NHS Choices

Lightning Process 'could help children with chronic fatigue syndrome', study claims

NHS Choices - Behind the Headlines -

"Controversial Lightning Process 'helps children with chronic fatigue syndrome'," reports The Guardian.

The story is based on a UK study investigating whether a treatment called the Lightning Process helped teenagers being treated for chronic fatigue syndrome (CFS), also known as ME (myalgic encephalomyelitis).

The study randomly split 100 young participants into two groups: those who received standard CFS/ME treatment and those who received the standard treatment plus the Lightning Process (LP).

LP treatment involved an intensive three-day group-therapy course aiming to teach participants how to use their brain to improve their body's health.

Researchers found those who received the LP were more active, less tired and less anxious after six months. At 12 months, they also had improved depression scores and school attendance.

However, this therapy is not recommended by the NHS, which currently suggests behavioural and exercise therapy for people with CFS/ME.

There are an estimated 250,000 people affected by chronic fatigue syndrome in Britain, according to the ME Association charity.

It's not known what causes CFS/ME, but there are a number of theories, such as it being triggered by an infection.

Living with the condition can be difficult, with extreme tiredness and other symptoms making everyday activities challenging.

As well as support from family and friends, it might also be useful for people with CFS/ME to talk to others with the condition and perhaps find a local support group.

Where did the story come from?

The study was carried out by researchers from the University of Bristol and the University of Nottingham in the UK. It was funded by the National Institute for Health Research and two charitable trusts: The Linbury Trust and The Ashden Trust.

The study was published in the peer-reviewed medical journal Archives of Disease in Childhood, part of BMJ Journals, and is free to read online.

The media reporting of this study was generally accurate, but the Daily Telegraph's suggestion that the therapy helps children get back to school cannot be certain – there are a range of possible explanations for why children in the LP therapy group had better school attendance.

What kind of research was this?

This was a randomised controlled trial involving teenagers who had been diagnosed with CFS/ME. They were randomised to receive either usual care, or usual care plus the LP.

The LP is a therapy developed from osteopathy, life coaching and neurolinguistic programming (a behavioural psychotherapy that "retrains the brain"), and is used for a variety of conditions.

CFS/ME is a long-term illness with a wide range of symptoms, the most common being extreme tiredness.

It can also cause sleep problems, concentration problems, muscle or joint pain, headaches, a sore throat, flu-like symptoms, feeling dizzy or sick, or a fast or irregular heartbeat.

Current accepted treatments in the UK health service include cognitive behavioural therapy (CBT); a structured exercise programme called graded exercise therapy; and medication to control pain, nausea and sleep problems.

What did the research involve?

The researchers randomised 100 children aged 12 to 18 with diagnosed CFS/ME to receive either specialist medical care (SMC) or SMC plus the LP, and followed them up at 3, 6 and 12 months.

There were 51 participants in the SMC-only group. The SMC focused on improving sleep, and using activity management to establish a baseline level of activity (including school attendance, exercise and social activity) that was then gradually increased.

Sessions were delivered by professionals such as doctors, psychologists and physiotherapists. The number and timing of sessions were agreed with the teenager and their family.

There were 49 participants in the SMC-plus-LP group. In addition to the same SMC, they attended an LP course consisting of three different sessions, lasting four hours each, on consecutive days. They attended in groups of two to five.

The first was a theory session looking at:

  • stress response
  • how the mind and body interact
  • how thought processes can be positive or negative

This was followed by a group session in which participants were asked to think about what they could take responsibility for and change.

The third was a practical session in which participants were asked to choose a goal they wished to achieve, such as being able to stand for a longer period of time. They were given different thinking strategies to perform before and during attempting to achieve the goal. They also chose a further goal, to be attempted at home.

Each participant was offered two follow-up phone calls.

Outcomes assessed were:

  • physical function, measured using the 36-Item Short-Form Health Survey Physical Function Subscale (SF-36-PFS)
  • quality of life using quality-adjusted life years (QALYs), measured using the EQ-5D-Y standardised instrument
  • fatigue, using the Chalder Fatigue Scale
  • pain, using the Visual Analogue Scale (VAS)
  • anxiety and depression, using the Hospital Anxiety and Depression Scale (HADS)
  • school attendance (days per week)
  • child's use of health services, educational services or health-related travel, and other family costs, using a questionnaire
What were the basic results?

At six months after randomisation, data from 81 participants showed that those in the SMC-plus-LP group were:

More active

They had better physical function compared with the SMC-only group according to the SF-36-PFS scale of 0 to 100, where lower scores indicate worse physical function. The SMC-plus-LP group's average increased from a baseline of 53 to 81.7, and the SMC-only group's increased from 56 to 70.2 (adjusted difference in means 12.5, 95% confidence interval [CI] 4.5 to 20.5).

Less fatigued

They had less fatigue, scoring 14.4 compared with 19.8 in the SMC-only group on a scale of 0 to 33, where higher scores indicate more fatigue (adjusted difference in means 4.7, 95% CI 7.9 to 1.6).

Less anxious

They had greater improvement in anxiety symptoms as measured by the HADS (scored from 0 to 21, with higher scores indicating worse symptoms) than the SMC-only group. The SMC-plus-LP average score was 6.1, compared with 9.0 for the SMC-only group (adjusted difference in means 3.3, 95% CI 5.6 to 1).

At 12 months after randomisation, data from 79 participants showed that the SMC-plus-LP-group were:

More active, less fatigued and less anxious

They still had better physical function, less fatigue and improved anxiety symptoms compared with the SMC-only group.

Feeling better

The SMC-plus-LP group also had greater improvement in depression symptoms on the HADS – scored from 0 to 21, with higher scores indicating more-severe symptoms (adjusted difference in means -1.7, 95% CI -3.3 to -0.2).

Attending school more often

School attendance, as measured by attendance in the previous week, was better for the SMC-plus-LP group, at 4.1 days on average, than the SMC-only group's 3.1 days (adjusted difference in means 0.9, 95% CI 0.2 to 1.6).

How did the researchers interpret the results?

The researchers concluded: "This is the first randomised trial investigating the effectiveness of the LP for any condition. It is the first trial that has demonstrated the effectiveness of an intervention other than CBT for paediatric CFS/ME.

"The addition of the LP to SMC improved physical function at 6 and 12 months in adolescents with CFS/ME and this difference increased at 12 months."

Conclusion

The results from this very small randomised controlled trial showed that people having LP therapy in addition to usual CFS/ME care had improved physical function, fatigue and anxiety symptoms at six months, and improved school attendance and depressive symptoms at 12 months.

However, there are a number of limitations to this research that need to be considered:

  • Participants in both groups improved, so both treatments were effective to some extent.
  • This was a very small trial, and the results analysis involved fewer than the 100 people recruited. It would need to be repeated in a much larger group to demonstrate more robust findings.
  • A number of outcomes were looked at, so it was very likely that some of them would return positive findings by chance – the improvements might not have been due to the LP therapy.
  • Participants were not blinded – they were aware of the group they were in; therefore, their self-reported outcomes might have been biased. They may have been more likely to report positive outcomes because they knew they were getting additional therapy in the LP group.
  • Of all those eligible to participate in the trial, fewer than 30% agreed to take part. The reason why the majority didn't want to is unknown.

As the LP therapy was given in addition to the usual CFS/ME care, it certainly cannot be suggested as a replacement for the current usual care.

There's no single way of managing CFS/ME that works for everyone and, if you have the condition, you should be offered a treatment plan based on your symptoms. Your doctor should discuss all options with you and make you aware of any benefits and risks.

Links To The Headlines

Chronic fatigue therapy 'could help teenagers', study says. BBC News, September 21 2017

Controversial 'light' treatment for young ME patients - endorsed by celebrities - DOES work despite being labelled as 'quack medicine'. Mail Online, September 21 2017

Controversial Lightning Process 'helps children with chronic fatigue syndrome'. The Guardian, September 20 2017

M.E. 'Lightning Process' trains the brain to ward off tired thoughts. The Daily Telegraph, September 20 2017

Links To Science

Crawley EM, Gaunt DM, Garfield K, et al. Clinical and cost-effectiveness of the Lightning Process in addition to specialist medical care for paediatric chronic fatigue syndrome: randomised controlled trial. Archives of Disease in Childhood. Published online September 20 2017

 

Many teenagers reporting symptoms of depression

NHS Choices - Behind the Headlines -

Summary

"One in four British girls hit by depression at 14 as experts blame increase in cyber bullying and academic pressure," says the Sun after a large study found 24% of 14-year-old girls in the UK report symptoms of depression.

The Millenium Cohort Study followed more than 19,000 children born in the UK in 2000 to 2001. Parents completed surveys when the children were aged 3, 5, 7, 11 and 14 about any emotional difficulties they were having. At age 14, the children also completed a short questionnaire about their mental health.

Levels of anxiety and depressive symptoms were similar for girls and boys up to the age of 11. At age 14, parents reported 12% of boys and 18% of girls had emotional problems. But when the 14-year-olds themselves were asked about their mental health, 9% of boys and 24% of girls reported depressive symptoms.

Though the statistics are worrying, it is important to note that these were responses to questionnaires and not formal diagnoses of depression so the real figures are likely to be lower. However, it is still of concern that so many children are struggling with emotional problems.

If you have concerns about yourself or a child, see your GP as there are many effective treatments available including talking therapies.

Find more information and advice for young people on mental health problems.

Where did the story come from?

The study was carried out by researchers from University College London, and was funded by the Economic and Social Research Council and the Government.

It was published by the Centre for Longitudinal Studies, an Economic and Social Research Council resource centre based at University College London and is free to read online (PDF, 554kb).

In general, the media reported the research accurately, although few explained that the children had not been formally diagnosed with depression and had only reported some symptoms in a questionnaire.

What kind of research was this?

This was a cohort study in which children born in the millennium were followed up over 14 years through questionnaires given to both parents and the children themselves.

This type of observational study is good for looking at patterns of illness in the population. However, it relies on people agreeing to take part so can be subject to selection bias whereby only people with an interest in the topic complete the survey.

What did the research involve?

The Millenium Cohort Study recruited the parents of 19,517 children born in 2000 to 2001 from England, Scotland, Wales and Northern Ireland.

When the children were aged 9 months, 3, 5, 7, 11 and 14 years, the parents answered questionnaires about their physical, emotional, social, cognitive and behavioural development. They also provided details about their family relationships, economic status and family life.

When the children were aged 3 and above, the questionnaires included the Strengths and Difficulties Questionnaire which includes parental concerns about behaviour problems, hyperactivity and bullying, and gives a score out of 10, with higher scores indicating greater problems.

When the children were aged 14, they completed the Short Mood and Feelings Questionnaire. This consists of 13 statements. Children are asked if they felt the statements were true, sometimes true or not true reflections of how they felt in the previous two weeks:

  • I felt miserable or unhappy.
  • I didn't enjoy anything at all.
  • I felt so tired I just sat around and did nothing.
  • I was very restless.
  • I felt I was no good anymore.
  • I cried a lot.
  • I found it hard to think properly or concentrate.
  • I hated myself.
  • I was a bad person.
  • I felt lonely.
  • I thought nobody really loved me.
  • I thought I could never be as good as other kids.
  • I did everything wrong.
What were the basic results?

Average scores on the Strengths and Difficulties Questionnaire (0 to 10) completed by parents were low overall (a lower score indicating lesser problems):

  • Behaviour problems were more likely at the age of 3, with a score of just below 3, which then reduced and stayed around 1.
  • Emotional symptoms gradually increased from 1 to just over 2 by the age of 14.
  • Hyperactivity was the biggest problem, scoring around 3 at all ages.
  • Peer problems scored between 1 and 2 at all ages.

The proportion of children reported to have emotional problems by their parents increased with age:

  • at the age of 3, it was 8%
  • by 11, this had risen to 12%
  • at 14, it was still 12% for boys but had increased to 18% for girls

The proportion of children reported to have behaviour problems varied with age:

  • at the age of 3, 20% of boys and 17% of girls
  • at 5, 11% of boys and 7% of girls – at 14, 15% of boys and 11% of girls

According to the Short Mood and Feelings Questionnaire completed by 14-year-old children:

  • 24% of girls reported high levels of depressive symptoms
  • 9% of boys reported high levels of depressive symptoms

Ethnicity and household income results indicate that children from all backgrounds and socioeconomic status can suffer from symptoms of depression:

  • Prevalence for girls ranged from 9% of Black African and 15% of Bangladeshi background to 25% of white and 27% of mixed race.
  • Mixed-race boys were also more likely to have symptoms of depression, at 13% compared to 3% of those of Indian ethnicity.
  • 18% of girls from the highest income bracket, 23% from the lowest and up to 27% of those from the second lowest bracket had symptoms of depression.
  • 12% of boys in the second lowest bracket going down to 6% in the highest bracket had depression symptoms.
How did the researchers interpret the results?

The researchers concluded that "children's perspectives about their mental health may be different from their parents". They say this "highlights the importance of obtaining young people's own perspective of their mental ill-health, alongside other perspectives".

Conclusion

This large cohort study highlights high levels of depressive symptoms in children and adolescents.

It is however important to note that these are symptoms – we don't know how many of the children would be diagnosed with depression.

When parents complete the Short Mood and Feelings Questionnaire, it is estimated that it will accurately identify 75% of children with depression and 73% of children without depression. But it is less accurate when children complete it. Recent research suggests that it can identify 60% of children with depression and 61% of children without depression.

Despite these limitations, the fact that so many children report symptoms is of concern. Various experts in the media have suggested reasons, ranging from greater awareness of mental health issues and therefore increased reporting, to greater pressure from social media. Further research is needed to identify the causes.

It is important to seek help early for children with emotional problems and your GP is the best place to start. You can also contact the charity Young Minds that offers information and help to both young people and their parents or carers.

Links To The Headlines

Quarter of 14-year-old girls 'have signs of depression' BBC News, September 20 2017

How a quarter of girls are hit by depression: Shocking figures show teenagers are struggling to cope with school, stress and pressures of social media Mail Online, September 20 2017

Teenage Blues One in four British girls hit by depression at 14 as experts blame increase in cyber bullying and academic pressure The Sun, September 20 2017

One in four teenage girls are depressed, by their own accounts The Daily Telegraph, September 20 2017

One in four girls have depression by the time they hit 14, study reveals The Guardian, September 20 2017

A quarter of all 14-year-old girls are depressed, research shows The Independent, September 20 2017

Quarter of girls are depressed at 14 in mental health crisis The Times, September 20 2017

Links To Science

Patalay P, Fitzsimons E. Mental ill-health among children of the new century (PDF, 554kb) Briefing paper from Centre for Longitudinal Studies, UCL Institute of Education. Published online September 20 2017.

Single-injection vaccine device still a long way off

NHS Choices - Behind the Headlines -

"Scientists invent injection that could deliver every childhood vaccine in one go," reports The Independent. Various media sources have run stories on a new injection they claim could allow multiple childhood vaccines to be delivered in a single jab.

This follows the development in the US of a method of making a tiny, multilayered biodegradable device, or microstructure, that can be given via injection. The device has several compartments that can be filled with solutions to be released at different points in time.

For the study, mice were given a single injection of the microstructure, which had been loaded with two fluorescently labelled sugar solutions. The researchers showed that the device could release the solutions at different times and that the delivery seemed to be better than in mice who received the solutions via two separate injections.

This device could have great medical potential, but it's important to realise that this is very early research.

More stages of testing in mice would be needed before we could think about human trials. There may be many as-yet-unknown obstacles in terms of safety and effectiveness when considering using the device for human immunisation.

Where did the story come from?

The study was carried out by researchers from the Koch Institute for Integrative Cancer Research at Massachusetts Institute of Technology (MIT) in the US and was funded by the Bill & Melinda Gates Foundation. Individual researchers received various additional funding grants.

The study was published in the peer-reviewed journal Science and is free to read online.

The media reporting was generally representative of the study and discussed the potential applications of such a device, as well as some of the hurdles that still remain.

What sort of research was this?

This was laboratory research describing the manufacture of a 3D microstructure that could be used for pulsed delivery of a drug or vaccine in a single injection.

The authors explained how 3D microdevices could be used for tissue engineering and drug delivery. Depending on size, shape and composition, the internal architecture of 3D microdevices offers greater potential than single-layer devices.

However, this research is still at the early experimental stage.

What did the research involve?

The researchers fully described the technique they used to create the microdevice. The methods are complex and only described in brief here.

The device was made of lactide-glycolide copolymers, the most widely used biodegradable polymers for human applications. The fabrication technique ("StampEd Assembly of polymer Layers" or SEAL) involves the technology used to produce computer chips.

The first layer of the microstructure is created using heated polymers in a silicone mould. This is then repeated, using microscopic alignment, to add layer upon layer to create structures smaller than 400 micrometres.

The process was tested by creating a number of different microstructures, including a 3D star, table and chair.

The researchers' main aim was to produce a microstructure that could be injected into the body and deliver timed pulses of different vaccines or drugs. They made a microstructure with hollow bases, filled these with a test solution and then carried out various experiments.

What were the basic results?

The researchers created a device that could give a controlled release of a substance. It delivered a fluorescently labelled test solution in a separate pulsed release, with no leakage prior to the set release time.

The sealed structures, filled with two labelled sugar solutions set to be delivered in separate pulsed releases, were then injected into a group of mice.

This group was then compared with mice that received the solutions via two separate injections timed to match the release from the microstructures. When tested after one week and then again after one month, levels of the test solutions were higher in the blood of the mice that received the single injection.

The microstructure and its pulse-release capacity were also stable under variations of temperature and acidity.

How did the researchers interpret the results?

The researchers said: "These experiments demonstrate that one injection of core-shell particles can induce a long-term antibody response, outperform multiple time-matched injections, and achieve twofold dose sparing."

Conclusion

Injection of a microstructure device that can give time-delayed release of a vaccine or drug could have great potential in medicine.

As the researchers noted, the structures are tiny and fully biodegradable, so they shouldn't cause a foreign-body reaction.

But they also mentioned the size – the lightweight device could only hold a small amount of solution. However, the researchers suggested that varying the wall thickness to create larger cores could greatly increase the device's capacity.

At this stage, the device has only been tested in a single experiment in mice. Further research in mice would be needed to see whether you could move on to testing it in humans. It's very difficult to stay at this stage which human vaccines the device could potentially be used for or what obstacles there could in terms of safety and effectiveness.

Various experts have given their response to the findings.

Dr Anita Milicic, senior scientist at the University of Oxford's Jenner Institute, said: "Single-dose vaccination has been a long-standing goal of the WHO [World Health Organization]: since the early 1990s researchers have been trying to create a vaccine formulation that is capable of delivering the equivalent of two or three prime-boost vaccinations with a single immunisation.

"Achieving this would circumvent many obstacles that immunisation coverage faces today: non-compliance, missed or delayed doses, logistical problems of vaccine storage and administration in hard to reach parts of the world, wastage of expired/unused doses, and so on."

Dr Kevin Pollock, honorary lecturer in infection, immunity and inflammation at the University of Glasgow, cautioned: "It may be as long as 15 to 20 years before such delivery systems could be used in vaccines.

"It is not yet well understood how the human immune system would respond as it is much more used to receiving a single dose, being allowed to recover and then being immunised again.

"This demonstrates the difficulty of going from in vitro or in vivo systems using mice to a vaccine ready to be rolled out in the NHS. This group are not even at this point. Therefore, there is much work to be done to consider the safety of these vaccines."

Find out more about the current childhood vaccination schedule in England.

Links To The Headlines

Scientists invent jab that could deliver every childhood vaccine in one go. The Independent, September 16 2017

New technology could allow multiple vaccines to be delivered in single jab. The Guardian, September 14 2017

Links To Science

McHugh KJ, Nguyen TD, Linehan AR, et al. Fabrication of fillable microparticles and other complex 3D microstructures Science. Published online September 15 2017

Women more likely than men to lose interest in sex

NHS Choices - Behind the Headlines -

"Women get bored of having sex with their partner after just a year together, a new study suggests," is the rather crass story in the Mail Online.

The news is based on research that actually found multiple factors increased the likelihood of both men and women reporting a lack of interest in sex.

The findings come from interviews with more than 10,000 men and women in the UK about their sex lives.

Lack of interest in sex was associated with being in poor health, being in longer relationships (for women), and living with your partner – and varied with age.

Those who found it easier to talk about sex were less likely to report a lack of interest.

Where did the story come from?

The study was carried out by researchers from the University of Southampton, University College London, the London School of Hygiene and Tropical Medicine, and the University of Glasgow.

It was funded by the Medical Research Council, the Wellcome Trust, the Economic and Social Research Council, the Department of Health, and the Scottish Government Chief Scientist Office.

The study was published in the peer-reviewed journal BMJ Open on an open access basis and is free to read online.

As you'd expect, the study was covered widely in the UK media. The reporting was generally accurate, though statements like "how women get bored of having sex with their partner after just 12 months" in the Mail Online generalise the findings somewhat.

We don't know why some people lack interest in sex – boredom isn't mentioned in the study, and the majority of women in relationships lasting longer than a year didn't actually report a loss of interest in sex.

What kind of research was this?

This cross-sectional survey looked at factors associated with reporting a lack of interest in sex and examined if – and how – these differ by gender.

This type of research is good for looking at the attitudes and behaviours of a large number of people, but only investigates them at a single point in time, so trends over time and longer term outcomes can't be assessed.

And it also doesn't show cause and effect – in other words, it can't show that any one of the factors investigated can on its own lead to a lack of interest in sex.

There may be many personal reasons for a lack of interest that weren't investigated in this study.

What did the research involve?

The research used data taken from the third UK National Survey of Sexual Attitudes and Lifestyles (Natsal-3).

The survey involved 4,839 male and 6,669 female respondents aged 16 to 74 who reported having one or more sexual partners in the past year.

This study looked at factors associated with a lack of interest in sex.

The computer-assisted interviews took place in participants' homes with professional interviewers. Computer-assisted self-interviews were used for more sensitive questions.

Participants who'd had one or more sexual partners in the past year were asked: "In the last year, have you experienced any of the following for a period of three or more months?". They were given a list of difficulties, including "lacked interest in having sex".

Those reporting lacking interest in sex for at least three months were then asked how they felt about this, from "not at all distressed" to "very distressed".

Those answering a little, fairly or very distressed were defined as lacking interest in sex and having distress about it respectively.

The researchers then looked at the likelihood that reporting a lack of interest in sex lasting three or more months was associated with a range of factors, including:

  • leaving school at 16
  • unemployment
  • poor health
  • current depression
  • frequency of sexual activity
  • recent masturbation
  • relationship status
  • ease of communication about sex
  • pregnant or having children
  • previous sexually transmitted infection diagnosis

Analyses were then broken down by gender and age groups.

What were the basic results?

Overall, 15% of sexually active men and 34.2% of sexually active women reported lacking interest in sex for at least three months before the interview.

Having sex five or more times compared with not at all in the past four weeks reduced the likelihood of reporting a lack of interest in sex by 61% in men (odds ratio 0.39, 95% confidence interval 0.30 to 0.51) and 59% in women (OR 0.41, 95% CI 0.34 to 0.49).

Compared with women who'd been in a relationship for less than a year, women in a relationship for 1 to 5 years were 45% more likely to lack interest in sex (OR 1.45, 95% CI 1.2 to 1.76), and those in relationships for 5 to 15 years were almost 2.5 times more likely to lack interest in sex (OR 2.37, 95% CI 1.96 to 2.86).

These findings were only true for women, with no significant increase in likelihood found for men.

Women in a steady relationship but not living with their partner were 41% less likely to lack interest in sex compared with those living with their partner (OR 0.59, 95% CI 0.49 to 0.71). There was no significant difference for men.

Men were most likely to lack interest in sex between the ages of 35 and 44, with 17.2% reporting a lack of interest (95% CI 14.5% to 20.4%), and women were most likely to lack interest between the ages of 55 and 64, at 38.8% (95% CI 34.5% to 43.2%).

Finding it difficult to talk about sex, having depressive symptoms, being in "fair" or "bad" health, and not feeling emotionally close when having sex all increased the likelihood of a lack of interest in sex for both men and women.

How did the researchers interpret the results?

The researchers concluded: "Both gender similarities and differences were found in factors associated with lacking interest in sex, with the most marked differences in relation to some relationship variables.

"Findings highlight the need to assess and, if appropriate, treat lacking interest in sex in a holistic and relationship-specific way."

Conclusion

This study appears to suggest that many factors increase the likelihood of both men and women reporting a lack of interest in sex. Overall, women seem to be more likely to lose interest than men.

While this large study provides some insight into the possible reasons behind having a lack of interest in sex, it has a few limitations:

As so many factors were considered, there were bound to be some that showed statistical significance – this could just be by chance.

The cross-sectional nature of the study means we can't be sure if the specific factors reported on caused the lack of interest, or vice versa.

People self-reported their sexual activity – this might lead to biased reporting, as people might under- or over-report certain factors.

If your sex life isn't fulfilling, there are steps you can take to make it better.

A good start is talking to your partner about how you feel about your current sex life in an honest and open way.

Read more advice about improving your sex life.

Links To The Headlines

Women 'more likely to lose interest in sex than men'. BBC News, September 14 2017

The one-year itch: How women get bored of having sex with their partner after just 12 months (but the interest in steamy nights doesn't fade for men). Mail Online, September 14 2017

Women are more likely to get bored of sex with a long-term partner, suggests new study. Metro, September 14 2017

Women are more likely to lose interest in sex if they move in with their boyfriend, expert warns. The Sun, September 14 2017

Women more likely to lose interest in sex in long-term relationships. The Daily Telegraph, September 14 2017

Women more likely to lose interest in sex after a year. The Times (subscription required), September 14 2017

Links To Science

Graham CA, Mercer CH, Tanton C, et al. What factors are associated with reporting lacking interest in sex and how do these vary by gender? Findings from the third British national survey of sexual attitudes and lifestyles. BMJ Open. Published online September 13 2017

Tattoo ink particles can spread into lymph nodes

NHS Choices - Behind the Headlines -

"Tattoos could give you cancer, new research suggests," is the entirely unsupported claim from the Mail Online.

The news come from a study that found evidence particles from tattoo ink can spread into lymph nodes – but it hasn't been proven that tattoo ink causes cancer.

Researchers used samples of skin and adjacent lymph nodes taken from six donors after autopsy.

Four of the donors had tattoos and were more likely to have substances like titanium in the lymph nodes. Lymph nodes are part of the lymphatic system, which in turn is part of the immune system.

The problem is the researchers didn't include important information about whether any of the donors had cancer, or what caused their deaths. This means it's not possible to claim that the tattoo ink particles found in lymph nodes cause cancer.

Tattoos have become far more popular in recent years, leading to concerns about their safety. The ink used in tattoos includes a mixture of organic and metal-based pigments and preservatives.

There's been little study of their effects on human health. This is partly because animal experiments are thought to be unethical, as tattoos are a matter of choice, not medical necessity.

Most safety concerns have focused on the need to ensure tattoo artists use sterile needles to prevent the spread of blood-borne diseases, such as hepatitis C.

We don't know whether the spread of ink particles into lymph nodes would have any significant impact on human health, let alone cause cancer.

Where did the story come from?

Researchers were from the German Federal Institute for Risk Assessment, Physikalisch-Technische Bundesanstalt, and the Institute of Forensic Medicine in Germany, and the Department of X-ray Spectrometry European Synchrotron Radiation Facility in France.

The research was published in the peer-reviewed journal Scientific Reports on an open access basis, so it's free to read online.

The Guardian's reporting is balanced and accurate. But the Mail Online's coverage is less accurate, focusing on the "controversial" chemical titanium dioxide found in some tattoo inks, stating it's been "linked to cancer".

There's no evidence titanium dioxide is linked to cancer except possibly when inhaled, which would usually only be a risk for people who work in manufacturing.

What sort of research was this?

This post-mortem research was carried out on tissue samples from people with and without tattoos.

The researchers used a variety of techniques, including X-ray fluorescence imaging, to measure levels of dyes and metals in skin and lymph nodes.

Lymph nodes are part of the body's immune system, and are located in the neck, armpits and groin.

Tiny foreign bodies such as nanoparticles of pigment can be swept up by lymph fluid or blood cells and transported to the lymph nodes.

The research doesn't tell us what effect these findings might have on people's health.

What did the research involve?

Researchers took samples of tattooed skin and lymph nodes from four people with tattoos and two people without to act as a control sample.

They ran a series of experiments to identify the types of pigments and particles in the skin and lymph nodes to see whether ink particles travelled to the lymph nodes and persisted there.

They also looked at tissue surrounding ink particles to see whether it differed from tissue not close to ink particles.

Using a range of techniques, they set out to answer four questions:

  • Do organic pigments travel from the skin to the lymph nodes?
  • Do people with tattoos have more potentially toxic metals in their skin and lymph nodes?
  • What size are particles from pigments, and what size are the particles that travel to lymph nodes?
  • Do the particles affect surrounding tissue?

They used a number of advanced spectroscopy techniques to analyse the tissue.

Spectroscopy involves analysing a sample of organic matter by measuring the wavelength of the spectrum of light it produces – different elements produce distinct lines on the spectrum.

What were the basic results?

The researchers found:

  • Organic pigments in both skin and lymph nodes from two of four tattooed donors. Two donors had no organic pigments in their lymph nodes, possibly because they were at low levels or had degraded. The most common organic compound in tattoo ink, carbon black, was "not accessible" with the methods used in the study.
  • Higher levels of five "toxic" elements in the skin and lymph nodes of people with tattoos. The elements identified were aluminium, chromium, iron, nickel and copper.
  • Traces of the element titanium (probably from the white pigment titanium oxide) in the skin and lymph nodes of people with tattoos. Micro-X-ray absorption showed this was "mostly" present in its more stable, less toxic, "rutile" form.
  • Particle size varied a great deal depending on the type of pigment. Smaller pigments were more likely to be found in the lymph nodes, although relatively large titanium oxide particles were also found in lymph nodes.
  • "Biomolecular" changes to tissue around pigment particles in the skin and lymph nodes. The researchers say the tissue near particles had higher levels of lipids and lower levels of proteins than similar tissue without particles.
  • They also found protein in the tissue around particles had a changed structure in both the skin and lymph nodes.
How did the researchers interpret the results?

The researchers said they found "strong evidence for both migration and long-term deposition of toxic elements and tattoo pigments" from tattoos on the skin into the lymph nodes.

They added they have found evidence for "alterations of biomolecules" in the tissues of skin affected by pigment particles, which may contribute to skin inflammation "and other adversities" connected with tattooing.

Conclusion

If you already have a tattoo, there's nothing in this study that should alarm you. It doesn't show that people with tattoos are more likely to get cancer, despite the scaremongering headlines.

The researchers explain how tattoo pigments are picked up as "foreign bodies" by the body's immune system and are then stored in the skin and lymph nodes.

But they can't tell us what effects this process has on our health. The researchers weren't told any medical information about the donor samples, such as any diseases they had (including cancer) or the cause of donors' deaths.

The study also has other limitations. It looked at samples from a small number of people, and an even smaller number of controls.

And some of the findings might not be linked to tattoos – for example, higher levels of iron in the lymph nodes might come from blood within the samples, and aluminium in armpit lymph nodes could be from antiperspirants.

If you're considering getting a tattoo, it might be worth thinking about whether you want to introduce pigments that include metals into your body unnecessarily.

While we don't know much about the possible effects now, harmful long-term effects can't be ruled out.

As well as asking a tattoo artist about the hygiene of their tattooing equipment, it may also be worth asking them about the types of pigments they plan to use and what's in them.

Titanium dioxide, for example, is known to increase inflammation and can delay healing.

Links To The Headlines

Why tattoos could give you cancer: toxins in inkings stay in your bloodstream for life and accumulate in lymph nodes. Mail Online, September 12 2017

Tattoo ink contaminants can end up in lymph nodes, study finds. The Guardian, September 12 2017

Links To Science

Schreiver I, Hesse B, Seim C, et al. Synchrotron-based ν-XRF mapping and μ-FTIR microscopy enable to look into the fate and effects of tattoo pigments in human skin. Scientific Reports. Published online September 12 2017

No change to alcohol guidelines for pregnancy

NHS Choices - Behind the Headlines -

"There is little evidence having the occasional drink while pregnant harms a baby," reports the Mail Online.

This follows a review of international research looking at whether low-to-moderate alcohol consumption – no more than 1 to 2 units, once or twice a week – was linked with adverse pregnancy outcomes. To put this in context, a pint of low-strength lager contains about 2 units of alcohol, a small glass (125ml) of 12% wine contains 1.5 units and a single shot of spirits contains 1 unit.

The review found that low-to-moderate alcohol consumption may slightly increase the risk of having a baby small for gestational age.

The Chief Medical Officers for the UK currently recommend that pregnant women, or those planning to become pregnant, avoid drinking any alcohol at all to keep risks to a minimum. Long-term health risks for the baby are greater the more alcohol you drink.

And as the researchers conclude, no evidence of harm is not the same as evidence of no harm: there could still be risks that haven't been identified.

However, the research does provide reassurance that women who have drunk small amounts of alcohol during pregnancy, or before they knew they were pregnant, are unlikely to have harmed their baby.

Where did the story come from?

The study was carried out by researchers from the University of Bristol in the UK. It was funded by the UK Medical Research Council, the University of Bristol, the National Institute for Health Research (NIHR) Collaboration for Leadership in Applied Health Research and Care West (CLAHRC West) at University Hospitals Bristol NHS Foundation Trust, and the Higher Education Funding Council for England.

The study was published in the peer-reviewed medical journal BMJ Open on an open-access basis, meaning it's freely available to read online.

Media reporting of the study was generally accurate and responsible, making it clear that it's probably still best to avoid alcohol during pregnancy.

Saying as The Guardian does, however, that "women worried by guidance advising abstinence should be told there is little evidence that the odd glass of wine causes harm to the baby" is a little misleading, as it could be interpreted to mean that there's definitely no harm in drinking. The reality is that there isn't enough research being done in the area, so we cannot firmly say whether or not it may be harmful.

What kind of research was this?

This was a systematic review and meta-analysis study looking at the effect of low-to-moderate alcohol intake in pregnancy (fewer than 2 UK units, no more than twice a week) on pregnancy and longer-term infant outcomes.

While this is a good way of summarising all evidence on a particular issue, systematic reviews will include any limitations of the studies reviewed. It wouldn't be ethical to randomise pregnant women to consume alcohol or not, so most studies are observational – such research cannot prove that a certain level of alcohol intake has directly caused any adverse outcomes.

It's also difficult to be sure of exact alcohol intake, and a range of other health and lifestyle factors may contribute to the outcome too.

What did the research involve?

Researchers looked at 24 cohort and two quasi-experimental studies (which don't involve randomisation) from a range of high-income countries, including the UK.

Low-to-moderate alcohol intake was defined as 32g a week (1 or 2 units, once or twice a week) as this was the "safe" threshold cut-off previously specified by UK guidelines. There has been a recent move among guideline development groups to recommend total abstinence during pregnancy.

Pregnancy outcomes assessed included:

  • stillbirth (pregnancy loss after week 24)
  • miscarriage (loss before week 24)
  • pregnancy duration and premature delivery (less than 37 weeks)
  • hypertensive disorders of pregnancy
  • gestational diabetes
  • baby born small for gestational age
  • birth size (weight, length and head circumference)
  • low birth weight (under 2.5kg)
  • low amniotic fluid, placenta previa and placental abruption
  • assisted delivery (using forceps, for example)
  • Apgar score at birth and admission to neonatal unit (Apgar scores assess the health of a newborn on a scale from 1 to 10, based on factors such as heart rate and breathing patterns)
  • congenital malformation

They also looked at features of foetal alcohol syndrome disorder (birth defects caused by heavy alcohol consumption in pregnancy), including childhood growth restriction, head size and circumference, developmental delays, behaviour problems, cognitive impairment and IQ, and facial malformations.

Researchers looked at whether study results had been adjusted for potential confounders, including socioeconomic status, smoking during pregnancy, maternal age and ethnicity.

What were the basic results?

Of the 24 studies, 17 were suitable to be pooled in a meta-analysis for four outcomes: birth weight, small for gestational age, premature birth and low birth weight (under 2.5kg).

There was modest evidence that low-to-moderate alcohol consumption gave an 8% increased risk of being small for gestational age compared with abstinence (odds ratio 1.08, 95% confidence interval 1.02 to 1.14).

This was from pooled results of seven studies, although 95% of the participants came from a single US study.

Low-to-moderate alcohol consumption had no significant effect on the likelihood of a low birth weight (six studies) or premature birth (nine studies). Seven studies also found no significant difference in the average infant birth weight between drinkers and non-drinkers.

For all other outcomes, there was not enough data to combine the results or reach firm conclusions.

How did the researchers interpret the results?

The researchers concluded there is "limited evidence for a causal role of light drinking in pregnancy, compared with abstaining, on most of the outcomes examined".

They added: "Despite the distinction between light drinking and abstinence being the point of most tension and confusion for health professionals and pregnant women and contributing to inconsistent guidance and advice now and in the past, our extensive review shows that this specific question is not being researched thoroughly enough, if at all."

Conclusion

The results of this review found that low-to-moderate alcohol consumption during pregnancy was linked with a slightly increased risk of having a baby small for gestational age.

However, there was no evidence for any other links, including any difference in the average birth weight of babies born to drinkers and non-drinkers.

There are some important limitations of the research to note:

• The evidence still doesn't prove that drinking directly increases the risk of a baby born small for gestational age. Studies were observational and varied widely in accounting for the extensive number of confounding factors that could be having an influence, such as maternal lifestyle and diet. And even when factors such as socioeconomic status were adjusted for, they may still have had some residual confounding effects.
• Because studies were observational, it's hard to be certain of exact alcohol intake. It may have varied week to week, and many women may not have been able to accurately judge the number of units of alcohol they had.
• As the authors acknowledge, there was little evidence available for many pregnancy and birth outcomes, and the studies weren't suitable for pooling. As such, we can't be sure that being small for gestational age – if this is a true risk – is the only one associated with drinking during pregnancy.

The research generally supports the opinion that it's difficult to say what a "safe" amount of alcohol is for women who are pregnant or trying for a baby.

The current advice from UK Chief Medical Officers is that, if pregnant or planning a pregnancy, the safest approach is not to drink alcohol at all. They say drinking in pregnancy can lead to long-term harm to the baby, with the risk becoming greater the more you drink.

They also advise that women who find out they're pregnant after already having drunk in early pregnancy should avoid further drinking but shouldn't worry unnecessarily, as the risks of their baby being affected are likely to be low.

Links To The Headlines

Little evidence that light drinking in pregnancy is harmful, say experts. The Guardian, September 11 2017

'Weak evidence' light alcohol use in pregnancy harms. BBC News, September 12 2017

Light drinking in pregnancy 'unlikely' to harm babies, but experts caution lack of evidence. The Daily Telegraph, September 11 2017

Light drinking during pregnancy 'may be OK' as researchers find limited evidence of harm. The Sun, September 12 2017

'No proof' that the odd glass of wine harms your baby, despite Government advice to abstain while pregnant. Mail Online, September 12 2017

Links To Science

Mamluk L, Edwards HB, Savovic J, et al. Low alcohol consumption and pregnancy and childhood outcomes: time to change guidelines indicating apparently 'safe' levels of alcohol during pregnancy? A systematic review and meta-analyses. BMJ Open. Published online September 11 2017

Avoid eating just before your bedtime, study recommends

NHS Choices - Behind the Headlines -

"It's not what you eat, it's when you eat that matters: study shows timing your meals right is the key to beating obesity," the Mail Online reports.

The headline was prompted by a small US study involving 110 university students.

Researchers gave them activity monitors to wear, measured their sleep patterns, and observed how much they ate and at what time.

The researchers were particularly interested in what they termed dim-light melatonin onset (DLMO). DLMO is when the body begins to wind down in preparation for sleep and starts producing the sleep hormone melatonin.

For most of us, our DLMO usually begins around 8pm. But the timing can vary if you do shift work.

The researchers found students with a higher body weight tended to eat more of their calories later in the day, closer to their DLMO.

This adds to previous evidence suggesting it's good to consume more of our calories earlier in the day, when we have more opportunities to be active ahead of us. Eating large, heavy meals late in the evening has also been linked with higher body fat.

But as a single study in a small, specific sample of students, this study provides little evidence that lifestyle and eating habits have a direct effect on body weight.

As advice goes, it may be sensible to consider whether regularly eating a large, heavy meal close to bedtime is the best thing for your health and wellbeing.

Eating earlier in the day may not make you magically thinner, but it may help prevent night-time indigestion.

Where does the study come from?

The study was conducted by researchers at Brigham and Women's Hospital and Harvard Medical School in the US, and the University of Murcia in Spain.

It was published in the peer-reviewed American Journal of Clinical Nutrition.

No external sources of funding are reported for the study, although the authors declared various conflicts of interest as many of them work, or have worked, for a wide range of commercial interests.

The Mail Online's coverage was accurate, but may have benefitted from noting the limitations of this small, cross-sectional study.

What kind of research was this?

This cross-sectional study aimed to see whether timing of eating, particularly eating at a later hour in the evening, was related to body clock and the amount of calories consumed.

The human body normally defaults to a 24-hour light-dark, wake-sleep cycle. Put simply, we wake up when it's light and go to bed when it's dark.

But with electrical lighting and modern lifestyles, we're now able to control our own wakefulness, and can stay awake and eat late into the evenings.

Various studies suggest eating at a time naturally reserved for sleeping could have adverse effects on weight and metabolic health.

This study observed the eating and activity patterns and body measurements of some university students across the course of a week.

You can observe links in this type of study, but you can't prove cause and effect.

What were the basic methods?

The study recruited 110 university students aged 18 to 22. They took part in a 30-day sleep-wake monitoring study, where they were instructed to wear a wrist actigraph monitor at all times.

An actigraph is a device that can provide a reasonably accurate estimate of time spent asleep by measuring physical activity and light exposure.

The students also kept daily sleep and exercise diaries. Sleep timing and duration was assessed from the actigraph monitor and correlated with the diaries.

For 7 consecutive days in the middle of the course, participants were asked to record all the food and drink they consumed.

They did this using a mobile app that allowed them to take photos of all the food they ate and record which meal or snack this was.

They also came in for a single night's sleep in the study lab, where they had saliva samples taken in dim-light conditions to measure levels of the sleep hormone melatonin.

Release of melatonin marks the start of the biological night, when our body clocks begin to shift into sleep mode.

Researchers assessed meals, calories consumed, and their timing against sleep, activity and body fat.

What were the results?

The study gives a breakdown of the average calories consumed and their timings.

There was no difference between students with higher and lower body fat in the timing of melatonin release.

But researchers noticed that for individuals with higher body fat, the midpoint of all the calories they consumed for the day was later than for leaner people, and 1 hour closer to the onset of melatonin release.

And those with a calorie intake-midpoint later in the day were also more likely to consume a greater number of calories at this time. People eating more calories later in the day also tended to have less sleep.

What do the researchers conclude?

The researchers said: "These results provide evidence that the consumption of food during the circadian evening and/or night, independent of more traditional risk factors such as amount or content of food intake and activity level, plays an important role in body composition."

Conclusions

Previous research suggests we may be better off consuming more of our calories earlier on in the day, when we have a full, active day ahead of us to use up the energy.

It's also been observed that people who consume large calorific meals late in the evening can have a higher body weight.

In a sense, the results of this study seem plausible and don't really say anything different from what's already been observed. But as this is a cross-sectional study, it can't really prove very much.

The study involved a small, select sample of US university students. Their results can't be applied to everyone, as they have different lifestyles and sociodemographics from the general population.

And a cross-sectional study can only show associations – it can't prove cause and effect.

The participants' body weight was assessed at the same time as their food intake and sleep patterns.

Though again it seems plausible, we can't assume that the students' lifestyle and eating habits have directly caused their current body weight.

This study will doubtless contribute to the body of evidence around timing of food intake, relationship to the sleep-wake cycle, and body weight. But it provides little proof as a single piece of evidence.

The best way to achieve and maintain a healthy weight is to eat a balanced diet high in fruit and vegetables and low in saturated fat and sugars, and to get regular exercise.

Read more advice on how to eat a healthy, balanced diet.

Links To The Headlines

It's not what you eat, it's when you eat that matters: study shows timing your meals right is the key to beating obesity. Mail Online, September 8 2017

Links To Science

McHill W, Phillips AJK, Czeisler CA, et al. Later circadian timing of food intake is associated with increased body fat. The American Journal of Clinical Nutrition. Published online September 6 2017

Could a Mediterranean diet be as good as drugs for acid reflux?

NHS Choices - Behind the Headlines -

"Why the Mediterranean diet is the best cure for acid reflux: Study found patients who ate plenty of fish and veg had fewer symptoms and avoided side effects of medication," the Mail Online reports.

Acid reflux, also known as gastro-oesophageal reflux disease (GORD), is a condition where stomach acid leaks back up into the gullet, causing pain. Standard treatment for GORD is a type of medication known as a proton-pump inhibitor (PPI), which reduces the amount of acid produced by the stomach.

This latest study looked at the medical records of people with GORD to compare whether taking PPI treatment or following a Mediterranean-style diet with alkaline water was better at reducing symptoms. A Mediterranean diet is largely based on vegetables, fruits, nuts, beans, cereal grains, olive oil and fish.

The study found the dietary changes were equally good at reducing symptoms as PPIs. This suggests dietary changes could be a first option to try for reflux symptoms, which may avoid the need for some people to take PPIs.

However, drug-free treatment may not be suitable for everyone (for example people whose symptoms are linked with stomach irritation or ulcers). Also, completely changing your diet can be complex and nutritional guidance may be needed.

Nevertheless, switching to a Mediterranean diet brings other health benefits such as reducing your risk of heart disease. Read more about the benefits of a Mediterranean diet.

 

Where did the story come from?

The study was carried out by researchers from New York Medical College, New York Eye and Ear Infirmary of Mount Sinai and The Institute for Voice and Swallowing Disorders, Phelps Hospital, all in the US.

No sources of funding are reported. One author served on the scientific advisory board of Restech Corporation (a company that specialises in GORD treatment), for which he received no financial compensation. There were no other conflicts of interest reported.

The study was published in the peer-reviewed medical journal JAMA Otolaryngology – Head & Neck Surgery on an open-access basis, meaning it is freely available to access online.

The Mail Online's reporting is misleading and contradicts itself with the headline suggesting fish was one of the main dietary components in the Mediterranean diet, then going on to describe how the diet consisted of "barely any dairy or meat including beef, chicken, fish, eggs and pork". Fish is not actually mentioned in the paper at all, we only know they were minimising intake of meat and dairy.

 

What kind of research was this?

This was a retrospective cohort study looking back at medical records of people with acid reflux who had either been prescribed usual medication (proton pump inhibitors or PPIs) or changed their diet to a Mediterranean style and alkaline water (water that is less acidic than tap water). It aimed to compare effects on reflux symptoms.

Gastro-oesophageal reflux (GORD) is when stomach acid rises up into the oesophagus (gullet), which can cause heartburn and indigestion. Standard treatment can involve removing dietary triggers (such as fatty foods) and medication with acid-blocking tablets called proton pump inhibitors (PPIs). PPIs can however have mild side effects such as headaches, diarrhoea or constipation, feeling sick, tummy pain and dizziness.

A cohort can look at associations, but as this study is looking back in time at what people have previously done, it can be hard to assess or control for confounding factors that could have had an influence.

 

What did the research involve?

Researchers looked back at medical records of people diagnosed with GORD between 2010 and 2015 in the US. They compared two cohorts, one being treated with PPI medication and the other with a Mediterranean diet and alkaline water to determine differences in the improvement of acid reflux.

The first cohort of 85 participants, on average aged 60, were treated between 2010 and 2012 with one of two PPI drugs (esomeprazole or dexlansoprazole [not used in the UK]) and asked to follow standard advice to cut out coffee, tea, chocolate, fizzy drinks, greasy, fried, fatty and spicy foods, and alcohol from their diet.

The second cohort of 99 participants, on average aged 57, were treated between 2013 and 2015 with alkaline water (pH >8.0) and a plant-based, Mediterranean-style diet, and also cut out the same things from their diet as the first group.

Participants of the second cohort were asked to replace all drinks with alkaline water and eat 90-95% of their diet as a plant-based diet with vegetables, fruits, wholegrains and nuts with less than 5 to 10% from animal-based products for six weeks. To meet this, participants had to limit animal products to only 2 or 3 meals a week containing 3 to 4 ounces of meat, with minimal intake of dairy.

Compliance with medication or diet was assessed by a questionnaire and verbal discussion and those not complying were excluded.

The outcome researchers were measuring was the change in reflux symptoms using the Reflux Symptom Index (RSI) after six weeks of treatment. The RSI is a scoring system based on how many symptoms of GORD a person has, and how troublesome those symptoms are.

A clinically meaningful change in RSI score was a reduction of at least 6 points.

 

What were the basic results?

A meaningful 6-point reduction was achieved by 54% of the medication group compared with 62.6% in the alkaline water and Mediterranean diet group. This was not a statistically significant difference, but the changes in overall scores were:

  • In the PPI group, RSI scores reduced by 27.2% (95% confidence interval [CI] 18.5% to 35.9%) from an average of 20.2 (95% CI 18.4 to 22) to 14.3 (95% CI 12.4 to 16.2).
  • In the Mediterranean diet and alkaline water group, scores reduced by 39.3% (95% CI 33.1% to 45.5%) from an average of 19.1 (95% CI 17.6-20.6) to 12.1 (95% CI 10.4-13.7).
  • The mean reduction was greater in the Mediterranean diet and alkaline water group (mean difference 12.1%, 95% CI 1.53 to 22.68).

 

How did the researchers interpret the results?

The researchers conclude that their "data suggest that the effect of PPI on RSI scores among patients with [GORD] is not significantly better than that of alkaline water and a plant-based, Mediterranean-style diet. In fact, our data suggest that the plant based approach is at least as good, if not better, than PPI therapy. Thus, we recommend that a patient with suspected [GORD] at least attempt a dietary approach prior to any pharmacological intervention".

 

Conclusion

The results of this relatively small cohort study seem to show that a plant-based Mediterranean diet with alkaline water is equally good as PPI medication at treating acid reflux symptoms when people also follow standard advice to cut out certain things from their diet.

This might suggest that the first port of call for people with gastro-oesophageal reflux could be to try a Mediterranean diet before going on PPI medication, to avoid potential side effects.

There are, however, some limitations to this research:

  • Cohort studies can only show links and cannot prove definite cause and effect, and retrospective cohorts such as this are even more limited than prospective cohorts. Prospective cohorts that follow people up over time have the advantage that they can at least assess and collect data on other factors that could be having an influence. When you have to rely on previously collected data, you cannot be sure that all relevant information has been collected.
  • We do not know exactly what people in each group were eating and we cannot tell what it was about the plant-based Mediterranean diet or alkaline water that might have provided a benefit. Food diaries or food frequency questionnaires might be one way to determine this in the future.
  • Follow-up was only six weeks, which is not much time to see longer-term outcomes. It might be that either PPIs or the Mediterranean diet have a different effect in the longer term.
  • We don't know for sure that the Mediterranean diet had no adverse effects – for example, it could have a detrimental effect on other health measures (such as vitamin and mineral levels). Therefore we can't say with confidence that it has no side effects compared with drug treatment.
  • For this reason there may be a need for guidance from dietitians. Changes to the diet often require self-control and it can be complex and difficult to achieve and maintain nutrition merely by doctor recommendation.
  • There will always be some people with reflux symptoms who need drug treatment, such as those with stomach irritation or ulcers.

Making changes to the diet and adopting a more Mediterranean-style diet might be one simple first option that people or practitioners could consider as a way of managing reflux. 

Links To The Headlines

Why the Mediterranean diet is the best cure for acid reflux. Mail Online, September 7 2017

Links To Science

Zalvan CH, Hu S, Greenberg B, et al. A Comparison of Alkaline Water and Mediterranean Diet vs Proton Pump Inhibition for Treatment of Laryngopharyngeal Reflux. JAMA Otolaryngogly – Head and Neck Surgery. Published online September 7 2017

Drinks industry accused of downplaying 'alcohol-cancer risk'

NHS Choices - Behind the Headlines -

"Drinks industry downplaying alcohol-cancer link," The Guardian reports as new analysis has been published looking at the accuracy of health information circulated by the alcohol industry on the link between alcohol and cancer.

Many people still don't appreciate that alcohol can increase the risk of a range of cancers, such as breast, liver and mouth cancer.

As part of their corporate and social responsibility goals, the UK alcohol industry shares health information to inform and encourage their consumers to drink responsibly.

But the industry has been accused of misrepresenting the evidence to favour their own interests.

Researchers wanted to see if the health information produced by the alcohol industry is scientifically accurate.

They found the industry and affiliated organisations use three main approaches when disseminating health information:

  • denial of the link between alcohol and cancer
  • misinterpretation of the risk
  • distraction by focusing on other risk factors for cancer, aside from alcohol consumption

Critics of the drinks industry have likened this approach to that of the tobacco industry in the 1960s and 70s, when the link between smoking and lung cancer was first proved.

The UK Chief Medical Officers' recommendation is men and women drink no more than 14 units a week, spread evenly over three days or more.

Where did the story come from?

The study was carried out by researchers from several institutions, including the London School of Hygiene and Tropical Medicine, the Karolinska Intitutet in Sweden, and the University of Tromsø in Norway.

No sources of external funding were reported.

It was published in the peer-reviewed journal Drug and Alcohol Review. It's available to read online for free on an open access basis.

Generally, the UK media coverage was balanced and accurate.

What kind of research was this?

This qualitative analysis aimed to investigate the comprehensiveness and accuracy of the health information disseminated by the alcohol industry on the links between alcohol and cancer.

It's well established that drinking alcohol is associated with an increased risk of at least seven types of cancer, including mouth, throat, oesophageal, liver, breast and colon cancers.

Alcohol is reportedly responsible for approximately 4% of new cancer cases every year.

Despite the volume of evidence, the alcohol industry has disputed the relationship between drinking alcohol and cancer.

This research highlights important themes and strategies used by the alcohol industry.

But it's unclear whether the sources and websites included in the research were chosen in a systematic manner.

A systematic review, where the search methodology is determined in advance, would be a better way to look into this thoroughly.

What did the research involve?

The researchers analysed websites and documents from 27 organisations linked to the alcohol industry.

They checked information published on cancer and alcohol between September and December 2016.

The websites were identified using the Global Alcohol Producers website and progress reports.

The researchers looked for related themes, and checked the reliability and validity of the content and whether representative scientific examples were used, before identifying the strategies the industry used to circulate the information.

What were the basic results?

The researchers found between 24 and 26 of organisational websites misrepresented or omitted scientific evidence confirming the link between alcohol consumption and cancer, particularly when discussing breast and colorectal cancers.

Three main strategies were identified.

Distortion

This is where the risk of cancer was mentioned, but the nature or size of that risk was obscured or misrepresented.

This was the most common strategy used by the alcohol industry.

The relationship between alcohol and cancer was presented in a highly complex way before implying that an independent link wasn't possible.

Three further approaches were found when this strategy was used:

  • Claiming or implying that the risk only applies to particular patterns of drinking, such as heavy drinking or consumption for long periods of time.
  • Claiming or implying that, as knowledge of the mechanism is incomplete, the evidence of a causal relationship isn't trustworthy, or there's a lack of consensus among experts.
  • Claiming protective effects of alcohol on some cancers, thus confusing the picture of overall risk.
Denial or omission

This involves denying or disputing any link with cancer, or deliberately failing to mention the relationship.

Five out of the 27 organisations denied there was any association between drinking alcohol and developing cancer.

Examples include inaccurate claims that light to moderate drinking doesn't lead to an increased risk of developing cancer.

And some sources listed the short- and long-term effects alcohol has on the body, such as cardiovascular disease, diabetes, alcohol dependence and liver cirrhosis, but failed to mention cancer.

Distraction

This involved focusing discussion away from the independent effects alcohol has on common cancers.

Eight organisations used this strategy – by discussing a wide range of other risk factors associated with cancers, the industry is able to minimise the role alcohol plays in their development.

For example, for the link between alcohol and breast cancer, organisations pointed out that individuals were at high risk if breast cancer ran in the family, or said it's also age-related.

How did the researchers interpret the results?

The researchers concluded: "Our analysis suggests that the major global alcohol producers may attempt to mitigate this risk by disseminating misleading information about cancer through their 'responsible drinking' bodies.

"The existing evidence of strategies employed by the alcohol industry suggests that this may not be a matter of simple error."

Conclusion

This qualitative analysis aimed to determine the accuracy of health information circulated by the alcohol industry on the links between alcohol and cancer.

It found the industry and affiliated organisations use three main approaches:

  • denial of the link between alcohol and cancer
  • misinterpretation of the risk
  • distraction by focusing on other risk factors

This analysis highlights how these strategies could be detrimental to public health.

Of course, it's possible, given this data was collected in 2016, that some of the websites and documents analysed by the researchers have since been updated.

Regardless, the researchers suggest their analysis has significant implications for both clinicians and policymakers.

They call for a full-scale investigation into how the alcohol industry represents the link between alcohol and cancer.

Current UK recommendations on alcohol advise that men and women drink no more than 14 units a week, with one unit equal to 10ml or 8g of pure alcohol.

Links To The Headlines

Drinks industry downplaying alcohol-cancer link – report. The Guardian, September 7 2017

Alcohol industry 'playing down' risk of cancer by using tobacco industry tactics. Sky News, September 8 2017

Links To Science

Petticrew M, Hessaei NM, Knai C, et al. How alcohol industry organisations mislead the public about alcohol and cancer. Drug and Alcohol Review. Published online September 7 2017

Can exercise offset some of the harms of regular drinking?

NHS Choices - Behind the Headlines -

"Adults who booze regularly but exercise for five hours a week are no more likely to die than teetotallers," the Mail Online reports.

A study suggests exercise may compensate for some, but certainly not all, of the harms associated with excessive alcohol consumption. This latest study looked at deaths from cancer and cardiovascular disease, as well as premature death in general (usually judged to be dying before the age of 75).

Researchers looked at around 10 years' worth of national survey data from UK adults aged over 40. Unsurprisingly, they found links between all-cause and cancer mortality in inactive people. But they also found increasing levels of physical activity generally removed the association with drinking habits. In fact, occasional drinking was associated with a significant reduction in all-cause mortality for the most active of people.

Although the study had strengths in its large sample size and regular follow-up, we can't be sure that any links observed were solely down to the interaction between alcohol and exercise. For example, people who are physically active may also avoid smoking and consume healthy diets. It is difficult to completely control for such influences when analysing data like this.

While regular exercise may mitigate against some of the harms associated with excessive alcohol consumption it certainly won't make you immune. Many world-class sportspeople, such as George Best and Paul Gascoigne, have had both their careers and lives blighted by drinking.

 

Where did the story come from?

The UK-based study was carried out by an international collaboration of researchers from Canada, Australia, Norway and the UK. The health surveys on which the study was based were commissioned by the Department of Health, UK. Individual study authors also reported receiving funding from the National Health and Medical Research Council and University of Sydney. 

The study was published in the peer-reviewed British Journal of Sports Medicine. 

The media coverage around this topic was generally overly optimistic, highlighting that by exercising, individuals can completely undo the harm caused by excessive alcohol consumption, which is untrue.

In particular, the Mail Online claimed "Adults who booze regularly but exercise for five hours a week are no more likely to die than teetotallers" which could send out the wrong message to the public.

 

What kind of research was this?

This cohort study analysed data from British population-based surveys: Health Survey for England (HSE) and the Scottish Health Survey (SHS) to investigate whether physical activity is able to moderate the risk between alcohol consumption and mortality from cancer and cardiovascular diseases.

Cohort studies like this are useful for assessing suspected links between an exposure and outcome. However, there are potentially other factors that have a role to play in such associations and therefore the study design doesn't allow for confirmation of cause and effect.

 

What did the research involve?

The researchers collected data on 36,370 men and women aged 40 or above from Health Survey for England (1994; 1998; 1999; 2003; 2004; and 2006) and the Scottish Health Survey (1998 and 2003). Among other things, the participants were asked about their current alcohol consumption and physical activity.

Alcohol intake was defined by six categories (UK units/week):

  • never drink (lifetime abstainers)
  • ex-drinkers
  • occasional drinkers (haven't drank anything in past seven days)
  • within (previous) guidelines: <14 units (women) and <21 units (men)
  • hazardous: 14-15 units (women) and 21-19 units (men)
  • harmful: >35 (women) and >49 (men)

Frequency and type of physical activity in the past four weeks was questioned and converted into metabolic equivalent task-hour (MET-hours, which are an estimate of metabolic activity) per week according to national recommendations:

  • inactive (≤7 MET-hours)
  • lower level of active (>7.5 MET-hours)
  • higher level of active (>15 MET-hours)

The surveys were linked to the NHS Central Register for mortality data and the participants were followed up until 2009 (HSE) and 2011 (SHS). There were 5,735 recorded deaths; deaths from cancer and cardiovascular disease were of most interest for this study.

The data was analysed for associations between alcohol consumption and the risk of death from all-causes, cancer and cardiovascular disease. The results were then analysed according to levels of physical activity.

Potential confounders (such as sex, body mass index and smoking status) were controlled for.

 

What were the basic results?

Overall, the study found a direct link between all levels of alcohol consumption and risk of cancer mortality. It also found that increasing levels of physical activity reduced this association with cancer mortality, and also reduced the link with death from any cause.

  • In individuals who reported inactive levels of physical activity (≤7 MET-hours), there was a direct association between alcohol consumption and all-cause mortality.
  • However, in individuals who met the highest level of physical activity recommendations a protective effect of occasional drinking on all-cause mortality was observed (hazard ratio: 0.68; 95% confidence interval (CI): 0.46 to 0.99). It should be noted that this result just skimmed the cut-off point for statistical significance.
  • In this high activity group, there was no link between all-cause mortality and alcohol consumption within guidelines, or even hazardous amounts, but the risk was still increased for those drinking harmful amounts.
  • The risk of death from cancer increased with the amount of alcohol consumed in inactive participants, ranging from a 47% increased risk for those drinking within guidelines to 87% increased risk for those with harmful drinking.
  • In people with higher activity levels (above 7.5 MET hours) there was no significant link between any amount of alcohol consumption and cancer mortality.
  • No association was found between alcohol consumption and mortality from cardiovascular disease, although a protective effect was observed in individuals who reported the lower and higher levels of physical activity (>7.5 MET-hours) and (>15 MET-hours) respectively.

 

How did the researchers interpret the results?

The researchers concluded "we found evidence of a dose–response association between alcohol intake and cancer mortality in inactive participants but not in physically active participants. [Physical activity] slightly attenuates the risk of all-cause mortality up to a hazardous level of drinking."

 

Conclusion

This study aimed to explore whether physical activity is able to moderate the risk between alcohol consumption and mortality from cancer and cardiovascular diseases. It found that increasing levels of physical activity reduced the association for death from both all-causes and cancer.

This study has strengths in its large sample size, comprehensive assessments and long duration of follow-up. The findings are interesting, but there a few points to bear in mind:

  • As the authors mention, cohort studies such as this are unable to confirm cause and effect. Though the researchers have tried to account for various potential health and lifestyle confounding variables, there is the possibility that others are still influencing the results. A notable one is dietary habits which weren't assessed. Also, for example, the former drinkers may have quit due to other health issues which may have introduced bias.
  • The study was unable to look at binge drinking levels of alcohol consumption which would have likely had important health implications.
  • Additionally, there is always the possibility with self-reported surveys that the participants either under or over-reported their drinking habits which can increase the chance of misclassification bias.
  • Though having a large sample size, fewer people reported harmful drinking levels, so links within this category may be less reliable.
  • The study has only looked at the link between alcohol and actually dying from cancer or cardiovascular disease. Links may be different if they looked at associations between alcohol and just being diagnosed with cancer or heart disease, for example.
  • The study is also only representative of adults over the age of 40.

Overall, maintaining a healthy lifestyle seems to be the best bet for reducing the risk of any chronic disease, be it through physical activity, balanced diet or reasonable alcohol consumption.

Current alcohol recommendations for both men and women are to drink no more than 14 units per week.  

Links To The Headlines

How exercise undoes the harm from drinking: Adults who booze regularly but exercise for five hours a week are no more likely to die than teetotallers. Mail Online, September 8 2016

Two hours a week of exercise could offset the dangers of alcohol. The Daily Telegraph, September 8 2016

Exercise can cut risk from alcohol-related diseases, study suggests. The Guardian, September 8 2016

Links To Science

Perreault K, Bauman A, Johnson N, et al. Does physical activity moderate the association between alcohol drinking and all-cause, cancer and cardiovascular diseases mortality? A pooled analysis of eight British population cohorts. British Journal of Sports Medicine. Published online August 31 2016

Statins cut heart deaths in men by 28% finds study

NHS Choices - Behind the Headlines -

"Statins cut the risk of dying from heart disease by 28% among men, according to the longest study of its kind," The Guardian reports.

Statins help reduce the level of low-density lipoprotein (LDL), or "bad cholesterol", in the blood. This in turn helps reduce the risk of cardiovascular disease (CVD).

Current UK guidelines recommend that people with a 1 in 10 chance of developing CVD at some point in the next 10 years should be offered statins.

The results of this new analysis led the researchers to conclude that more people with high cholesterol should be offered statins.

Researchers looked at data for a sub-group of men who had high cholesterol, but no signs of heart or circulation problems, at the start of the study.

They analysed the effects of taking statins or a placebo during the five-year trial and after a 20-year follow-up period.

People took statins or not as recommended by their doctor during the follow-up period.

The researchers say men who took statins during the trial period were about 25% less likely to get heart disease or have a major event like a heart attack or stroke during the trial, and in the 20 years afterwards.

The study provides evidence to back current recommendations that people at risk of heart disease benefit from taking statins.

But it doesn't provide evidence that younger people should take them (as some papers reported) as everyone in the study was over the age of 45.

 

Where did the story come from?

The researchers were based at Imperial College London, the University of Glasgow, Università degli Studi di Milano, the University of Western Australia, and the Academic Medical Centre Amsterdam.

The study was published in the peer-reviewed journal Circulation. It was funded by Sanofi, a statin manufacturer.

It was based on an original study funded by statin manufacturers Bristol-Myers Squibb and Sankyo. Several of the researchers reported receiving fees from multiple drug manufacturers.

The UK media seems to have missed the point that this isn't a new study, but a new analysis of a landmark study that took place mainly in the 1990s.

Several reports refer to it as a "major new study", and the Mail Online says people were randomised to take either a statin or placebo for 20 years – even though the randomisation period lasted only five years.

Most news stories say the study means young people should be taking statins, which seems to be based on comments from one of the researchers, who also seems to have said that women would benefit as well, even though no women took part in the trial.

 

What kind of research was this?

This was a post-hoc (after the event) analysis of results from a previously published randomised control trial with a 20-year observational follow-up period. The main results from the study have already been published.

Post-hoc analysis is less reliable than initial analysis because researchers already know the main results – this means they can be accused of "cherry-picking" results to prove the point they wish to make.

In this case, they wanted to see the effects of statins on people who had high cholesterol, but no heart or circulation disease, at the start of the study.

 

What did the research involve?

The original study – known as the West of Scotland Coronary Prevention Study (WOSCOPS) – was an early statin trial.

WOSCOPS recruited 6,595 men aged 45 to 64 with LDL cholesterol levels over 155mg/decilitre, and randomly assigned them to take pravastatin (a relatively weak statin) or placebo.

The trial ran from 1989 to 1995. After it finished, the men were followed up for another 20 years, during which time they and their doctors decided whether they wanted to take statins or not.

Results for the original trial and follow-up period have been published already.

This new analysis looked at one sub-group – 5,529 men with no evidence of cardiovascular disease at the start of the study. Researchers looked separately at results for those with LDL cholesterol above or below 190mg/decilitre.

They recorded the men who'd either developed coronary heart disease (non-fatal heart attack plus death from coronary heart disease) or had a major cardiovascular event (death from cardiovascular disease, non-fatal heart attack, or non-fatal stroke) during the trial or at the 20-year follow-up.

 

What were the basic results?

During the trial period, men who took pravastatin were:

  • 27% less likely to have coronary heart disease (hazard ratio [HR] 0.73, 95% confidence interval [CI] 0.59 to 0.89)
  • 25% less likely to have a major cardiovascular event (HR 0.75, 95% CI 0.62, 0.91)

Results for men with and without cholesterol over 190mg/decilitre had very similar results.

After 20 years of follow-up, men who'd originally taken pravastatin were:

  • 26% less likely to have coronary heart disease (HR 0.74, 95% CI 0.65, 0.84)
  • 21% less likely to have a major cardiovascular event (HR 0.79, 95% CI 0.71 to 0.88)

Again, results were similar between those with higher and lower cholesterol levels.

 

How did the researchers interpret the results?

In the paper, the researchers concluded their analysis "provides for the first time evidence for the benefits of LDL-C lowering for the primary prevention of [coronary heart disease] in individuals with primary elevations of LDL-C ≥190 mg/dL", and that this "may help reinforce current recommendations for this group of patients".

But they seem to have gone further in their comments to reporters. Lead researcher Professor Kausik Ray told The Daily Telegraph that millions of people in their 20s and 30s could benefit from taking statins.

 

Conclusion

This new analysis found that men without cardiovascular disease who were prescribed a statin were less likely to go on to develop heart disease or have a major cardiovascular event.

These findings from the five-year randomised controlled trial are useful – there's been a lot of debate about whether giving statins to people without any cardiovascular disease is helpful.

But it's harder to draw conclusions from the longer-term results, as these were from a non-randomised observational period. Potential confounding factors – such as the men's attitude to medicine, risk and health – may have influenced the results.

The study has other limitations we should bear in mind:

  • A post-hoc analysis is less reliable than a primary analysis because researchers are better able to cherry-pick the results they want.
  • The original study was carried out more than 20 years ago. Statins used today are usually stronger than those in the WOSCOPS study, and people's lifestyles nowadays are different. For example, more than 40% of men in the study smoked – this is much higher than today's smoking levels. The results may not be applicable to people today.

  • The researchers found little difference between outcomes for men with higher or lower cholesterol levels. That makes it hard to back up their conclusions that cholesterol is the most important factor and people with raised cholesterol are most in need of treatment, regardless of other factors like age.

Guidelines from the National Institute for Health and Care Excellence (NICE) in the UK recommend that people are offered statin treatment if their risk of a cardiovascular event, such as a heart attack or stroke, is at least 10% over 10 years.

People in this category should discuss the options with their GP. NICE has a decision aid to help people make up their minds.

Lifestyle measures that can reduce your cholesterol and risk of CVD include:

  • eating a healthy, balanced diet
  • exercising regularly
  • maintaining a healthy weight
  • limiting the amount of alcohol you drink
  • stopping smoking

Read more advice about treating high cholesterol.

Links To The Headlines

Statins cut the risk of heart disease death by 28% among men, study shows. The Guardian, September 6 2017

Statins DO work: Cheap pills slash heart attack and stroke deaths by 28% in men, 20-year study finds. Mail Online, September 7 2017

Millions of healthy younger adults ‘should take statins to prevent heart attacks’. The Sun, September 7 2017

Statins cut heart deaths by 28%. The Times (subscription required), September 7 2017

Links To Science

Vallejo-Vaz AJ, Robertson M, Catapano AL, et al. LDL-Cholesterol Lowering for the Primary Prevention of Cardiovascular Disease Among Men with Primary Elevations of LDL-Cholesterol Levels of 190 mg/dL or Above: Analyses from the WOSCOPS 5-year Randomised Trial and 20-year Observational Follow-Up. Circulation. Published online September 6 2017

Zika virus may be useful in treating brain tumours

NHS Choices - Behind the Headlines -

"Zika virus used to treat aggressive brain cancer," BBC News reports. Animal and laboratory research suggests a modified version of the virus could possibly be used to target and destroy cancerous cells.

The Zika virus was first discovered in 1947. It hit the headlines in 2016 when an epidemic of the virus began quickly spreading through parts of South and Central America.

The virus, spread by mosquitoes, rarely causes serious problems in adults. But it can lead to birth defects, specifically microcephaly (a small, not fully developed head), if a woman contracts the virus when pregnant.

The virus has the ability to cross from the blood into the brain, so researchers wanted to see if it could be used to treat a very aggressive type of brain cancer called glioblastoma.

Glioblastoma is hard to eradicate with conventional treatments because the stem cells that drive the growth of the cancer tend to recur after the more developed cancer cells are killed by chemotherapy or removed surgically. Average survival is only two years after diagnosis.

So far, using Zika virus to treat glioblastoma has only been researched in cultured cells and tissue in the laboratory, as well as in mice.

Results have been encouraging, but we don't know if the treatment would work in humans. And more work is needed to find out if the virus can be engineered so it's safe to use.

Where did the story come from?

The work was carried out by researchers from the University of California, Cleveland Clinic, Washington University School of Medicine, and the University of Texas Medical Branch, all in the US.

The research was funded by grants from the US National Institutes of Health and the US National Cancer Institute.

It was published in the peer-reviewed Journal of Experimental Medicine.

BBC News and the Mail Online gave balanced and accurate reports of the study, although their headlines overstated the stage the research is at.

What kind of research was this?

This laboratory-based research involved several phases of experiments using:

  • cells grown in the laboratory
  • human brain tissue extracted during surgery
  • mice

These types of experiments are all useful ways to investigate the action of a potential treatment in the laboratory before it can be tested properly in humans.

Researchers wanted to test the theory that Zika virus would infect and kill glioma stem cells (the cells that primarily drive the cancer) while sparing normal, non-cancerous brain cells.

What did the research involve?

Researchers tested the effect of different strains of Zika virus in several settings on:

  • glioma stem cells and more mature glioma tumour cells grown in the laboratory after being removed from patients, and cells in artificially grown "organoids" that mimic the arrangement of cells in the brain
  • tissue specimens of glioma tumours taken during surgery
  • non-cancerous brain tissue samples
  • mice injected with glioma cells that had grown into brain tumours

The researchers also looked at the effects of the West Nile virus, which is related to the Zika virus.

They used two strains of "natural" Zika virus, as well as a strain engineered to infect mice, as mice aren't usually susceptible to Zika.

They also looked at the effect of a strain of Zika engineered to be less likely to spread and cause disease in humans, in combination with an existing chemotherapy (temozolomide) that targets more mature glioma cells.

In the mouse experiments, the researchers randomly selected half the mice for treatment with Zika and half to act as a control group. They measured how much the tumours grew in the week after treatment and how long the mice lived.

What were the basic results?

Zika virus was much more likely to infect and kill glioma stem cells than other types of cells in the brain, including mature glioma cancer cells.

Glioma stem cells reproduced and grew in uninfected cultures, but they didn't reproduce when infected with either type of natural Zika virus. More of the glioma stem cells infected with Zika died.

In newly taken surgical samples, Zika virus infected more of the human glioblastoma tissue than normal brain tissue.

By contrast, West Nile virus infected all types of brain cells, whether cancerous or not, both in cultured cells and tissue samples.

In the mouse experiments, mice injected with adapted Zika virus showed slower tumour growth and lived longer – more than 50 days, compared with between 28 and 35 days for those not treated with Zika virus.

Engineered Zika virus tested alongside conventional chemotherapy on cultured glioma tumour cells also seemed to slow growth of tumour stem cells and improve the effects of the conventional chemotherapy.

How did the researchers interpret the results?

The researchers said the Zika virus "may offer a tailored therapy that could be used in combination with conventional therapies". They say it could help halt the recurrence of glioma stem cells after the mature tumour cells have been removed.

But they warned this research is only the "first step" in developing Zika virus as an anti-cancer therapy, and said "safety remains a paramount concern" with future use of the virus.

Conclusion

This is an interesting piece of research that shows how knowledge in one field of medicine can sometimes be applied to another field with surprising results.

But it's important to be realistic about the stage of research. This is very much a "proof of concept" study, and tests on cells, tissues and mice don't necessarily translate into a safe and effective treatment for humans.

The study has several limitations, but the fact the treatment so far hasn't been tested on humans is the most important. For one thing, Zika virus doesn't naturally infect mice, so researchers had to use a specially engineered virus that's different from the virus that infects humans.

Also, the glioma tumours in mice were taken from mouse models, so they weren't the same as human glioma tumours. The researchers say there are "technical challenges" to overcome before they can test human-derived glioma cells in mice.

They say it may be possible to make the Zika virus safe enough to use in glioma treatment, possibly by injecting it into tumour sites at the same time as surgery to remove tumours.

But clinical trials of such a therapy are still some way off.

Links To The Headlines

Zika virus used to treat aggressive brain cancer. BBC News, September 5 2017

Zika can kill brain tumors like John McCain's, study shows – paving the way to a groundbreaking new use for the mosquito-borne virus. Mail Online, September 5 2017

Links To Science

Zhu Z, Gorman MJ, McKenzie LD, et al. Zika virus has oncolytic activity against glioblastoma stem cells. The Journal of Experimental Medicine. Published online September 5 2017

Older babies 'sleep better' in their own room

NHS Choices - Behind the Headlines -

"Babies who sleep in separate rooms from their parents have earlier bedtimes, take less time to nod off and get more shut eye," the Mail Online reports on the results of an international survey looking at sleeping locations and outcomes in infants aged 6 to 12 months.

The parents of more than 10,000 infants aged 6 to 12 months completed an app-based questionnaire. As this was a US-based study, the results were split into two categories: the United States and international (Australia, Brazil, Canada, Great Britain and New Zealand).

The results showed babies who slept in separate rooms slept longer, got to sleep quicker, and were more likely to have a bedtime routine than those who slept in the same bed or room as their parents. Parents were also less likely to perceive bedtime as difficult.

The results seem to confirm the findings of a much smaller study we discussed back in June.

But a range of external factors, such as home environment, breastfeeding, and interaction with family and other caregivers, might also affect babies' sleep.

We can't say for certain that separate rooms are better for all infants. The study didn't look at the effect of babies sharing a room with a sibling, for example.

Current NHS guidance recommends keeping your baby in the same room as you in a separate cot for the first six months.

Placing your baby on their back to sleep from the very beginning, for both day and night sleeps, will reduce the risk of sudden infant death syndrome (SIDS).

 

Where did the story come from?

The study was carried out by researchers from Saint Joseph's University, Philadelphia, the Children's Hospital of Philadelphia, and Johnson and Johnson Consumer, all in the US.

It was funded by Johnson & Johnson, a multinational medical devices, pharmaceutical and consumer packaged goods manufacturing company, who also developed the mobile app used in this research.

There doesn't seem to be any conflict of interest on the part of the researchers, as the results of the study had no obvious commercial implication.

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

The Mail Online generally reported accurately on the results of the study itself, but got muddled by claiming that the findings "contradict guidelines by the American Academy of Pediatrics (AAP), which recommends babies sleep in the same room as their parents for at least the first six months to reduce their risk of sudden infant death syndrome (SIDS)".

This is neither true nor relevant – the study didn't look at the first six months of life, it investigated infants aged 6 to 12 months.

 

What kind of research was this?

This cross-sectional study used a questionnaire on an app to examine babies' sleep patterns, behaviours and problems in both a US and international sample of infants.

The researchers aimed to see if sleeping arrangements (where the infant slept) affected these sleep-related outcomes.

This type of research can identify patterns and associations between sleep location and sleep outcomes at a specific snapshot in time, but can't show trends over time or look at longer term outcomes.

It also can't determine cause and effect – in other words, that where a baby sleeps directly causes certain sleep outcomes. A range of other factors could also influence this.

Also, it's possible that parents of babies with underlying sleep problems unrelated to where they sleep just prefer to put them in the same bedroom because it's easier for them if their child wakes in the night.

 

What did the research involve?

The research involved 6,236 infants and their parents from the US, and 3,798 participants from Australia, Brazil, Canada, Great Britain and New Zealand, who all had infants aged between 6 and 12 months. It looked at the association between sleep location and sleep outcomes.

Participants completed a smartphone app-based expanded version of the Brief Infant Sleep Questionnaire (BISQ). They also reported demographic information. The app, Johnson's Bedtime Baby Sleep, was free and publicly available.

The questionnaire recorded expected developmental changes in infants and the potential influence of environmental factors.

It asked questions on:

  • sleep location in relation to parents: room-share, bed-share or separate sleeping (sharing with siblings was excluded)
  • infant daytime and night-time sleep patterns
  • sleep-related behaviours, such as how long it takes to fall asleep or how many times an infant wakes during the night

The app also included:

  • an electronic sleep diary
  • information on bedtime routines
  • lullabies
  • an online intervention – the intervention uses sleep data gathered by the app and then provides customised advice based on the data provided

 

What were the basic results?

The researchers found 37.2% infants aged 6 to 12 months from the US, and 48.4% in the international sample, slept in a separate room from their parents.

US infants sleeping in a separate room:

  • had significantly earlier bedtimes (20:08pm) than those room-sharing or bed-sharing (20:43pm and 20:52pm, respectively) – they also took less time to get to sleep (32.04 minutes versus 45.67 and 42.31, respectively)
  • woke up less in the night (2.00) than room-sharers (2.35) or bed-sharers (2.61), had a greater longest stretch of sleep (6.75 hours versus 5.88 and 5.33), and had a longer night-time sleep (9.57 hours versus 8.81 and 8.89)
  • were more likely to be reported as having a consistent bedtime routine (72.8% versus 56.0% room-share versus 51.5% bed-share) and more likely to fall asleep independently (35.5% versus 30.3% versus 17.4%)
  • resulted in fewer parents perceiving bedtime to be difficult (27.1% versus 37.1% room-share versus 42.3% bed-share) or their child having problems falling asleep (33.1% versus 43.6 room-share versus 48.1% bed-share)

Similar results were found for the international sample.

 

How did the researchers interpret the results?

The researchers concluded: "These results indicate that infants aged 6 to 12 months who sleep in a separate room have better parent-reported sleep outcomes in terms of increased sleep duration and sleep consolidation, as well as better sleep health practices (i.e. conforming with commonly recommended sleep behaviours) and parent perception of infant sleep."

 

Conclusion

This study seems to show that parents of infants aged 6 to 12 months who sleep in a separate room report better infant sleep outcomes, such as sleep times and sleep duration, than parents who keep their infant in the same room or bed.

These findings are similar to a study covered in June 2017, which found "independent sleepers" slept for longer aged nine months than room-sharers.

But there are some considerations that need to be taken into account:

  • This questionnaire-based study didn't follow infants over a long period of time, so we only know about their sleep behaviours and patterns at one particular time, not over a long period.
  • Many external factors might also contribute to sleep patterns and behaviours, including breastfeeding, interaction with family members and caregivers, having siblings, the home environment, and possibly cultural differences.
  • Parent-reported answers may not be accurate. For example, not all parents are going to closely time how long it takes their child to fall asleep or what their longest stretch of sleep is. There could also be potential for some bias in reporting, such as under-reporting sleep disruption in case this is perceived as them not coping well.
  • The majority of caregivers who responded to the questionnaire were mothers. The results might have been different if other caregivers had responded.

If your baby is over the age of six months, there are no known health reasons why they can't sleep safely in their own room as long as they're always placed on their back to sleep.

Get advice about sleep problems in young children.

Links To The Headlines

Babies who sleep in SEPARATE rooms from their parents have earlier bedtimes, take less time to nod off AND get more shut eye. Mail Online, September 4 2017

Links To Science

Mindell JA, Leichman ES, Walters RM. Sleep Location and Parent-Perceived Sleep Outcomes in Older Infants. Sleep Medicine. Published online August 12 2017

One in 10 men aged 50 'have the heart of a 60-year-old'

NHS Choices - Behind the Headlines -

"One-tenth of 50-year-old men have a heart age 10 years older than they are," BBC News reports. This is the finding of an analysis of 1.2 million people who used the NHS Heart Age Test.

The principle behind the test is that you can "age" your heart through unhealthy behaviour such as smoking and being obese.

Underlying conditions like high blood pressure and high cholesterol, which often have no noticeable symptoms, can also age the heart.

An obese smoker in their 50s who has high blood pressure and high cholesterol could have the heart of a 60- or 70-year-old.

The quick and simple test tells you the age of your heart compared with your actual age, and shows how many years you can expect to live in good health without having a heart attack or stroke.

The test was first launched two years ago, and initial results show 1 in 10 men aged 50 who took the test has a heart age of at least 60.

It also shows many people are unaware of their blood pressure. The test could be a good way of raising public awareness of cardiovascular health and the simple lifestyle changes that can reduce their risk.

If you want to know what your blood pressure and cholesterol levels are, a practice nurse at your local GP surgery can test these for you. Call your surgery for advice.

Where does the analysis come from?

The analysis was carried out by Public Health England (PHE), a Department of Health agency responsible for improving public health and protecting the public against health emergencies and hazards.

PHE launched the One You campaign in 2016 to help people live longer, happier lives with a particular focus on awareness of heart health.

PHE reports that every month, 7,400 people die from heart disease or stroke in the UK, with a quarter of these deaths in people under 75.

Most could be prevented through better awareness of heart health and by people making positive lifestyle choices.

As part of the campaign, PHE are encouraging people to take a simple three-minute online Heart Age Test. 

What is the test?

The test asks you a set of questions about factors known to have an effect on cardiovascular disease risk.

These include:

  • age, gender and ethnicity
  • weight and height – used to calculate your body mass index (BMI)
  • if you or a close relative under 60 has known cardiovascular disease
  • whether you smoke, or used to smoke
  • if you have diabetes, rheumatoid arthritischronic kidney disease or atrial fibrillation
  • whether you know your total cholesterol
  • if you know your blood pressure or have been on blood pressure treatment

It then tells you your heart age and the age, on average, you could expect to live to without having a heart attack or stroke.

It gives you a breakdown of your results, including your BMI and information on your cholesterol or blood pressure level (if you knew these), or alternatively recommends you get these checked.

It then gives you individual advice, such as ways you can lower your cholesterol or blood pressure through diet or activity.

It links to various recognised sources of advice on lifestyle, diet and activity, such as the British Heart Foundation and NHS Choices.

It also tells you where you can go locally for advice or testing, and whether you're eligible for the NHS Health Check.

The NHS Health Check is like a medical "MOT" for adults in England aged 40 to 74. It's designed to spot the early signs of stroke, kidney disease, heart disease, type 2 diabetes and dementia.

What do the test results show so far?

The Heart Age Test was launched in February 2015, and PHE has analysed 1.2 million test results so far.

The main finding reported is that 1 in 10 men aged 50 who've taken the test were found to have a heart age of at least 60, and around half of people who took the test didn't know their blood pressure.

PHE says 5.6 million people in England may have high blood pressure and not know it. The results suggest the test could play an important role in giving people a wake-up call about their heart health and what they can do to improve it.

Various experts have given their thoughts on the test.

Associate Professor Jamie Waterall, Lead for Cardiovascular Disease Prevention at PHE, said: "We should all aim for our heart age to be the same as our real age – addressing our risk of heart disease and stroke should not be left until we are older.

"The Heart Age Test is really important as it gives an immediate idea of heart attack and stroke risk, with no doctor's appointment needed."

Katherine Jenner, CEO of Blood Pressure UK, commented: "Getting your blood pressure tested in your nearest pharmacy or health centre can be the first important step to prolonging your life.

"Making simple changes, like doing more activity or quitting smoking, can reduce this risk, and PHE is urging adults to lower their heart age before it is too late."

What can I do about improving my heart health?

Although we can't change some risk factors for cardiovascular disease – such as age, gender, ethnicity and genetics – there are ways you can reduce your risk:

  • take regular exercise
  • eat a healthy diet high in fruit and vegetables and low in saturated fat, salt and sugar
  • quit smoking
  • drink alcohol in moderation and drink no more than 14 units a week

Get more advice on heart health.

Links To The Headlines

Tenth of men aged 50 'have heart age 10 years older'. BBC News, September 4 2017

How 50 is the new 60 as our hearts are ageing too fast: Unhealthy lifestyles mean one in five middle-aged men have an organ of someone who is a decade older. Mail Online, September 4 2017

Bad habits leave one man in six with an 'older' heart. The Times, September 4 2017

New insight into how excess belly fat may increase cancer risk

NHS Choices - Behind the Headlines -

"Belly fat releases proteins that fuel the growth of malignant [cancerous] cells," the Mail Online reports.

It's long been known that obesity is an independent risk factor for a number of cancers, including breast, bowel and liver cancer. But it's less clear why this is the case.

This question has become more pressing, as it's estimated obesity will soon overtake smoking as the leading preventable cause of cancer in the developed world.

A new study has investigated the possible biological mechanisms behind this link. Researchers focused on visceral adipose tissue, the fat that coats internal organs. Visceral fat leads to a bigger waist size and more belly fat.

The researchers found excess visceral fat stimulated the growth of normal, healthy cells and may promote cancerous change by releasing a protein called fibroblast growth factor-2 (FGF2).

But visceral fat wasn't able to stimulate growth when cells lacked FGF2 receptors. Receptors are specialised parts of cells designed to respond to certain chemical signals.

The researchers suggest the findings could pave the way for important cancer prevention strategies targeting FGF2. But this research is still in its very early stages.

Maintaining a healthy weight is one of the most effective ways of reducing your risk of cancer, as well as a number of other serious health conditions. 

Where did the story come from?

The study was carried out by researchers in the US from several institutions, including Michigan State University and the Yale School of Medicine.

Although the study wasn't directly funded by any organisation, individual authors received grants from different funding bodies, including the US National Institutes of Health and the Office of the Assistant Secretary of Defense for Health Affairs' Breast Cancer Research Program.

The study was published in the peer-reviewed journal Oncogene. It's available on an open access basis and can be read for free online.

Generally, the Mail Online's coverage was accurate. Their coverage also referenced a narrative review from July 2017 on the influence of visceral fat on health outcomes, but we're unable to comment on the accuracy of the reporting on that study.

What kind of research was this?

This animal and laboratory study aimed to investigate the relationship between excess body fat, specifically fat around the organs (visceral adipose tissue), and cancer risk.

There's plenty of evidence to confirm the link between having excess visceral fat and the risk of developing cardiovascular disease and type 2 diabetes.

Recent evidence suggests excess visceral fat may also be linked to the risk of developing breast and colon cancer.

But the exact biological mechanisms aren't well understood. The researchers hoped to study in more detail how visceral fat causes a normal, healthy cell to progress into a cancerous one.

Early-stage research is very useful for improving our understanding of mechanisms that occur at a cellular level. But even though mice are genetically similar to humans in many ways, we aren't identical.

That being said, regardless of whether human or animal cell lines are being studied, there could be external factors playing a role in the association that can't be explored, such as whether or not someone smokes.

What did the research involve?

The study involved both research in mice and tests on human fat cells in the laboratory.

The mice were either fed a low-fat diet, high-fat diet or normal diet, and were induced to grow cancerous cells using ultraviolet-B rays. Their visceral fat was then collected and any tumours were analysed.

The researchers also obtained samples of visceral fat tissue from mice and cancer-free obese human subjects. They studied whether incubating this tissue with the epithelial cells that line organs caused cancer.

What were the basic results?

The researchers found visceral fat tissue stimulated the growth of a protein called fibroblast growth factor-2 (FGF2) in some cases if the FGF2 receptors were present.

This in turn stimulated the growth of epithelial cells, which may have the possibility of turning malignant (cancerous).

In the live mice, the researchers also discovered that circulating levels of FGF2 were associated with the formation of non-melanoma tumours.

How did the researchers interpret the results?

The researchers suggest that the release of FGF2 could be a pathway by which visceral adipose tissue leads to tumour generation.

They concluded that, "These data therefore suggest FGF2 stimulation of [FGF2 receptors] as a previously unappreciated link between [visceral adipose tissue] and cell transformation.

"This key finding begins to inform how [high-fat diets] and/or visceral adiposity elevate cancer risk, previously suggested only via epidemiological studies." 

Conclusion

This animal and laboratory study investigated the possible cellular relationship between excess body fat – specifically fat around the body organs – and cancer risk.

It seems one key mechanism by which excess visceral fat could stimulate healthy cells to develop into cancerous ones could be through FGF2 levels.

The researchers hope their study could pave the way for possible cancer prevention strategies by stopping FGF2 production in obese people with excess belly fat.

They even go as far as suggesting that blocking FGF2 receptors could be one part of a treatment approach after a diagnosis of breast or skin cancer.

But it's too early to speculate about the implications of this research. Early-stage animal and laboratory studies like this one are useful for better understanding mechanisms that occur at a cellular level.

We don't know that this is the whole answer. Various genetic, health and lifestyle factors are likely to be play a combined role in the association between body fat and cancer development.

Find out more about losing weight.

Links To The Headlines

How having a thicker waist raises your cancer risk: Belly fat releases proteins that fuel the growth of malignant cells, study finds. Mail Online, August 31 2017

Links To Science

Chakraborty D, Benham V, Bullard B, et al. Fibroblast growth factor receptor is a mechanistic link between visceral adiposity and cancer. Oncogene. Published online August 7 2017

Going to university may cut your risk of heart disease

NHS Choices - Behind the Headlines -

"Why gaining a degree could help you live longer," The Daily Telegraph reports. A new gene study found people with genes associated with spending longer in education had around a 33% reduced risk of developing heart disease.

One of the practical difficulties about assessing the effects of education on heart health is the long gap between a person's time at school and university and the expected time when someone would be vulnerable to heart disease. The researchers estimated that the average length between the two could be around 50 years.

So researchers attempted to overcome this difficulty by looking at genetic variations known to be associated with spending more or less time in education. And then seeing if these variants had any corresponding effects on heart disease risk.

They found those with "longer education genes" (said to translate to around 3.6 years more in education) had a lower risk of heart disease than those with "shorter education genes".

And people with "longer education genes" were less likely to smoke and be overweight, both of which could contribute to heart disease risk.

But the use of these gene markers was very much an exercise in educated guesswork. We have no idea whether all people with "longer education genes" went to university, and similarly, whether people with "shorter education genes" left school at 16.

Not everyone wants (or can afford) to go to university. However, you can reduce your risk of heart disease by having a healthy, balanced diet, being physically active and not smoking.

 

Where did the story come from?

The study was carried out by researchers from academic and research institutions from the UK, Poland, Lithuania, the Czech Republic, Russia, Brazil, Estonia and Italy.

It was funded by a range of institutions, including the Wellcome Trust, the Medical Research Council and the National Institute for Health Research. None of the funders had a role in the design, data collection, analysis, interpretation, or writing of the study.

The study was published in the peer-reviewed medical journal BMJ on an open-access basis, meaning it is freely available to read online.

The Daily Telegraph reported the research accurately, explaining that better educated people were also less likely to smoke, and more likely to have a lower BMI and a more favourable blood fat profile, all of which probably contributed to their lower risk of heart disease.

The Mail Online's reporting was more misleading, suggesting that a definite cause and effect relationship between time spent in education and heart disease risk had been proven. At best you could say that a possible relationship between the two may exist.

 

What kind of research was this?

This was a study looking at whether educational attainment (as measured by looking at the genetic variants linked to years of schooling) can affect the risk of developing coronary heart disease.
 
Coronary heart disease is a major cause of death worldwide and happens when the heart's blood supply is blocked or disrupted by a build-up of fatty substances causing narrowing and hardening of the coronary arteries. Known risk factors for developing coronary heart disease include smoking, having high blood cholesterol levels and having diabetes but the role of a person's education levels is not known.

 

What did the research involve?

Researchers analysed data from 707,903 participants mostly of European origin, to determine if there is a genetic link supporting the idea that education is a causal risk factor in the development of coronary heart disease (CHD).

They also aimed to see whether education influences other risk factors for cardiovascular disease.

They looked at 162 independent genetic variants associated with educational attainment, previously identified by the Social Science Genetic Association Consortium. These genetic variants were used as a proxy for randomly assigning 543,733 participants to "more education" or "less education".

The researchers then compared the CHD risk of the two groups of participants – using data from the Coronary Artery Disease Genome wide Replication and Meta-analysis plus the Coronary Artery Disease Genetics Consortium (CARDIoGRAMplusC4D) – to see if participants with genetic variants for longer education had a different CHD risk than those with genetic variants for shorter education.

They also looked at observational studies to see if there was an association between education and risk of CHD, using data collected between 1983 and 2014. They looked at data analysed from 164,170 participants from the National Health and Nutrition Examination Surveys (NHANES) and the Health, Alcohol, and Psychosocial factors In Eastern Europe (HAPIEE) study.

 

What were the basic results?

The data from the genetics study showed there were 63,746 CHD events (fatal and non-fatal).

  • A genetic predisposition towards 3.6 years extra education was linked with a 33% reduced risk of CHD (odds ratio [OR] 0.67, 95% confidence interval [CI] 0.59 to 0.77).
  • An extra 3.6 years of education (due to genetic predisposition) was linked with a 35% lower likelihood of smoking (OR 0.65, 95% CI 0.54 to 0.79), a lower body mass index (BMI) (OR 0.17, 95% CI 0.26 to 0.08) and more favourable blood lipids (triglycerides) (OR 0.14, 95% CI 0.22 to 0.06).

 

How did the researchers interpret the results?

The researchers conclude that this "study found support for the hypothesis that low education is a causal risk factor in the development of coronary heart disease. Potential mechanisms could include smoking, body mass index, and blood lipids. In conjunction with the results from studies with other designs, these findings suggest that increasing education may result in substantial health benefits."

 

Conclusion

This study indicates there may be some genetic support for the idea that spending longer in education contributes to lowering the risk of CHD. The researchers also demonstrate that this may be because people who spend longer in education have a lower BMI and are less likely to smoke.

However, there are some limitations to this research that need to be considered:

  • The genetic variations identified as being associated with education may not be markers for education at all, but more basic biological pathways.
  • The authors do not account for the fact that differences in education might be due to brain function, which also influences mental health, lifestyle and behaviour choices, all of which are likely to contribute to cardiovascular health.
  • The research does not address whether the link between "longer education genes" and decreased risk of CHD might be down to educational ability rather than just length of time spent in education.
  • The increased time in education might have led to increased wealth for many of the participants, which may contribute to the decreased risk of CHD.

You don't need to get a degree to reduce your risk of heart disease. You can lower your risk by having a healthy, balanced diet, being physically active and not smoking.

Read more advice about preventing heart disease.

Links To The Headlines

Why gaining a degree could help you live longer. The Daily Telegraph, August 31 2017

Having a degree helps cut heart attack risk by a third: Researchers say better educated people are less likely to smoke and do more exercise. Mail Online, August 31 2017

Links To Science

Tillmann T, Vaucher J, Okbay A, et al. Education and coronary heart disease: mendelian randomisation study. British Medical Journal. Published online August 30 2017

Sitting for 20 minutes less a day won't make you 'more muscly'

NHS Choices - Behind the Headlines -

"Spending just 20 minutes less sitting a day reduces blood sugar levels, improves cholesterol AND even makes you more muscly," is the Mail Online's overly optimistic claim.

Researchers in Finland recruited people who worked in offices and had young children for a study investigating whether training could help cut the amount of time the parents spent sitting. Regular, prolonged periods of sitting puts people at risk of developing diseases such as diabetes and heart disease.

Despite a programme of counselling and a lecture aimed at making people more active during work and leisure hours, people sat for only 21 minutes less for every eight hours during the first three months of the study, and only during leisure time. By the end of the year-long study, people were only sitting for 8 minutes less than those in the control group.

Researchers reported "some small positive changes" in blood sugar during the first three months, and in cholesterol biomarkers and lean leg mass at the end of the study, compared with parents who had not received the intervention. It's not clear how clinically important these changes were.

While it's true that every little helps, there's very much a dose-dependent relationship when it comes to the benefits of exercise: the more you do, the more you benefit.

You should aim to at least meet the minimum physical activity guidelines for adults.

Where did the story come from?

The study was carried out by researchers from the University of Jyväskylä in Finland. It was funded by the Finnish Ministry of Education and Culture, the Ellen and Artturi Nyyssönen Foundation, the Juho Vainio Foundation and the Yrjö Jahnsson Foundation. It was published in the open-accesspeer-reviewed PLOS One medical journal so is free to read online.

The Mail Online's interpretation of the study does not stand up to much scrutiny.

The 20-minute figure cited in the headline was sustained for only three months and, rather than making people "more muscly", lean leg mass stayed about the same in people who were on the programme. It's just that those who weren't on the programme lost lean leg mass.

Reduced blood sugar levels lasted only three months, and the changes in proteins related to cholesterol metabolism were small and of uncertain importance.

What kind of research was this?

This was a cluster randomised controlled trial (RCT). In cluster RCTs, groups of people are randomised, rather than individuals. In this case, neighbourhoods in the Finnish city of Jyväskylä were randomised, with the people living in them recruited to either the control or intervention arm of the study. RCTs are usually good ways to measure the effect of an intervention.

However, in this study, the intervention – a lecture and counselling about reducing sedentary time – was not "blinded". People knew whether or not they were receiving the lecture and counselling, which reduces the reliability of the results.

What did the research involve?

Researchers picked 14 neighbourhoods in the city of Jyväskylä, with seven randomly assigned to receive the intervention programme and seven to act as controls.

They recruited parents who had children aged three to eight in kindergartens and infant schools in the 14 neighbourhoods. The parents were recruited either individually or as pairs. There were 133 participants overall, with 71 parents from the intervention neighbourhoods and 62 from the control neighbourhoods.

Parents from the intervention neighbourhoods underwent the study programme of a lecture followed by counselling sessions. Researchers looked to see how activity levels and sedentary time changed over a year, and whether physical assessments also changed.

Everyone had a physical assessment and tests, including measurements of physical activity, at the start of the study, and after 3, 6 and 12 months. These included body composition, blood pressure, and blood tests to measure insulin resistance, cholesterol and blood sugar.

People were excluded from the study if starting body mass index was above 35 (which could be considered as being morbidly obese if they had other health problems), they were pregnant at the start of the study, they had long-term illnesses or if the child had a disability that delayed their development of movement skills.

Diet was assessed through participants keeping diaries for three weekdays and a weekend day at the beginning and end of the study, and on a weekday at three, six and nine months.

The intervention group's lecture explained the potentially harmful effects of being too sedentary. During counselling sessions, parents set goals to reduce their sedentary time at work and at home. During follow-up phone calls, they discussed their progress towards the goals and any problems they'd had achieving them.

The researchers compared the difference between the change from baseline between parents in the intervention and the control groups for:

  • total sedentary time
  • work sedentary time
  • weekday leisure sedentary time
  • weekend leisure time
  • light activity time
  • moderate to vigorous activity time
  • breaks from sitting per hour during sedentary time

These were measured by giving people an accelerometer to wear (a device similar to a fitness tracker) for seven days at five points during the study year.

What were the basic results?

After three months, parents who went through the programme showed no changes in their total, workplace or weekend sedentary time compared with parents in the control group, but they were doing better on weekday leisure time:

  • Compared with the control group, for every 8 hours, they sat for 21.2 minutes less (95% confidence interval [CI] -37.3 to -5.1).
  • After 12 months, they were sitting for just 7.9 minutes less than the control group (95% CI -24.0 to 8.3). This difference wasn't statistically significant – it could have been down to chance.

In the first three months, the programme group did more moderate to vigorous physical activity than the control group, but that was because the control group's levels of activity dropped, not because the programme group did more activity.

There were a few differences in people's biochemical and physical test results.

Out of 12 tests of body composition and blood pressure, there was only one difference (lean leg mass, or muscle) between the groups after 12 months. However, this was mainly because the control group had lost muscle, whereas the programme group's stayed about the same (mean difference between groups 0.48%, 95% CI 0.18 to 0.77).

Of 14 biochemical test results, only two – involving levels of a protein called apolipoprotein A1, related to the metabolism of cholesterol – showed a difference between the two groups after 12 months.

How did the researchers interpret the results?

The researchers said their results showed their intervention "induced a small beneficial intervention effect on weekday sedentary leisure time throughout the whole year". They added that "some small positive changes in biomarkers were observed" at the same time.

They also noted that the initial decrease in overall sitting time achieved in the first three months of the study was not maintained over the year.

Conclusion

Despite the encouraging headlines, the study showed it isn't easy to get people to reduce their overall sedentary time. It's interesting that people were better able to make changes at home – especially when both parents had been through the programme – than in the office.

Future programmes could look at whether workplace interventions, which might include group activities or changes to the office environment, are more successful at reducing time spent sitting.

We don't know the clinical significance of the small changes in some of the physical and biochemical results found in the programme group.

It's surprising that any changes were found at all when the difference in activity levels was so small. One possibility is that the small number of participants and the large number of tests threw up some misleading results.

There are several other limitations to the study:

  • It was subject to selection bias. Only 30% of people contacted showed any interest in participating, meaning those who did were likely to be more motivated in the first place, so the results may not be applicable to the general population.
  • People may have changed their usual activity level when wearing the accelerometer.

Any effort to help people become less sedentary is to be applauded, but it's likely most people will need to do more than just sitting down for a few minutes less to make a big difference to their long-term health.

While 20 minutes more exercise a day is certainly better than none, if you have been inactive for a while, you should aim to gradually build up your activity levels until you meet the recommended minimum for adults.

Read more advice about getting started with or returning to exercise.

Links To The Headlines

Spending just 20 minutes less sitting a day reduces blood sugar levels, improves cholesterol AND even makes you more muscly. Mail Online, August 30 2017

Links To Science

Pesola AJ,  Laukkanen A, Heikkinen R, et al. Accelerometer-assessed sedentary work, leisure time and cardio-metabolic biomarkers during one year: Effectiveness of a cluster randomized controlled trial in parents with a sedentary occupation and young children. PLOS One. Published online August 24 2017

Results of global fats and carbs study not very relevant for UK

NHS Choices - Behind the Headlines -

"Eating a low-fat diet 'increases your risk of dying young by 25%'," is the stark but somewhat misleading report in The Sun. The study the headline is based on mainly looked at people in lower- and middle-income countries, where diets are very different, so the results may not be relevant to the UK.

Many previous studies linking high levels of saturated fat to heart disease and early death were carried out in high-income countries, such as the UK and US, where heart disease and consumption of saturated fats are both relatively high. The resulting recommendations that people avoid a high-fat diet may not be very relevant in countries such as Bangladesh and Zimbabwe, where eating enough may be a more pressing concern than weight gain. That's why this latest study focused on lower- and middle-income countries.

The results of this latest study suggest people who get more than three quarters of their total calories from carbohydrates have a 28% higher risk of death than those who get about half their calories from carbs.

However, people from lower- and middle-income countries are more dependent on refined carbohydrates, such as white rice. These are known to be less healthy than unrefined sources, such as brown rice and wholemeal bread, which are more readily available in the UK.

The researchers say their results suggest global dietary guidelines should be revised. However, their recommendations – that carbohydrates should provide 50 to 55% of energy intake and fat around 35% – are in line with existing UK dietary guidelines.

The whole "fats vs carbs" debate is arguably a bit of a sideshow: the truth is that, based on the latest UK obesity statistics, many of us simply eat too much.

Where did the story come from?

The study was carried out by researchers from universities and research centres in 18 countries around the world: Canada, Sweden and the United Arab Emirates (high-income countries); Argentina, Brazil, China, Chile, Colombia, Iran, Malaysia, occupied Palestinian territory, Poland, South Africa and Turkey (middle-income countries); and Bangladesh, India, Pakistan and Zimbabwe (lower-income countries).

It was funded by many local and national organisations, and by several pharmaceutical companies. The results were presented at the European Society of Cardiology Congress in Barcelona, Spain, and published in the peer-reviewed medical journal The Lancet.

The reporting of this study in the UK media was generally poor. None of the sources made clear the limited relevance of the study to the UK. For example, The Sun reported: "Cutting back on butter, cheese and meat raised the risk of an early death." But people in the study in countries such as India were unlikely to be "cutting back" on cheese and meat – it's more likely they were unable to afford to eat a lot of it, or that their traditional diet did not include much meat or dairy.

The Independent said: "Consuming high levels of all fats cuts early death rates by up to 23%." However, the report does not mention that these "high" levels were around 35% of calorie intake – around the average for the UK.

What kind of research was this?

This was a population-based cohort study using food-frequency questionnaires to sample adults aged 35 to 70 in 18 countries. Researchers wanted to see whether the dietary balance of fat, protein and carbohydrate was linked to people's chances of dying from any cause, or having a major cardiovascular event such as a heart attack, stroke or heart failure.

Cohort studies, like all observational studies, may be affected by confounding factors. This means we can't be sure that one factor (diet) is directly linked to another (death or cardiovascular disease).

What did the research involve?

Researchers recruited adults from 18 countries – 3 high-income, 11 medium-income and 4 lower-income. People filled in questionnaires about their diet, and were assessed for a range of health and lifestyle factors.

They were followed up at three, six and (for those who could be contacted) nine years to see what had happened to them. The groups were then divided into "quintiles", or fifths, from the highest consumption of different nutrients recorded to the lowest.

After adjusting for confounding factors, the researchers looked to see how diet was linked to chance of death or cardiovascular disease.

They recruited 148,723 people, of whom 135,335 remained after excluding those with missing data, a history of cardiovascular disease or who gave implausible answers on their dietary questionnaire.

The questionnaires were designed to be suitable for the country or region being sampled, and all of them mapped back to a method for translating food (potatoes, butter) into food types (carbohydrates, saturated fats).

The researchers adjusted their figures to account for:

  • age
  • sex
  • education level
  • smoking
  • physical activity
  • waist:hip ratio

They also looked at whether the people had diabetes, whether they lived in an urban or rural location, and their total calorie intake.

Asian countries – which had much higher levels of carbohydrate consumption than other countries – were also analysed separately to see if the results held true across different regions.

What were the basic results?

Of the 135,335 people in the study, 1,649 died of cardiovascular disease and 3,809 died from other causes.

The researchers compared the group of people who ate the most carbohydrate (average 77.2% of calories) with those who ate the least (average 46.4% of calories). They found:

  • People who ate the most carbohydrate were 28% more likely to have died than those who ate the least (hazard ratio [HR] 1.28, 95% confidence interval [CI] 1.12 to 1.46).
  • There was no difference in the risk of having major cardiovascular disease (HR 1.01, 95% CI 0.88 to 1.15).

They compared people who ate the most total fat (35.3%) with those who ate the least (10.6%). They found:

  • People who ate the most fat were 23% less likely to have died than those who ate the least (HR 0.77, 95% CI 0.67 to 0.87).
  • There was no difference in risk of having major cardiovascular disease (HR 0.95, 95% CI 0.83 to 1.08).

Looking at different types of fat, they found that every type – saturated, polyunsaturated and monounsaturated – revealed a similar pattern. However, when they plotted the results on a graph, it didn't go in a straight line, suggesting that both too much and too little fat could be a problem.

How did the researchers interpret the results?

The researchers said: "We found that high carbohydrate intake (more than about 60% of energy) was associated with an adverse impact on total mortality and non-cardiovascular disease mortality. By contrast, higher fat intake was associated with lower risk of total mortality."

They added: "Individuals with a high carbohydrate intake might benefit from a reduction in carbohydrate intake and increase in consumption of fats."

However, they also warned that the study "does not provide support for very low carbohydrate diets", saying that "a certain amount of carbohydrate is necessary to meet short-term energy demands during physical activity, and so moderate intakes (eg 50 to 55% energy) are likely to be more appropriate than either very high or very low carbohydrate intake".

Conclusion

The results of the study have been presented in the media as if they overturn all current dietary guidelines. In the UK at least, that is completely misleading. The study results support the UK guidelines, having found that people who get around 50% of their calories from carbohydrates and 35% from fat, as recommended by Public Health England, were likely to live the longest.

There are some limitations to the study, not least that observational studies cannot prove cause and effect.

For example, the very low fat and high carbohydrate levels of diets found among some participants in the study might simply represent poverty – rice, flour and sugar tend to be much cheaper than animal products such as butter and meat. It's not a surprise that people living on diets where most of their energy comes from nutrient-poor sources, such as white rice, are likely to live shorter lives. However, this does not apply widely in the UK.

The researchers may have a point that global guidelines for diet need to be revised in the light of these international findings, particularly in parts of the world where under-nutrition is more of a problem than obesity. However, UK guidelines are already in line with the study findings.

For more information about a healthy diet, see the Eatwell Guide.

Links To The Headlines

Eating a low-fat diet 'increases your risk of dying young by 25%'. The Sun, August 29 2017

Low-fat diets could increase the risk of an early death: Major study challenges decades of advice as it reveals fat has a PROTECTIVE effect. Mail Online, August 29 2017

Low-fat diets could kill you, warns major study. The Independent, August 29 2017

Low-fat diet could kill you, major study shows. The Daily Telegraph, August 29 2017

Links To Science

Dehghan M, Mente A, Zhang X, et al. Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. The Lancet. Published online August 29 2017

Anti-inflammatory drug may help prevent heart attacks

NHS Choices - Behind the Headlines -

"Anti-inflammatory drug 'cuts heart attack risk'," BBC News reports. A major study found canakinumab – an anti-inflammatory drug originally designed to treat rheumatoid arthritis – could also reduce the risk of having another heart attack in people who have already had one.

The study included more than 10,000 people who'd already had a heart attack. They were assigned to receive either injections of the drug canakinumab or a placebo.

Canakinumab is what's known as a monoclonal antibody – an engineered antibody designed to modify the immune system. It turns off the process of inflammation, making it useful for serious inflammatory conditions like rheumatoid arthritis.

Not everyone who has a heart attack has raised cholesterol levels, so it's unclear whether giving statins to these groups of patients would reduce the risk of another heart attack. The researchers wanted to see if a drug that reduces inflammation would be of more use.

After four years, researchers found people who received the higher doses of canakinumab (150mg or 300mg) were significantly less likely to have had another heart attack or a stroke, or to have died from cardiovascular disease.

But people taking the drug had a higher risk of developing fatal infections. Though this outcome was rare, it's a serious risk that needs investigation.

We also need to see how the drug compares with other treatments currently used for people who've had a heart attack.

Where did the story come from?

The study was carried out by a large team of researchers from an extensive number of organisations worldwide, including Brigham and Women's Hospital, Harvard Medical School, and Baylor College of Medicine in the US, Novartis in the US and Switzerland, and the Federal University of São Paulo and the University of São Paulo Medical School in Brazil.

It was funded by Novartis, the company that manufactures canakinumab. It was published in the peer-reviewed New England Journal of Medicine.

Overall, the media coverage of this story was well balanced, although the headlines didn't mention that the study only looked at people who'd already had a heart attack.

Many newspapers claimed that canakinumab was "better than statins", but this isn't really a useful comparison and doesn't reflect what was done in the study.

If canakinumab was licensed as a preventative medication, it's likely it would be given to people who wouldn't benefit from taking statins.

The papers acknowledged this treatment has potential downsides and more research is needed before it could be used in routine care.

What kind of research was this?

This placebo-controlled randomised clinical trial aimed to see whether the anti-inflammatory drug canakinumab (given at a specific dose of 50mg, 150mg or 300mg) could reduce the risk of further cardiovascular events in people who'd had a heart attack and had blood markers of inflammation.

Canakinumab is a monoclonal antibody given by injection. It's currently licensed in the UK for the treatment of a selection of rare inflammatory conditions.

As prior research supports the role of inflammatory processes in the build-up of fatty deposits in the arteries (atherosclerosis), it's thought anti-inflammatory drugs could affect the risk of heart attacks.

The study was very large, well-conducted and well reported. Its design, as a randomised controlled trial, is ideal for looking at how canakinumab might affect heart attacks.

What did the research involve?

Researchers enrolled people who'd previously had a heart attack (myocardial infarction) and lived in one of the 39 countries where the research took place.

The participants also had a raised blood level (2mg per litre or more) of an inflammatory marker called high-sensitivity C-reactive protein (hs-CRP). Raised levels of this protein may indicate people at risk of having further heart attacks.

People weren't allowed to take part in the study if they had:

  • a history of chronic or recurrent infections
  • previous cancer (except basal cell skin cancer)
  • suspected or known problems with their immune system
  • a history or high risk of tuberculosis or diseases related to HIV
  • been using other anti-inflammatory treatments

The 10,016 people recruited to the study were split into four groups to receive either a placebo (3,344 people) or canakinumab at either 50mg (2,170 people), 150mg (2,284 people) or 300mg (2,263 people) doses.

The placebo, 50mg and 150mg doses were given by injection every three months. People receiving the 300mg dose initially had two injections a fortnight apart before switching to every three months.

Participants were monitored over the next four years. The researchers were mainly interested in whether the participants had any further heart attacks or a stroke, or died from cardiovascular disease during this time.

Other outcomes of interest included hospitalisation for unstable angina and need for surgery to improve blood flow to the heart. The researchers also looked at any negative reactions to the treatment.

They analysed all participants in their assigned treatment groups, even if they stopped or changed treatment. This is known as an intention to treat analysis.

What were the basic results?

After four years, a total of 1,490 participants had experienced the main combined outcome of heart attack, stroke, or death from cardiovascular disease.

Overall, there was an average of 4.5 of these events per year per 100 people in the placebo group.

The risk in the treatment groups was:

  • 50mg group – 4.11 events per year per 100 people (not statistically significant compared with placebo)
  • 150mg group – 3.86 events per year per 100 people (a 15% lower risk compared with placebo, hazard ratio 0.85, 95% confidence interval 0.74 to 0.98)
  • 300mg group – 3.90 events per year per 100 people (a 14% lower risk, hazard ratio 0.86, 95% confidence interval 0.75 to 0.99)

When combined with other outcomes, the 150mg dose was considered the best.

The researchers found people taking any dose of canakinumab were at higher risk of fatal infections like sepsis. The rate of death from infection was 0.31 per 100 people in the treatment groups, compared with 0.18 in the placebo group.

A low white blood cell count was far more common in the treatment group compared with the placebo group, which could make people vulnerable to infections.

A similar pattern was found with a reduction in platelets, the cells that help keep blood sticky and prevent excessive bleeding, though no increased bleeding risk was reported.

Consistent with the known effects of the drug, treatment was also linked with fewer reports of arthritis and gout.

How did the researchers interpret the results?

The researchers concluded that the 150mg dose every three months led to a significant reduction in recurrent cardiovascular events compared with placebo.

The drug also reduced the inflammatory marker hs-CRP, which the researchers suggest indicates a reduction of inflammation overall.

They also noted that treatment had no effect on cholesterol levels.

Conclusion

This well-conducted study shows promising signs that canakinumab may reduce the risk of future heart attacks and other cardiovascular events in people who've had them in the past.

But before any changes are made to the current licensing of this drug, further research is needed to confirm the beneficial effects and the optimal dose.

Most importantly, researchers will need to focus on the observation that the drug lowered white blood cell counts and increased the risk of fatal infection.

They estimated around 1 in every 300 people taking canakinumab would die of a fatal infection. This number, while low, is still a concern if you're planning to potentially treat thousands of people.

It also remains to be seen how this drug compares with existing drugs used in the secondary prevention of heart attack.

Many people could potentially be eligible for this treatment, so we need to be sure that the benefits outweigh any risks.

Links To The Headlines

Anti-inflammatory drug 'cuts heart attack risk'. BBC News, August 28 2017

Best heart drug since statins: New injection could save thousands of lives by preventing heart attacks and also slash cancer risk. Mail Online, August 27 2107

Heart attack and cancer deaths could be cut by new drug. Sky News, August 28 2017

Wonder drug breakthrough could save thousands of lives from heart attacks and cancer. Daily Mirror, August 27 2017

New wonder drug hailed as biggest breakthrough in fight against heart attacks and cancer. The Daily Telegraph,  August 27 2017

Links To Science

Ridker PM, Everett BM, Thuren T, et al. Anti-inflammatory Therapy with Canakinumab for Atherosclerotic Disease. The New England Journal of Medicine. Published online August 27 2017

Reports that 'women have more stamina' look a little weak

NHS Choices - Behind the Headlines -

"Women have more stamina than men," is the definitive sounding, yet entirely unsupported headline in The Times.

The study the headline is based on involved just nine women and eight men. Researchers asked each participant to do an exercise similar to calf raises (where the calves are used to lift a weighted bar or similar) 200 times.

It found that although men were more powerful and faster to begin with, they also became exhausted more quickly.

But the study was carried out in a lab and performance might differ to real life physical activity. It also didn't look at cardiovascular fitness and only investigated one muscle in the body – other muscles might perform differently.

For many people in England, it's not stamina that's the problem – it's actually taking part in exercise in the first place.

Read more advice about fitness and exercise.

 

Where did the story come from?

The study was carried out by researchers from the University of Oregon in the US and the University of Guelph and University of British Columbia in Canada. The study did not report funding sources.
 
The study was published in the peer-reviewed journal Applied Physiology, Nutrition, and Metabolism.

While the body of The Times and the Mail Online's reporting was accurate, both used misleading headlines. As discussed, The Times' headline was far too definitive for such a small study, while the Mail's claim that "the greater staying power of females means they can beat men in gruelling ultra-marathons – extreme running and cycling events that can last days" is entirely unfounded.

 

What kind of research was this?

This was a laboratory based study comparing a small number of men and women doing repetitive exercises similar to calf raises and looking at the effect of repetition on fatigue.

This type of research is good at looking at the mechanics behind why there might be differences in things like muscle fatigue between men and women. However, it cannot prove that women are better than men at endurance events as this depends on a range of things, including overall fitness. Ability also depends on training levels and preferred type of exercise.

 

What did the research involve?

Researchers took nine women and eight men from a local university in the US, all of whom were fairly physically active. They aimed to see if women were less likely to tire following a calf raise exercise repeated many times, and to examine if certain muscle-related factors were responsible for the fatigue.

Male and female participants were matched for age and physical activity levels and were asked to complete a calf raise-type exercise. They did 3-4 calf raises at maximum voluntary contraction (MVC), a measure of muscle strength. This provided the baseline MVC for each participant.

They were then asked to perform 200 of these calf raise exercises at 30% of MVC and were encouraged to carry them out as quickly and forcefully as possibly for all contractions.

They measured muscle performance by looking at:

  • peak power – calculated using the maximum force applied and the speed the exercise was completed
  • rate of force development (a measure of explosive strength) – calculated using the change in force applied divided by the change in time
  • rate of speed development – calculated using the change in speed divided by the change in time

 

What were the basic results?

Women had a lower MVC (lower muscle strength), slower speed and less peak power than men. They were also lighter and shorter than men.

But immediately after the fatigue task (200 reps) had ended:

  • women had a 15% less fatigue-related change in peak power (force and speed of exercise compared with men) – in other words, they tired less
  • the change in force applied at peak power was 11% less for women compared with men
  • women showed less change in power and speed at peak power over time compared with men

 

How did the researchers interpret the results?

The authors conclude that their study "indicates that females are less fatigable than males when performing fast unconstrained velocity shortening plantar flexions and this sex-related difference is, at least partially, a result of time-dependent mechanical factors within the muscle that contribute to rapid power production."

 

Conclusion

This study in a small number of students in the US indicates that when repeating the same calf-raising movement, women showed less fatigue in terms of force applied and time taken to complete the exercise.

Some UK media outlets directly link this to women being better than men at lengthy aerobic exercise activities such as ultra-marathons and long distance cycling.

However a number of factors might mean this is not necessarily the case:

  • This was undertaken in a laboratory using seated exercise and participants might perform differently when undertaking physical activity normally.
  • Only one muscle was investigated – other muscles in the body might perform differently.
  • The study used a very small number of participants and the results cannot necessarily be generalised to the whole population.
  • The participants were an average age of 21-22, so while this might be relevant for younger adults, it might not apply to older adult populations.
  • While women showed less of a change (i.e. tired less) in things such as power and speed, they had lower scores on these parameters to start with – they were slower, less powerful and weaker. So the link with marathons and activities might not necessarily be true.
  • There are a range of other factors that might affect fatigue in these situations – such as sleep, caffeine intake, blood sugar levels, and previous physical activity.
  • We do not know if women retain this advantage of reduced fatigue over longer periods of time carrying out more reps. It's possible men level out the fatigue over time.

The best way to increase your stamina is to gradually increase the amount of exercise you do each day. Read more about getting started with exercise.

Links To The Headlines

Women have more stamina than men. The Times, August 25 2017

Women DO have more stamina than men and will soon be beating them in marathons. Mail Online, August 24 2017

Links To Science

Lanning AC, Power GA, Christie A, Dalton BH. Influence of sex on performance fatigability of the plantar flexors following repeated maximal dynamic shortening contractions. Applied Physiology, Nutrition and Metabolism. Published online June 21 2017

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