups – particularly the most active groups – were much smaller. These small numbers mean the analyses are less able to detect differences between these small groups and the sedentary group, even if they do exist.

Overall, the study does not impact the current physical activity recommendations for adults.

While it is important that people do not push themselves over their limit, in general, the more common problem is people not doing enough exercise to meet these recommendations.

 

Where did the story come from?

The study was carried out by researchers from the Frederiksberg Hospital in Denmark and other research centres in Denmark and the US. The study was funded by the Danish Heart Foundation.

The study was published in the peer-reviewed Journal of the American College of Cardiology.

The Daily Telegraph’s headline – “Fast running is as deadly as sitting on couch” – is too sensationalist given the limitations to the study, which are not mentioned.

While BBC News and the Daily Mail commit the journalistic sin of stating “too much of x is bad for you”; an entirely uninformative statement of the obvious. “Too much” of anything is bad for you. That is what “too much” means; a quantity that is so excessive it poses a threat to wellbeing.

A more useful statement would be explaining how much is too much, but unfortunately this study cannot conclusively provide this information.

 

What kind of research was this?

This was a prospective cohort study aiming to find out what the ideal “dose” of jogging would be for lengthening your life. The researchers report that although people who are physically active have longer lives, the ideal dose of exercise (in terms of intensity, duration and frequency) for achieving the greatest impact on lifespan is not known.

The researchers’ previous study on jogging suggested that jogging up to 2.5 hours in total a week, over up to three sessions, at a slow or average pace was associated with the lowest risk of death during follow-up. Jogging more or less than this was not associated with a reduced risk of death. The researchers investigated this further in the current study.

While people could be randomly assigned to different patterns of exercise, it is unlikely that they would continue to exercise as instructed over their entire lifetime. Therefore a cohort study is likely to be the most feasible way of comparing the effect of people’s normal physical activity patterns on a long-term outcome such as lifespan/risk of death. As with all studies of this type, the main limitation is that people who are physically active may also have other habits (such as healthy eating) that influence their likelihood of death. The researchers need to take these confounders into account in their analyses to try to isolate the effect of the physical activity pattern alone.

 

What did the research involve?

The researchers identified healthy joggers and healthy non-joggers taking part in the Copenhagen City Heart study. They followed these people up over two years to identify any people who died in that period. They then compared the risk of death in light, moderate and strenuous joggers with that of non-joggers.

The Copenhagen City Heart study took a random sample of nearly 20,000 white adults aged 20 to 93 living in Copenhagen in January 1976. Participants were sent a survey four times during follow-up. For the current study, researchers excluded people who had a history of heart disease, stroke or cancer.

The current study looked at data on physical activity collected from 2001 to 2003, the fourth time survey data had been collected from participants. The sample included original participants from 1976 and an additional sample of younger individuals. The recruitment of these additional people was reported in previous publications, and not in the current study.

The study assessed what type and how much physical activity people did in their leisure time. People were considered “sedentary” if they were almost entirely inactive in their leisure time e.g. reading, watching TV, or doing only very light activity such as gentle walking for less than two hours a week.

Those who jogged were asked about their pace, total time jogging per week, and frequency of jogging per week. This information was used to categorise them as:

  • light joggers – less than two and a half hours a week at a slow or average pace (about five miles an hour) three times a week or less
  • moderate joggers – between light and strenuous jogging in terms of pace, duration, and frequency – so for example, could be at a slow pace but more than three times a week, or up to a fast pace two and a half to four hours in total in up to three sessions a week
  • strenuous joggers – for more than four hours a week at a fast pace (more than seven miles an hour) at any frequency, or two and a half to four hours a week at a fast pace more than three times a week

Participants were followed up to 2013, and researchers managed to follow up almost all participants. Anyone who died in this period was identified through a national death register.

Analyses compared 1,098 joggers versus 413 sedentary non-joggers. The researchers analysed the data in a way that took into account differences in age between joggers and non-joggers. Analyses were also adjusted for characteristics that the participants reported in the surveys:

  • gender
  • smoking
  • alcohol intake
  • diabetes
  • education

 

What were the basic results?

Joggers tended to be younger (average age around 40 compared to 61 in non-joggers), have lower blood pressure and body mass index (BMI), and be less likely to smoke or have diabetes. The joggers ranged in age from 20 to 86 years, and the non-joggers from 21 to 92 years.

During follow-up there were 28 deaths among the 1,098 joggers (2.6%) and 128 deaths among sedentary non-joggers (31%).

Quantity

Analyses by quantity of jogging found that those jogging between one and 2.4 hours a week were less likely to die during follow-up than sedentary non-joggers. Those jogging for more time each week did not differ from sedentary non-joggers in risk of death.

Frequency

Analyses by frequency of jogging found that those jogging up to three times a week were less likely to die during follow-up than sedentary non-joggers. Those jogging more frequently did not differ from sedentary non-joggers in risk of death.

Pace

Analyses by pace of jogging found that those jogging at an average pace were less likely to die during follow-up than sedentary non-joggers. Those jogging at a slow or fast pace did not differ from sedentary non-joggers in risk of death.

Overall jogging “dose”

When combining all of these factors together, the researchers found that after adjusting for confounders, only light jogging was associated with significantly lower risk of death than sedentary non-joggers. Moderate joggers did have a slightly lower risk of death, but this difference was not large enough to rule out with a high level or certainty the possibility of the difference happening just by chance (it was not statistically significant).

 

How did the researchers interpret the results?

The researchers conclude that their findings show that light and moderate joggers have a lower risk of death than sedentary non-joggers during follow-up. However, strenuous joggers did not differ in their risk of death during follow-up to those who are sedentary. They note that more research is needed before this finding could be incorporated into physical activity recommendations for the general public.

Conclusion

This study has suggested that light to moderate jogging could be associated with living longer compared with being sedentary, but strenuous jogging might not be.

Due to the fact that this data was collected prospectively, there are considerable limitations. The main limitation is that although the total number of joggers was quite high (around 1,000), once these joggers were split up by duration, frequency and pace of jogging, some of the individual groups were much smaller. This was particularly the case in the most active jogging categories (those who jogged more often, for longer, and at a higher pace). This reduces the ability of the analysis to detect differences between these smaller groups and the sedentary group.

For example, there were only 36 people who were classed as “strenuous” joggers, and only two of these people died. These small numbers mean that we cannot say with certainty that there is definitely no difference between people in the most active jogging categories and the people who are sedentary.

The authors also note that even slow jogging would count as vigorous exercise, and strenuous jogging would be considered heavy vigorous exercise. This is important to bear in mind when considering the current UK physical activity recommendations for adults to be active daily and either:

  • 150 minutes of moderate activity per week in bouts of 10 minutes or more
  • 75 minutes of vigorous activity spread across the week

In addition, while the authors took various factors that could affect their results into account, such as age, these adjustments may not have removed their effect completely. They acknowledge that their study cannot determine whether the jogging patterns themselves directly caused the differences in risk of death seen. Jogging was also only assessed once in the study, and activity patterns may have changed over time. Also, death was the only outcome assessed, so we don’t know what the associations with other outcomes such as general fitness and quality of life were.

Overall, the study does not contradict the current physical activity recommendations and the issue of people not doing enough exercise is more likely to be a concern than people over-exercising.

Too many people in the UK are failing to meet the recommended levels of physical activity. This is reflected in the latest obesity statistics.

Still, it’s never too late to start – read more advice about how you can gradually increase your activity and fitness levels.

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

Links To The Headlines

Too much jogging 'as bad as no exercise at all'. BBC News, February 3 2015

Fast running is as deadly as sitting on couch, scientists find. The Daily Telegraph, February 3 2015

Stop that binge jogging! Three times a week is best for you... and too much is as bad as doing nothing. Daily Mail, February 3 2015

Links To Science

Schnor P, O’Keefe JH, Marott JL, et al. Dose of Jogging and Long-Term Mortality. The Journal of the American College of Cardiology. Published online February 2015

Categories: Medical News

Teen screen time linked to less sleep

Medical News - Tue, 02/03/2015 - 14:30

"Teenagers sleep less when they have more computer screen time, says study,” The Guardian reports.

The study involved almost 10,000 older teens in Norway and included any device that had a screen, such as tablets, laptops, smartphones, games consoles, PCs and TVs. It found that those who used electronic devices in the hour before going to bed took longer to fall asleep. They were also more likely to feel they needed at least another two hours sleep more than they actually got. The same was true of those who spent at least two hours of their leisure in various forms of screen time. The more time a teenager spent on electronic devices, the less sleep they tended to get.

It’s important to note that the researchers did not assess whether any of the differences seen had any impact on the teens’ daily lives or health. Also, the study design means that we cannot interpret this as saying that device usage directly causes lack of sleep, as they were both measured at the same time. In some cases, teenagers unable to sleep may have used a device out of boredom.

However, it is important to stress that getting enough sleep is important for all age groups.

 

Where did the story come from?

The study was carried out by researchers from Uni Research Health and other research centres in Norway. It was funded by Uni Research Health and the Norwegian Directorate for Health and Social Affairs.

The study was published in the peer-reviewed BMJ Open. As the name suggests, this is an open-access journal, meaning the study can be accessed for free online here.

While the UK media reported the findings of the study accurately, they did not mention that this type of study cannot identify cause and effect.

The suggestion by some sources that restricting screen time in the evening would improve sleep also cannot be proven by this study. However, reducing activities that might replace or distract from sleep may improve sleep patterns.

 

What kind of research was this?

This was a cross-sectional study looking at whether there was a relationship between the amount of time that adolescents spend using electronic devices and how much sleep they get.

The researchers say that electronic devices have been used much more in the past decade, including by teens. This could be one factor contributing to the “shift towards poorer sleep” in adolescents seen over the same period. Several studies have found that more device usage is linked to less sleep. This body of research mainly focused on one or two devices (often TV and computers), and it has been suggested that more research is needed on newer devices and assessing different measures of sleep and sleep problems.

While the study design can tell us whether certain characteristics tend to occur together (e.g. more screen time and less sleep), it cannot tell us if one causes the other. The study also cannot tell us how these characteristics have changed over time.

 

What did the research involve?

The researchers assessed electronic device use, as well as sleep, in 9,843 adolescents aged 16 to 19 years old. They analysed whether those who used screens or electronic devices more tended to sleep different amounts to those who used them less.

The adolescents all lived in one county in Norway (Hordaland) and were taking part in the youth@hordaland study. This study invited all adolescents born from 1993 to 1995, and all students attending secondary school in 2012 in Hordaland to participate. Looking at devices and sleep was not the main aim of the study, which focused on mental health problems. Teens who agreed to participate (53% of those asked) were sent a web-based questionnaire to fill out.

The teens were asked about their use of six different electronic media devices and whether they used them in the bedroom during the hour before they went to sleep. The devices were:

  • PC
  • Cell phone
  • MP3 player
  • Tablet
  • Games console
  • TV

They were also asked how much time they spent on various on-screen activities outside of school hours on weekdays.

The teens were also asked:

  • their typical bedtimes and getting up times in the week and on weekends
  • how long it took them to fall asleep once in bed
  • how much time they spent awake due to waking up in the night
  • how much sleep they needed to feel rested

The researchers used this information to find out how much “sleep deficit” the teens had by subtracting how much sleep they actually reported having from how much they said they needed.

They looked at the difference in sleep among those using devices for different amounts of time.

 

What were the basic results?

The researchers found that most of the teens used electronic devices in the hour before going to sleep – between about 30% and 90%, depending on the device. Boys spent about six-and-a-half hours on leisure “screen time” on weekdays, and girls spent about five-and-a-half hours.

Using any electronic device in the hour before sleep was associated with an increased likelihood of taking more than an hour to fall asleep once in bed and also with needing at least two hours more sleep than they actually had. The same was true of any leisure screen time activity of over two hours.

The more time a teen spent on electronic devices, the less sleep they tended to get. In addition, those who used multiple devices also tended to be more likely to take at least an hour to fall asleep than those using just one device.

They found no differences between boys and girls in their analyses of the relationship between devices and sleep.

 

How did the researchers interpret the results?

The researchers conclude that adolescents frequently use electronic devices during the day and at bedtime. Those who used these devices more tended to sleep less. They say this suggests that “recommendations on healthy media use could include restrictions on electronic devices”.

 

Conclusion

This large cross-sectional study found that older teens who use their electronic devices more tend to sleep less.

The findings are unlikely to come as much of a surprise and it supports findings from previous studies on “screen time”. The new aspect of this research is that it has studied newer devices such as tablets, MP3 devices and phones, as well as PCs and TV. All of them seemed to have similar associations with sleep. The researchers say they did not assess why the teens were using the devices – for example, whether they were doing homework. They also note that some of the differences seen were small, and they did not assess whether they had any impact on the teens’ daily lives or health.

However, the study design means that we cannot interpret this as saying that device usage directly causes lack of sleep, as they were both measured at the same time. It is also possible that teens who cannot sleep use the devices to entertain themselves.

Another limitation is that the study did not take into account any other characteristics of the teens in their analyses. They also only used the teens’ own reports of their sleep patterns.

Overall, the practical implications of the study are probably limited. However, getting enough sleep is important for all age groups. Read more information and advice about children and sleep.

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

Links To The Headlines

Teenagers sleep less when they have more computer screen time says study. The Guardian, February 3 2015

Banish smartphones and computers from bedroom to get a good sleep, say scientists. The Daily Telegraph, February 2 2015

Too much exposure to smartphone screens ruins your sleep, study shows. The Independent, February 3 2015

Teenagers who use screen for more than four hours a day 'take longer to fall asleep and get poorer quality rest'. Mail Online, February 3 2015

Laptops and phones are causing teens to lose sleep. Daily Express, February 3 2015

Links To Science

Hysing M, Pallesen S, Stormark KM, et al. Sleep and use of electronic devices in adolescence: results from a large population-based study. BMJ Open. Published online February 2 2015

Categories: Medical News