NHS Choices

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

Regular exercise for the over-50s 'sharpens the mind'

NHS Choices - Behind the Headlines -

"Doing moderate exercise several times a week is the best way to keep the mind sharp if you're over 50," BBC News reports.

A review of existing data found both aerobic exercise and strength training appeared to improve cognitive functions, such as memory, attention, and how well people carry out tasks. 

The review brought together information from 39 studies in the biggest summary of the effects of exercise on mental ability to date.

Previous summaries of research have had unclear results. But this study found most types of moderate to vigorous exercise had a positive effect as long as sessions lasted at least 45 minutes.

The researchers say doctors should recommend people take part in exercise on as many days a week as possible.

Importantly, the study found people benefited even if they were already showing signs of mental decline. This means exercise might help those with early signs of dementia stay mentally alert for longer.

The study provides yet another reason to keep active in later life – both the mind and the body should benefit.

It's recommended that adults do at least 150 minutes of exercise a week, ideally through a combination of aerobic and strength training exercises.

Where did the story come from?

The study was carried out by researchers from the University of Canberra and Australian National University, both in Australia. No funding information was provided. 

It was published in the peer-reviewed British Journal of Sports Medicine on an open access basis, so it's free to read online.

The study was widely reported, with somewhat conflicting and inaccurate advice in the headlines.

The Daily Telegraph and the Daily Express say people only need exercise for 45 minutes a week, although most of the studies included exercise programmes twice a week or more.

The Sun says "walking benefits the brain more than cycling" – but the study didn't present any evidence for this.

The intensity rather than the type of exercise was important, so moderate-intensity cycling should be as good as moderate-intensity walking or running.

What kind of research was this?

This was a systematic review and meta-analysis of randomised controlled trials (RCTs) of exercise programmes.

A meta-analysis of RCTs is a good way to summarise and pool evidence to show whether a particular intervention (in this case, exercise) affects a particular outcome (in this case, cognitive function).

What did the research involve?

Researchers looked for any RCTs that compared an exercise programme with a control group, among adults over 50 living at home, with at least one test of cognitive function (mental ability) as an outcome.

They excluded studies where exercise was not the only intervention – for example, exercise plus brain training – to focus the study on exercise alone.

They then pooled the results between exercise groups and control groups to find the standard mean difference from baseline cognitive function.

Researchers also analysed the results by:

  • type of exercise (aerobic, resistance/strength training, a combination of the two, yoga and tai chi)
  • intensity (low, moderate or high)
  • duration of exercise session (less than 45 minutes, 45 minutes to an hour, more than an hour)
  • length of programme (4-12 weeks, 13-26 weeks, more than 26 weeks)
  • frequency of exercise sessions (two or fewer, 3 or 4, 5-7)

Tests of cognitive function included overall cognition, attention (such as ability to process information quickly), executive function, long-term memory, and short-term working memory.

All the studies were assessed for risk of biases, such as publication bias. The researchers did not exclude any studies based on the date of publication or type of exercise.

What were the basic results?

The study found, overall, taking part in an exercise programme had a small to moderate positive effect on cognitive function, although this varied considerably from one study to another.

People's mental abilities at the start of the study made no difference to the results – people were likely to benefit even if they already showed signs of mild cognitive decline.

Looking at the different types of exercise separately, the authors found:

  • all types of exercise studied except yoga showed a positive effect on cognitive function
  • aerobic and resistance training (such as weight training) showed similar effects, suggesting that both types of exercise are important
  • studies where exercise duration was 45 minutes to an hour showed better results than shorter or longer exercise sessions
  • all lengths of exercise programme, and programmes with all frequencies of sessions, had a positive effect – there were no clear differences between them
  • moderate and vigorous exercise showed better results than low-intensity exercise

The type of control group made a difference. Where people in the control group had either no intervention or a sedentary intervention (such as attending lectures or a computer course) the difference in cognitive function compared with exercise was notable.

However, when the control group did stretching exercises or attended social events, the difference was small enough that it could have been down to chance – in other words, it wasn't statistically significant.

The quality of the evidence was assessed as "moderate" overall. It's not possible to blind people in exercise studies as to whether or not they're doing exercise, which means the studies all have a risk of bias from people knowing whether or not they're being treated.

How did the researchers interpret the results?

The researchers say their findings "suggest that an exercise programme with components of both aerobic and resistance-type training, of at least moderate intensity and at least 45 minutes per session, on as many days of the week as possible, is beneficial to cognitive function in adults aged more than 50 years".

They say future studies should accept as a starting point that exercise is beneficial, and concentrate on ways to "refine the prescription" to identify the best exercise programme to benefit brain function.

Conclusion

It's no surprise to hear that exercise has health benefits – but not everyone knows that it's good for your brain as well as your body.

This study provides evidence that, even for people with some signs of declining mental function, regular moderately intense exercise has a positive effect.

There are a few minor caveats, however. Although the study showed tai chi is beneficial, this was based on only four trials.

And it's not completely clear how often people need to exercise. The study found any number of weekly sessions showed a benefit, but it's reasonable to think more sessions would be more beneficial.

The reasons why physical exercise benefits mental function are thought to include better blood flow to the brain, which keeps nerve cells healthy and supplied with oxygen, lower inflammation and less cellular damage.

Current guidelines for exercise for adults in the UK are to do at least one of the following:

  • 150 minutes of moderate aerobic activity, such as cycling or fast walking, every week, and strength exercises on two or more days a week that work all the major muscles (legs, hips, back, abdomen, chest, shoulders and arms)
  • 75 minutes of vigorous aerobic activity, such as running or a game of singles tennis, every week, and strength exercises on two or more days a week
  • a mix of moderate and vigorous aerobic activity every week (two 30-minute runs plus 30 minutes of fast walking equates to 150 minutes of moderate aerobic activity) and strength exercises on two or more days a week

Other ways you can reduce your risk of dementia include:

Links To The Headlines

Exercise 'keeps the mind sharp' in over-50s, study finds. BBC News, April 25 2017

Doctors should prescribe exercise to the over-50s to 'help prevent dementia' as walking 'benefits the brain more than cycling'. The Sun, April 24 2017

45 minutes' exercise a week boosts brain power in over-fifties. The Daily Telegraph, April 24 2017

45 minutes of exercise for over-50s can 'significantly' improve brain function, study finds. Daily Mirror, April 24 2017

Exercise keeps dementia at bay: Running and walking 'significantly' boosts brain power. Daily Express, April 24 2017

Links To Science

Northey JM, Cherbuin N, Pumpa KL, et al. Exercise interventions for cognitive function in adults older than 50: a systematic review with meta-analysis. British Journal of Sports Medicine. Published online April 24 2017

Four cups of coffee 'not bad for health' suggests review

NHS Choices - Behind the Headlines -

"Drinking up to four cups of coffee a day carries no health risk, experts say. Scientists said those who stick to that limit have no need to worry," reports The Sun.

This was based on a review of studies that looked at the effects of caffeine on health. The researchers specifically investigated the effect of having more or less than 400mg of caffeine a day for adults (the equivalent of four cups of coffee), or 300mg/day (three cups) for pregnant women.

These amounts (400mg for adults and 300mg for pregnant women) were the recommended upper daily limits from a previous large-scale review of caffeine safety carried out in 2003.

Overall, the researchers found the available evidence suggests that consuming up to these amounts of caffeine doesn't have a negative effect on bone health, heart health, behaviour or on reproduction and development.

They found links with increased anxiety, higher blood pressure and headaches. Though these symptoms may not necessarily lead to adverse health outcomes in the long term, they need further research.

Currently the NHS recommends pregnant women have no more than 200mg of caffeine a day – less than the recommended upper limit in this study. Pregnant women should aim to stick to the 200mg a day limit as it will reduce any risks even further.

One important thing to remember is that caffeine is present in lots of products other than coffee, including tea, cola drinks, energy drinks and chocolate.

 

Where did the story come from?

The study was carried out by researchers from various institutions in the US, with most of the authors coming from ToxStrategies, a company that manufactures and processes drugs for human use.

The study was published in the peer-reviewed journal Food and Chemical Toxicology and is open-access, meaning it is free to read online.

The study was funded by the North American Branch of International Life Sciences Institute Caffeine Working Group. Grants were also received from the American Beverage Association and the National Coffee Association. The authors claim these funders had no input into the systematic review.

The Mail Online emphasised the positive side for coffee drinkers, "Coffee lovers rejoice – drinking up to four cups of your favourite beverage each day won't damage your health."

One problem with the media's emphasis on cups of coffee is that caffeine is found in many things besides coffee, including chocolate, coke, tea and energy drinks. Moreover, the claim that the research was based on 740 studies is wrong. Although the reviewers looked at a large number of papers, evidence on the main outcomes was only available from 381 studies.

 

What kind of research was this?

This systematic review aimed to look for studies published between 2001 and 2015, investigating the potential negative effects of caffeine. The researchers specifically aimed to look at effects in four healthy population groups – adults, pregnant women, adolescents and children.

It aimed to review the benchmark conclusions of a previous review in 2003 that had recommended caffeine intakes of:

  • ≤400mg/day in adults (about 4 cups of coffee per day)
  • ≤300mg/day in pregnant women
  • ≤2.5mg/kg per day in children and adolescents

A systematic review is useful for summarising all the relevant evidence in a specific health area but the strength and quality of the evidence is only as good as the gathered studies.

Often the difficulty with studies assessing food and drink exposures – such as the amount of caffeine – is that other health and lifestyle factors could influence the findings.

 

What did the research involve?

This systematic review was built around the question "For [population], is caffeine intake above [dose], compared to intakes [dose] or less, associated with adverse effects on [outcome]?" In other words: for a set population, is caffeine intake above a set amount, compared to the set amount or a lower intake, linked to health risks?

The researchers aimed to assess healthy adults, pregnant women, adolescents (aged 12 to 19 years), and healthy children (aged 3 to 12 years).

The levels of caffeine consumption compared for the different population groups were:

  • Healthy adults: 400mg/day compared with less
  • Healthy pregnant women: 300mg/day compared with less
  • Healthy adolescents and children: 2.5mg/kg per day compared with less

The outcomes of interest were:

  • Cardiovascular: assessed by looking at mortality, blood pressure, heart rate, heart rate variability and cholesterol.
  • Bone and calcium: assessed by looking at bone mineral density and osteoporosis and risk of fracture or fall. 
  • Human behaviour: assessed by looking at anxiety, anger, depression, headache, sleep, problematic or risk-taking behaviour.
  • Development and reproduction: assessed by looking at fertility, miscarriage, stillbirth, preterm birth, fetal growth and birth defects.

Forms of caffeine included coffee, tea, chocolate, cola drinks, energy drinks, energy shots, supplements, medicines, caffeinated chewing gum, caffeinated sports gel, and caffeinated sports bars.

Researchers searched three literature databases for English language studies meeting these criteria published between January 2001 and June 2015.

A total of 381 individual studies were included. Most of these (63%) were described as "controlled trials" – though these may not necessarily all have been randomised trials. The other studies were observational.

Most studies (79%) reviewed the adult population and 14% reviewed pregnant women. Very little evidence was available for adolescents (4% of studies) and children (2%).

 

What were the basic results?

The researchers were not able to pool the study results in a meta-analysis, and instead gave a narrative summary of the effects. Nearly all evidence relates to adults.

Cardiovascular

400mg/day of caffeine is not associated with significant concern for cardiovascular mortality. Six of nine observational studies assessing mortality found that higher intakes of up to 855mg/day did not affect mortality.

If blood pressure alone is considered, 400mg/day may be too high – studies generally suggested that intakes both above and below this level were associated with increased blood pressure (by a few mmHg). However, this small rise may not necessarily have an adverse effect on cardiovascular risk. There were no adverse effects on heart rate, heart rate variability or cholesterol.

Bone and calcium

Most of the data supports that 400mg/day in healthy adults is not harmful with respect to bone mineral density and osteoporosis. It also supports that an intake of 400mg/day is not associated with concern regarding risk of fall or fracture.

Human behaviour

400mg/day can lead to increases in measures of anxiety, sleep problems and may increase the chance of getting a headache. Headaches were observed in people who had previously been drinking levels of coffee just below the maximum recommended amount but no longer did.

Consumption of coffee led to delays in getting to sleep and decreases in quality of sleep. Caffeine intake did not influence anger, depression or confusion.

Development and reproduction

Up to 400mg/day does not seem to affect fertility. 300mg/day was not associated with increased risk of miscarriage, stillbirth, preterm birth, and the birth defects assessed in these studies. There was no conclusion on risk of 300mg/day or more on fetal growth.

 

How did the researchers interpret the results?

The researchers concluded that "evidence generally supports that consumption of up to 400mg caffeine/day in healthy adults is not associated with overt, adverse cardiovascular effects, behavioral effects, reproductive and developmental effects, acute effects, or bone status.

"Evidence also supports consumption of up to 300mg caffeine/day in healthy pregnant women as an intake that is generally not associated with adverse reproductive and developmental effects."

 

Conclusion

It appears that previous recommendations from the 2003 Health Canada review into the effects of caffeine on health remain suitable. Health Canada recommended a maximum daily coffee intake of 400mg/day for healthy adults and 300mg/day for pregnant women.

Although this review looked at a large number of studies and found that the evidence overall supports these recommendations, there are some limitations to the research:

  • The number of studies providing evidence for each health outcome varied.
  • Some results were based on a large number of studies, others on a much smaller number. This means the strength of evidence for different health outcomes varied.
  • Most evidence comes from observational studies. This means we can't be sure that other health and lifestyle factors aren't influencing the findings. Even if randomised controlled trials were possible, it is often difficult to make sure people stick to a given caffeine level and are assessed for long enough to measure adverse outcomes. 
  • The methods and quality of the individual studies will have varied. Studies will have differed in the way they measured caffeine intake or how they assessed health outcomes. This could have made the findings of individual studies inconsistent and difficult to directly compare.
  • We don't know that observations on measures such as blood pressure, anxiety and sleep would necessarily have led to negative overall health outcomes.
  • People may not accurately recall how much caffeine they consumed and state lower levels, particularly if they had a negative health outcome. We also don't know whether caffeine intake reflects recent or long-term intake. Studies may have differed in the period of assessment.
  • Lastly, there was very little evidence available for caffeine intake in children and adolescents.

Currently the NHS recommends having no more than 200mg of caffeine a day if you are pregnant, which is less than the upper limit for pregnant women in this research. Pregnant women should aim to stick to NHS advice.

Find out more in Should I limit caffeine in pregnancy?

Links To The Headlines

4 coffees 'no harm'. The Sun, April 24 2017

Coffee lovers rejoice: Drinking 4 cups a day is not bad for your health, study finds. Mail Online, April 24 2017

Good news caffeine lovers, drinking up to four coffees a day is NOT bad for your health. Mirror Online, April 23 2017

Links To Science

Wikoff D, Welsh BT, Henderson R, et al. Systematic review of the potential adverse effects of caffeine consumption in healthy adults, pregnant women, adolescents, and children. Food and Chemical Toxicology. Available online April 21 2017

Children with regular bedtimes 'less likely to become obese'

NHS Choices - Behind the Headlines -

"Regular bedtimes make children less likely to be obese as adults," is the slightly misleading Mail Online headline. This follows a study looking at the link between household routines in early childhood and obesity at age 11.

Researchers analysed data about children in the UK that had been collected as part of a previous large study (the UK Millennium Cohort Study).

Parents were asked questions about their child's routines at three years of age, including whether they had a regular bedtime. The children then had their height and weight measured at age 11 to see if they were obese.

The study looked at whether there was a link between obesity at age 11 and certain routines earlier in life. They found young children with an inconsistent bedtime were almost twice as likely to be obese aged 11 as those with a regular bedtime.

But this doesn't prove an irregular bedtime directly causes obesity by itself. It could be that children with irregular bedtimes are more likely to have a less healthy lifestyle overall. For example, they may have a poorer diet and exercise less – neither of which was measured in this study.

Also, the parents in the study weren't asked how much sleep the child actually got, which is likely to be an important factor.

Overall, this study alone doesn't prove that an irregular bedtime during childhood directly increases the risk of later obesity. 

Where did the story come from?

The study was carried out by researchers from The Ohio State University College of Public Health, Temple University, Philadelphia, and University College London. Funding was provided by the National Institutes of Health and the UK Economic and Social Research Council.

The study has been accepted for publication by the International Journal of Obesity. However, it has not yet gone through the full review process, so some further changes could be made ahead of the final publication.

Despite the Mail Online saying regular bedtimes make children less likely to be obese "as adults" the study only went as far as 11 years of age.

Media reports also claimed the study found that watching lots of TV was linked to a higher risk of obesity, but the researchers actually found no link between the two after several other factors had been taken into account.

In general, the media stories might have benefitted from considering the other limitations to this research, notably the fact that other environmental and lifestyle factors could have influenced the results.

What kind of research was this?

This was a cohort study that used data collected as part of the ongoing UK Millennium Cohort Study to see whether household routines when a child is three, such as sleep times and meal times, are linked with child obesity at the age of 11.

As the researchers say, young children benefit from regular routines and a previous study has suggested that this is likely to help them regulate their behaviours as older children and adults. However, no previous studies have looked at whether household routines and self-regulation are linked with later obesity.

The main limitation with this study is that although it can find links, it is very difficult to pin down a single cause, such as sleep, to a general health outcome like obesity. It is most likely that obesity is influenced by a variety of environmental and lifestyle factors.

What did the research involve?

The study used data collected as part of the UK Millennium Cohort Study (MCS), which in 2000-2002 recruited 19,244 nationally-representative families with a baby aged nine months in the household. A first home assessment was carried out when the child was nine months, followed by repeat assessments at three, five, seven and 11 years of age.

When the child was aged three household routines were assessed. This included asking parents whether the child went to bed at regular times or ate meals at regular times. Those who replied "always" were said to have regular routines, while those who replied "sometimes" or "never" were regarded as inconsistent.

Child self-regulation was also assessed at age three using the Child Social Behaviour Questionnaire. Parents were asked to reply "not true", "somewhat true", "certainly true" or "can't say" to questions around child emotions (such as whether they're easily frustrated) and cognitive self-regulation (for example, whether they persist with difficult tasks).

At age 11 the child's height and weight were measured to see if the child was obese. The researchers modelled the links between child sleep and self-regulation aged three and obesity aged 11. They took account of various potential confounders that could be having an influence, such as ethnicity, parent's age at child's birth, educational level, household size and income.

The final sample included 10,995 children who had full assessment data available. 

What were the basic results?

At the age of three 41% of children always had a regular bedtime, 47% had regular mealtimes, and only around a quarter (23%) were restricted to viewing no more than one hour of TV a day. At age 11, 6.2% of children were obese. Obesity was more common in families with lower educational level and lower household income.

Having regular bed and meal times and limited TV viewing were all linked with better emotional regulation, but only regular meal times were associated with better cognitive regulation.

When adjusted for all confounders, children with inconsistent bedtime at three years of age were almost twice as likely to be obese aged 11 (odds ratio 1.87, 95% confidence interval 1.39 to 2.51). Poor emotional regulation was also linked with increased risk (OR 1.38, 95% CI 1.11 to 1.71).

TV viewing wasn't linked with risk of obesity and, interestingly, children with inconsistent mealtimes were actually less likely to be obese.

How did the researchers interpret the results?

The researchers conclude: "Three-year-old children who had regular bedtimes, mealtimes, and limits on their television/video time had better emotional self-regulation. Lack of a regular bedtime and poorer emotional self-regulation at age 3 were independent predictors of obesity at age 11."

Conclusion

This study aimed to look at whether child routines and behavioural regulation are linked with child obesity aged 11. The study made use of data collected at regular home assessments for a large, nationally representative UK sample.

The data suggests that inconsistent bedtimes are linked with increased likelihood of the child being obese at age 11. But before drawing firm conclusions about this, there are a couple of points to bear in mind.

  • Though the researchers have tried to adjust for sociodemographic factors, there is a high possibility that this link is being influenced by confounding factors. The most likely confounding factors apparently missing from the analysis are diet and physical activity. It could be that inconsistent bedtimes are linked with less healthy lifestyle patterns in general, and together these all contribute to risk of obesity. It's very difficult to accurately blame a single factor such as sleep.
  • Sleep routines weren't assessed in much depth. Parents were only given very brief options when asked if their child has regular bedtimes – "always", "usually", "sometimes" or "never". It's not always possible to be accurate and these responses may mean different things to different people. It also gives no indication of the duration or quality of the child's sleep.
  • This study doesn't include any analysis of how the child's sleep patterns or behaviour have changed between three and 11 years of age. For example, the child may have been having problems with behaviour and difficulties going to bed around the age of three but this may have settled down in the years since.
  • Obesity has only been assessed at 11 years of age. This doesn't tell us whether the child is going to be obese in later adolescence or adulthood.

Overall this supports understanding that it can be helpful for young children to have regular routines. But this study provides no proof that if a child doesn't have a regular bedtime, this will directly increase their risk of later obesity. 

Links To The Headlines

Regular bedtimes stop children from becoming overweight, study finds. The Telegraph, April 24 2017

Regular bedtimes make children less likely to be obese as adults: Scientists find link between family structure and behaviour that affects possibility of gaining weight. Mail Online, April 24 2017

Children who go to bed late are more likely to grow up to be obese, study reveals. The Sun, April 24 2017

Links To Science

Anderson SE, Sacker A, Whitaker RC, et al. Self-regulation and household routines at age three and obesity at age eleven: Longitudinal analysis of the UK Millennium cohort study. International Journal of Obesity. Accepted article preview online 24 April 2017

Reported link between diet drinks and dementia and stroke is weak

NHS Choices - Behind the Headlines -

"Diet drinks triple your risk of stroke and dementia," the Daily Mail reports, as US research found a link between daily intake and increased risk. However, the chain of evidence is not as strong as reported.

The researchers analysed data from an ongoing US cohort study to see if consumption of sugar or artificially sweetened drinks was linked with risk of stroke or dementia 10 years later. Several thousand people were included in the study, and during follow-up 3% had a stroke and 5% developed dementia.

Overall, when taking account of all health and lifestyle factors that could have an influence (confounders), the researchers actually found no link between artificially sweetened drinks and risk of dementia.

The figures reported in the media came from a model that wasn't adjusted for all confounders, such as diabetes, that could explain part of the link.

For stroke the links with artificially sweetened drinks were inconsistent. There were no overall links when looking at longer term patterns.

The study does not give definitive "cause and effect" proof that drinking artificially sweetened drinks will lead to stroke or dementia. Still, the lead author's reported statement that it is healthier (not to mention cheaper) to just drink water is sound advice.

 

Where did the story come from?

The study was carried out by researchers from Boston University School of Medicine and Tufts University, Boston. The long-term cohort study is funded by the National Heart, Lung, and Blood Institute, the National Institute on Aging and the National Institute of Neurological Disorders and Stroke.

Individual researchers of this particular analysis received funding from additional sources including the National Health and Medical Research Council. The researchers declare no conflict of interest.

The study was published in Stroke, a peer-reviewed journal of the American Heart Association, on an open-access basis so you can read it for free online.

The Guardian gave a good overview of the research while making clear that no cause and effect had been proven.

The Daily Mail's headline – "Diet drinks TRIPLE your risk of stroke and dementia" – is somewhat misleading as it is based on unadjusted data. Though the authors themselves included this information in the abstract of the study.

Several independent experts in the field have also advised caution in taking the results of this research as being conclusive, until further research is conducted. 

 

What kind of research was this?

This was a prospective cohort study, using data collected from the ongoing Framingham Heart Study Offspring, to see whether drinking sugar or artificially sweetened drinks was linked with risk of stroke or dementia.

The researchers say how previous research has linked both types of soft drink with cardiovascular disease, like stroke, but dementia had yet to be examined.

This type of large cohort can find links, but it's very difficult to prove that any individual factor, such as drinks, is directly responsible for a health outcome. Food questionnaires can be subject to inaccurate recall and it's hard to account for all other health and lifestyle factors that can have an influence. 

 

What did the research involve?

The Framingham Heart Study Offspring cohort started in 1971, enrolling 5,124 people living in the community of Framingham, Massachusetts. They had assessments every four years up to 2014.

The assessments at waves five (1991–95), six (1995–98), and seven (1998–2001) included food frequency questionnaires that assessed dietary intake over the previous 12 months. This included questions on sugar-sweetened and artificially-sweetened drinks, among many other food and drink items. Responses for intake ranged from "never or less than once per month" to "six or more per day".

The researchers pooled the most common response categories for each drink to come up with ranges that weren't directly comparable:

  • total sugary drinks: <1 per day, 1 to 2 per day, and >2 per day
  • sugar-sweetened drinks: 0 per week, ≤3 per week, and >3 per week
  • artificially sweetened drinks: 0 per week, ≤6 per week, and ≥1 per day

The 10 year risk of new-onset stroke or dementia started from the last food and drink assessment wave (1998–2001) onwards.

Stroke cases were identified by monitoring hospital admissions, medical records, and asking about stroke at each assessment cycle. Diagnoses of stroke were confirmed by doctors using valid criteria.

Dementia was detected by routine Mini-Mental State Examination at each study assessment. Those with cognitive impairment were flagged for a full review by doctors, and diagnoses of dementia were again made using valid diagnostic criteria.

Links between drinks and stroke or dementia were adjusted for the following confounders:

  • age
  • gender
  • educational level
  • total calorie intake and diet quality
  • physical activity
  • smoking history
  • waist-hip ratio
  • blood cholesterol levels
  • history of high blood pressure
  • history of diabetes

 

What were the basic results?

The researchers analysed 2,888 people aged above 45 years (average 62) for the stroke assessment, and 1,484 adults aged above 60 years (average 69) for the dementia assessment.

During follow-up there were 97 cases of stroke (3% of the cohort), 82 of which were caused by a clot (ischaemic). There were 81 new diagnoses of dementia (5%), 63 of which were consistent with Alzheimer's.

Stroke

When adjusted for all confounders, there was no link between any consumption of either total sugary drinks or sugar-sweetened drinks and risk of stroke.

They did find significant links for artificially sweetened drinks when looking at recent history. Recent consumption of artificially-sweetened drinks (at the 1998–2001 assessment) was linked with risk of stroke: compared with none:

The risk was slightly higher when restricting the analysis to ischaemic stroke cases only.

For overall intake across all assessment periods, however, there was no significant link between artificially-sweetened drinks and strokes – this was only found again when restricting to the smaller number with ischaemic stroke.

The reported figure of a tripled increase with artificially-sweetened drinks comes from an HR of 2.67 (95% 1.26 to 6.97) for one or more drinks per day – but this was in the model that was not fully adjusted for all health factors – and for ischaemic stroke only.

Dementia

In the fully adjusted model there were no significant links for risk of dementia (or Alzheimer's specifically) from total sugary drinks, sugar-sweetened drinks or artificially-sweetened drinks.

Again, the reported figure of a tripled risk increase with artificially-sweetened drinks comes from an HR of 2.89 (95% 1.18 to 7.07) for one or more drinks per day – but this was again in the model that was not fully adjusted – and for Alzheimer's only.

 

How did the researchers interpret the results?

The researchers conclude: "Artificially sweetened soft drink consumption was associated with a higher risk of stroke and dementia."

 

Conclusion

The researchers used data from a large ongoing cohort study to look for links between consumption of sugary and artificially sweetened drinks and risk of stroke or dementia.

This cohort study benefits from the large overall sample size, long period of data collection, careful and valid diagnostic assessments, and adjustments for a number of confounders. However, care must be taken when interpreting these results – particularly if latching on to the maximal tripled risk figures reported in the media.

There are several points to consider:

Small numbers

The new number of strokes and dementia in this study was small, just 3% and 5% of the cohort, respectively. The most common category for consumption of artificially sweetened drinks in the full cohort was actually zero.

The paper doesn't report how many of the 97 people with stroke or 81 with dementia were in the highest consumption categories, but it's likely to be few. The numbers will get even smaller when restricting to the 82 with ischaemic stroke and 63 with Alzheimer's.

Analyses with smaller numbers can be less accurate, as indicated by the rather wide confidence intervals on the tripled associations.

Variable consumption measures

As said above, the researchers grouped consumption categories according to the most common response. The categories for the three different drinks aren't consistent, which makes it quite difficult to compare them with one another.

Overall this makes it very difficult to conclude with any certainty that artificially sweetened drinks carry more risk than sugary drinks.

Inconsistent links

In the fully adjusted model, links between artificially sweetened drinks and stroke were only found for the last food and drink assessment taken at wave seven.

There was no statistically significant link for stroke when looking at cumulative intake over all assessments – only when restricting to ischaemic strokes only.

Overall this makes it difficult to give any conclusive answer about the strength of the links with artificially-sweetened drinks. Arguably the cumulative, overall pattern, should give the most reliable indication – and this found no link.

Recall in food frequency questionnaires

Food frequency questionnaires are a validated measure for assessing food and drink consumption. However, people may not be able to accurately recall how much and how often they have consumed a particular drink over the past year.

Potential influence of confounders

As highlighted, the triple figures came from models that hadn't adjusted for health related factors. Full adjustment for all health and lifestyle factors gave more tentative links. Even then this analysis may not have been able to adjust for all factors that could be having an effect.

If there is a link it may not have been directly caused by artificially sweetened drinks. For example people with diabetes or obesity may be more likely to consume artificially sweetened drinks and are also more likely to develop stroke and some forms of dementia.

Generalisability

Lastly, this is a sample from one region of the US only. Lifestyle habits – including drink consumption – may differ and the findings may not have been the same if studying other samples.

Overall the various limitations mean that this study does not give definitive proof that drinking artificially sweetened drinks will increase risk of stroke or dementia.

When it comes to the healthiest drink to have on a day to day basis you can't go wrong with plain old tap water.  

Links To The Headlines

Stroke and dementia risk linked to artificial sweeteners, study suggests. The Guardian, April 20 2017

Could a diet drink a day increase your risk of dementia or a stroke? ITV News, April 21 2017

People who consume one diet drink a day 'three times more likely to suffer stroke or dementia'. The Independent, April 21 2017

Diet drinks TRIPLE your risk of stroke and dementia - and are FAR more dangerous than drinks sweetened with sugar. Daily Mail, April 21 2017

Links To Science

Pase MP, Himali JJ, Beiser AS, et al. Sugar- and Artificially Sweetened Beverages and the Risks of Incident Stroke and Dementia - A Prospective Cohort Study. Stroke. Published online April 20 2017

Cycling commuters have lower rates of heart disease and cancer

NHS Choices - Behind the Headlines -

"Want to live longer? Reduce your risk of cancer? And heart disease? Then cycle to work," BBC News advises, prompted by a new study that found UK commuters who cycled to work had lower rates of cancer and heart disease, compared to other types of commuters.

The study was well designed as it included more than 200,000 adults working full time away from their homes and aged between 40 and 69 years. Commuting on a bicycle was associated with a lower risk of cardiovascular diseasecancer and death from any cause, while those walking to work only had a lower risk of cardiovascular disease.

This observational evidence adds to other studies to confirm the benefits of physical activity and active commuting in reducing the risk of these conditions.

The main strength of the study is that it made use of real world data on lifestyle and health outcomes. It also adjusted for a wide range of other factors that might affect the risk of cardiovascular disease or certain types of cancer.

As it is often difficult to fit exercise into our daily routine, commuting by foot or bike could be a useful way of achieving recommended levels of  physical activity.

Read more advice about getting started with cycling (if you've not done so since childhood, or ever) and the health benefits of cycling.

 

Where did the story come from?

The study was carried out by researchers from the University of Glasgow. The UK Biobank (the resource that provided the data used in the study) is supported by the Wellcome Trust, Medical Research Council, Department of Health, Scottish government, and Northwest Regional Development Agency.

Funding for the study was also received from the Welsh Assembly government and British Heart Foundation.

The study was published in the peer-reviewed medical journal the BMJ on an open-access basis so you can read it for free online.

The main facts of the study have been reported accurately in the UK media, including a note that it is not possible to determine clear cause and effect.

 

What kind of research was this?

This was a prospective cohort study which aimed to investigate the association between active commuting and cardiovascular disease, cancer and death.

This type of study is useful for looking at data collected over a long period of time, but an inherent weakness of this study design is that it can only highlight possible associations, and not prove cause and effects.

 

What did the research involve?

Between April 2007 and December 2010 over 500,000 adults aged between 40 and 69 years were recruited to the UK Biobank, an ongoing large prospective study set up to improve the prevention, diagnosis and treatment of a wide range of illnesses.

Participants were recruited from across the country, had biological measurements taken, provided blood, urine and saliva samples for future analysis, and gave detailed information about themselves. They agreed to have their health followed for life (or at least 25 years).

At the start of the study the mode of transport used for commuting was recorded using an electronic questionnaire. The participants were asked "In a typical day, what types of transport do you use to get to and from work?" One or more of the following options could be selected:

  • car/ motor vehicle
  • walk
  • public transport
  • cycle

These were then grouped into five commuting categories:

  • non-active (car/motor vehicle and/or public transport only)
  • walking only
  • cycling (cycling, or cycling and walking)
  • mixed mode walking (non-active plus walking)
  • mixed mode cycling (non-active plus cycling, or non-active plus cycling and walking)

During the follow-up period the main outcomes of interest were deaths from any cause, which was obtained from death certificates held by the National Health Service Information centre, and the incidence of cardiovascular disease and cancer, which was established using hospital episode statistics and Scottish morbidity records.

Data was collected on confounding factors, including:

  • sociodemographic factors such as level of deprivation and ethnicity
  • smoking status
  • body mass index
  • leisure time
  • occupational and physical activity
  • sedentary behaviour
  • dietary intake

 

What were the basic results?

A total of 263,540 adults (52.4% of the total recruited to the Biobank), with an average age of 52.6 years, joined this sub-study. Only those in paid employment were included.

During the follow-up period of around five years 2,430 people died, 496 of which were due to cardiovascular disease. There were an additional 3,748 cancer events and 1,110 cardiovascular events.

Cycling was the mode of commuting most strongly linked to reduced risk of death, cardiovascular disease and cancer. When compared to the non-active group the following was seen:

  • 41% lower risk of death from any cause (hazard ratio [HR] 0.59, 95% confidence interval [CI] 0.42 to 0.83)
  • 52% lower risk of death from cardiovascular disease (HR: 0.48, 95% CI: 0.25 to 0.92)
  • 46% lower risk of cardiovascular events (HR: 0.54, 95% CI: 0.33 to 0.88)
  • 40% lower risk of dying from cancer (HR: 0.60, 95% CI: 0.40 to 0.90)
  • 45% lower risk of a cancer event (HR: 0.55, 95% CI: 0.44 to 0.69)

Mixed mode cycling (e.g. train and bike) also saw reduced risk of death from cancer and cancer events.

Walking to work was associated with some reduced risk, but this was only for death from cardiovascular disease (HR: 0.64, 95% CI: 0.45 to 0.91) and the incidence of cardiovascular disease events (HR: 0.73, 95% CI: 0.54 to 0.99).

Cancer risk was not significantly reduced in those who walked to work, including mixed mode walking. Mixed mode cycling did not appear to protect against cardiovascular death or new cardiovascular disease.

 

How did the researchers interpret the results?

The researchers conclude that commuting on a bicycle was associated with a lower risk of cardiovascular disease, cancer and death from all causes. People who walk to work also have a lower risk of CVD even after adjusting for potential confounders.

Encouraging and supporting active commuting could reduce risk of death and the burden of important chronic conditions.

 

Conclusion

This prospective cohort study has established that active methods of commuting to work, either walking or cycling, are associated with reduced risk of death, cardiovascular disease and cancer.

Overall this was a well-designed study based on a large collection of real-world data from the UK. The researchers controlled for key socioeconomic and lifestyle confounders.

Although this is an observational study, confidence in the link is improved by its consistency with existing knowledge and research on the benefits of physical activity and the graded response in the results.

Participants from the UK Biobank who were in paid employment were included and are thought to be reasonably representative of the middle-aged general population. Similar links in younger adults can't be assumed.

A limitation of this study is that the participants volunteered to take part and therefore may be healthier than the rest of the population. However, this bias is unlikely to undermine the findings.

It makes sense that those who have a more active lifestyle would reduce their risk of cardiovascular disease or certain types of cancer.

If you are finding it hard to fit the recommended levels of physical activity into your daily routine then using a bike to commute, if possible, could be an ideal solution.

Read more about getting started with cycling.

Links To The Headlines

Cycling to work can cut cancer and heart disease, says study. BBC News, April 20 2017

Cycling to work ‘could halve risk of cancer and heart disease’. The Independent, April 20 2017

Cycling to work almost ‘HALVES the risk’ of developing heart disease and cancer, study claims. The Sun, April 20 2017

Cycling to work 'halves the risk of heart disease and cancer': Study finds that biking just a short distance is far more beneficial than walking. Mail Online, April 19 2017

Cycling to work could help you live longer and greatly reduces the chance of developing cancer, study reveals. The Daily Telegraph, April 20 2017

It's good to hear cycling to work reduces your risk of dying. But that's not why I do it. The Guardian, April 20 2017

Links To Science

Celis-Morales CAC, Lyall DM, Welsh P, et al. Association between active commuting and incident cardiovascular disease, cancer, and mortality: prospective cohort study. BMJ. Published online April 19 2017

Two older drugs could be 'repurposed' to fight dementia

NHS Choices - Behind the Headlines -

"Depression and cancer drugs offer hope for dementia sufferers," Sky News reports. The headline is prompted by a study looking at the effect of two drugs – one used to treat depression and another being trialled for cancer treatment – on neurodegenerative diseases.

Neurodegenerative diseases are conditions that cause progressive damage to the brain's functions, such as Alzheimer's disease, Parkinson's disease and CJD (aka "Mad Cow Disease").

Mice infected with diseases mimicking neurodegenerative diseases were treated with the two drugs: trazodone hydrochloride (used to treat depression and anxiety) and dibenzoylmethane (a drug that could be useful for prostate and bowel cancer).

Both drugs restored memory, reduced signs of neurodegeneration and were safe for the mice in the doses given.

This is exciting early-stage research that might lead to trials in humans to see if they remain safe and effective. An additional bonus is that trazodone has already been licensed for use in older adults, so we have a good understanding of how safe the drug is. This means that clinical trials for trazodone in treating neurodegenerative diseases could conceivably start straight away. But it could take much longer for the drug to come to market for this purpose (and this is not guaranteed to happen).

While there is no guaranteed way to prevent dementia, you may be able to reduce your risk by regular exercise, eating a healthy diet, quitting smoking if you smoke and moderating your consumption of alcohol.

 

Where did the story come from?

The study was carried out by researchers from the University of Cambridge, University of Nottingham and the Medical Research Centre Toxicology Unit in Leicester, UK. The study was funded by the Medical Research Council in the UK and a grant from the Alzheimer's Society and Alzheimer's Drug Discovery Foundation.

The study was published on an open-access basis in the peer-reviewed scientific journal Brain, a Journal of Neurology. You can read it for free online or download a PDF version.

The UK media's reporting of the study was generally accurate and acknowledged that this was early-stage research carried out on mice.

The Mail Online was perhaps a little over-optimistic regarding trazodone, the drug used for depression, suggesting "as it has already been proven safe for humans, it could be on the market in two years". As research in humans for its potential role in neurodegenerative disorders has not even started, it is likely to be much longer before it can be considered for marketing.

 

What kind of research was this?

This was experimental laboratory research on mice that looked at the effect of different compounds on brain impairment and the nervous system.

Experimental research such as this on mice is necessary to look at the mechanisms of certain drugs that may have an effect on disorders such as dementia. However, as dementia covers a range of complex neurodegenerative disorders which do not affect mice, researchers are only able to study some of the pathways that may be involved.

As the authors acknowledge, this is early-stage research that offers the potential for new treatments for dementia in humans. However, it does not necessarily mean they have discovered a cure or even that the treatment will make it past human clinical trials.

 

What did the research involve?

Researchers looked to restore normal brain functioning in mice that had been infected with neurodegenerative-like diseases by testing two drugs, trazodone hydrochloride and dibenzoylmethane. These two drugs had been whittled down from a list of 1,040 from the National Institute for Neurological Disorders and Stroke, through testing on worms among other things.

A major factor contributing to neurodegenerative diseases such as Alzheimer's and Parkinson's is the response to problems with proteins in the brain.

In people with Alzheimer's, protein production is reduced, causing damage to nerves and memory loss. By "switching" protein production back on, neurodegeneration has been found to be stopped in its tracks. As the compounds that were able to do this were not judged to be suitable for humans, the researchers looked at whether any of the 1,040 drugs also had this effect.

Mice were infected with a prion disease (which can cause CJD), an infectious disease, or a type of genetic dementia, both of which cause neurodegeneration. Seven weeks later, they were treated with either trazodone hydrochloride, a drug used to treat depression, or dibenzoylmethane, a drug currently being trialled as an anti-cancer compound.

The researchers then used an object recognition test to see if mice remembered objects they had already seen and what object was new. They also looked at signs of brain damage as well as brain shrinkage, a sign of neurodegenerative disease.

 

What were the basic results?

Trazodone hydrochloride and dibenzoylmethane restored memory and reduced brain shrinkage, which is a sign of neurodegenerative disease in mice either infected with the prion disease or given a type of genetic dementia.

For the prion-infected mice, survival time was also extended.

Both trazodone hydrochloride and dibenzoylmethane were found to restore protein production in the mice, an indication of neurodegeneration being halted.

Previously, drugs also attempting to reduce neurodegeneration by the same pathway have been found to be toxic to the pancreas. Reassuringly, both drugs were found to be safe for the mice at the given dose and neither were found to be toxic to the pancreas.

 

How did the researchers interpret the results?

The researchers concluded that these two compounds "therefore represent potential new disease-modifying treatments for dementia."

They suggest that "trazodone in particular, a licensed drug, should now be tested in clinical trials in patients."

 

Conclusion

This early stage experimental research has demonstrated a beneficial neurological effect of trazodone and dibenzoylmethane on mice with diseases mimicking neurodegenerative diseases.

It is important to acknowledge that this is animal research and therefore the drugs might not have the same effect when they are trialled on humans.

That being said, trazodone is already an approved drug for depression and sleep problems and has therefore already passed safety tests. If the mechanisms of neurodegeneration in humans and mice are similar, it is possible trazodone could be used in the future in treating Alzheimer's and other neurodegenerative diseases.

These early tests are promising. However, these drugs need to be proven effective and safe in people with neurodegenerative diseases before becoming available.

Even if these are proven safe and effective, it is often a lengthy process from the start of human clinical trials to drugs being marketed and available to healthcare providers. This is especially true for long-term conditions where progression may be slow. Therefore, it could well be several years before these drugs are available for the treatment of neurodegenerative diseases.

Links To The Headlines

Depression and cancer drugs offer hope for dementia sufferers – study. Sky News, April 20 2017

Experts excited by brain 'wonder-drug'. BBC News, April 20 2017

Could cancer drugs help slow down dementia? ITV News, April 20 2017

Depression drug that could slow Alzheimer's: Treatment found to reduce brain shrinkage in early tests. Mail Online, April 20 2017

Drug already prescribed to millions of Brits ‘may protect against Alzheimer’s’. The Sun, April 20 2017

Links To Science

Halliday M, Radford H, Zents KAM, et al. Repurposed drugs targeting eIF2α-P-mediated translational repression prevent neurodegeneration in mice. Brain. Published online April 19 2017

Frog slime could protect us against future flu epidemic

NHS Choices - Behind the Headlines -

"'Potent' new molecule in frog slime may give us new way to beat flu epidemics, say boffins," The Sun reports.

Researchers looked at secretions from the skin of a south Indian frog called Hydrophylax bahuvistara. They found it contained a peptide (a short chain of amino acids) which could kill certain flu viruses in the lab. They called this peptide "urumin" – after a curved sword that comes from the same region of India as the frog.

They also found that urumin was able to protect mice from the flu virus. Only 3 in 10 mice given urumin died from the infection, compared to 8 in 10 mice which weren't treated with urumin.

Research into urumin is still at an early stage, too early to say that this is a "cure" for flu. While it was effective against several types of flu virus in the lab – including the one that caused the 2009 swine flu pandemic – it didn't work against others.

Still, despite these limitations, this is welcome news. Current antivirals have proved to have limited effectiveness against flu, and there is always the concern that a new flu pandemic could emerge.

Researchers are likely to continue to study urumin and make sure it is effective and safe enough to be tested in humans.

 

Where did the story come from?

The study was carried out by researchers from Emory University and the Icahn School of Medicine at Mount Sinai in the US, and the Rajiv Gandhi Center for Biotechnology in India. Sources of funding weren't clear, but one author acknowledged a grant from the Kerala State Council for Science, Technology and Environment.

The study was published in the peer-reviewed scientific journal Cell.

The Daily Telegraph and Mail Online suggest the peptide was found in "frog snot", which isn't strictly correct as the study looked at skin secretions. The Sun and the Daily Mirror preferred the term "frog slime", which is arguably more accurate.

There were suggestions in the media that the urumin peptide could be a possible "cure" for flu. This suggestion is probably unwarranted given that we already know it does not kill all strains of flu.

The flu virus has many different varieties, and the peptide seemed good at killing one particular sub-type of influenza A called H1N1 (which includes strains such as swine flu, and the infamous Spanish flu of 1918-19), but not other sub-types, such as H3N2 (which is another common cause of seasonal flu).

The Mail Online does raise a good point in that the body can break down peptides like the one tested in this study, so researchers will need to find a way to stop this happening.

 

What kind of research was this?

This was laboratory and animal research looking for new antiviral molecules in the skin secretions of a south Indian frog. Frogs are known to secrete substances from their skin that protect them from bacteria and viruses.

These substances – called peptides – can also destroy some human viruses in the lab. The researchers in the current study wanted to see if any of the peptides could destroy the human flu virus.

This type of research is useful for identifying new substances that might be effective as human medicines. When these potential new drugs are found, they then need to go through a long period of testing to ensure they are safe and effective enough before they can be tested on humans. Once they reach this stage they have to go through tough tests to confirm their safety and how well they work before they can be used more widely.

 

What did the research involve?

The researchers collected skin secretions from a type of south Indian frog, and then returned them to the wild unharmed. They analysed these secretions to identify the peptides (small chains of amino acids) they contained. They then tested each peptide to see if it could kill the human flu virus in the lab.

They also tested whether the peptide harmed human cells in the lab to make sure it was not toxic to human cells.

Once they identified a suitable peptide they tested whether it could treat live mice which had been infected with a large dose of the flu virus.

They gave one group of mice a dose of urumin and another group an inactive control liquid into their nasal passages five minutes before infecting them with the flu virus. They then gave them urumin or control daily for the next three days and compared how the infection affected the mice's weight (as ill mice lose weight), how many mice died, and how much flu virus was present in their lungs.

The researchers also tested urumin on other viruses that infect humans – including HIV, hepatitis C, Ebola, Zika, and Dengue viruses.

 

What were the basic results?

The researchers identified 32 peptides in the mucus collected from the frogs' skin. They identified four peptides which could kill more than half of a sample of the human H1N1 flu virus in the lab. They selected the peptide which was least harmful to human cells in the lab for further study, and they named it "urumin".

They found that urumin was effective at killing different types of H1N1 flu viruses in the lab – including the type which caused the 2009 swine flu pandemic. Urumin killed at least 60% of each of the eight types of H1N1 tested. It was also good at killing seven strains of H1N1 that were resistant to antiviral medicines such as Tamiflu.

The researchers found that urumin did this by targeting the part of the virus's structure that is shared across different "H1" strains, called the "stalk region". However, urumin was not as good at killing a different strain of flu (H3N2), where it killed less than half of the four samples tested.

Urumin protected live mice against the flu virus. Infected mice treated with urumin lost less weight and had less flu virus in their lungs. Urumin also reduced deaths; 70% of the mice treated with urumin survived compared to only 20% of those given the inactive control.

The researchers found that urumin did not have an effect on the other human viruses they studied.

 

How did the researchers interpret the results?

The researchers concluded that they had identified a peptide called urumin in the skin secretions of a south Indian frog which can kill H1 strains of the human flu virus. They say urumin "has the potential to contribute to first-line anti-viral treatments during influenza outbreaks".

 

Conclusion

This study has identified a substance in the mucus secreted by a south Indian frog which can kill certain types of flu virus.

Researchers often turn to natural substances with known health-giving properties to find potential new drugs for humans. For example, aspirin was developed based on a compound found in willow bark – which had been used in traditional medicine for hundreds of years.

Some other drugs – such as some chemotherapy and anticlotting drugs – have also been developed from chemicals found in plants.

By isolating the substances that have an effect the researchers can make sure they are pure and adapt and them to make them as safe and effective as possible for human use. This is another example of this process, using an animal's natural defences to identify substances that could help protect humans.

It also offers yet another compelling reason why we should make an effort to prevent different species, both animal and plants, from becoming extinct. Potential treatments for human disease could be lost forever if a species disappears.

As yet, tests on urumin are in the early stages. So far it has only been shown to be effective at killing some types of flu viruses in the lab but not others, and researchers will want to test it against a wider range of flu viruses.

The path to developing new drugs is long, and it will be a while before we know if urumin is suitable for testing in humans, and whether it will be successful in these tests. We certainly can't yet say if it will be a "cure" for "most" strains of flu as suggested by the Mail Online.

Flu viruses are hard to combat, because they mutate and change so rapidly. Therefore it is important the researchers continue to do studies such as this, to look for ways that they can be treated.

Flu is unpleasant for most of us, but it can be serious, and potentially life-threating for more vulnerable groups, such as people over the age of 65, and people with long-term conditions, such as asthma or heart failure.

Read more advice about who should get the flu vaccination.

Links To The Headlines

‘Potent’ new molecule in frog slime may give us new way to beat flu epidemics, say boffins. The Sun, April 19 2017

Frog slime could revolutionise anti-flu drugs - and help to prevent deadly epidemics. Daily Mirror, April 19 2017

Frog slime compound ‘blows up’ flu virus, scientists discover. The Independent, April 19 2017

Frog snot gives hope for flu cure. The Daily Telegraph, April 18 2017

Links To Science

Holthausen DJ, Lee SH, Kumar VTK, et al. An Amphibian Host Defense Peptide Is Virucidal for Human H1 Hemagglutinin-Bearing Influenza Viruses. Immunity. Published online April 18 2017

Touchscreen-using toddlers may sleep less

NHS Choices - Behind the Headlines -

"'Touchscreen-toddlers' sleep less," BBC News report. Results from a survey of UK parents suggest every hour a child spends using a touchscreen device was associated with an hour's less sleep a night.

Reports such as this are likely to cause concern to many parents, as touchscreen devices, such as smartphones and tablets, are now widespread in most UK houses. The devices are often used as an easy form of entertainment for bored toddlers (and bring some much-needed relief for tired parents).

More than 700 parents took part in a survey that found 75% of children use a touchscreen on a daily basis. A link between levels of use and a reduction in daily sleep was found; however this one-off assessment does not prove that one thing has caused the other.

Many other environmental influences may be involved. Also, despite some of the more worrying headlines, such as The Daily Telegraph's "Ipads could hinder babies' sleep and brain development," the researchers did not look at the effect on developmental milestones. This is an area certainly worth researching, given the rise of "touchscreen toddlers".

It is well known that sleep is important for young children as it has a role in development. Any environmental influences found to reduce the quality of sleep should be limited. Read more advice about how much sleep children need as well as helpful tips that can help improve the quantity and quality of your child's sleep.

 

Where did the story come from?

The study was carried out by researchers from the University of London and was funded by a Philip Leverhulme Prize.

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

The media reported on this study accurately, pointing out that it is not possible to prove that screen use is responsible for reducing sleep from this study.

However, the Telegraph and the Mail Online overstepped the mark by saying that reduction in sleep may increase a child's risk of doing badly at school.

 

What kind of research was this?

This was an online parental survey that aimed to see whether the use of touchscreen devices, such as mobile phones and tablets, is associated with reduced quality of sleep in infants and toddlers aged between 6 and 36 months.

Surveys are not able to prove that one thing causes another. Also, as all data is parent-reported, we can't rule out the possibility of recall bias or differences in how parents measure and interpret their child's sleep patterns and use of media devices.

However, it is possible to find potential links and see how these match with other similar research.

In this case, heavy use of screen media, such as TV and video games, is known to contribute to poor sleep. So it's important to establish if a similar effect can be seen with portable devices, which reports suggest are more widely used these days.

 

What did the research involve?

Between June 2015 and March 2016, UK-based parents of infants and toddlers aged 6 to 36 months completed an online questionnaire. Parents were invited to join the survey from Birkbeck Babylab database, Goldsmiths Babylab database and study advertisements from various news agencies, magazines, and charities, including the National Childbirth Trust.

The main areas of focus in the questionnaire were:

  • demographic information – age, sex and mother's level of education
  • child's media usage – frequency and duration of touchscreen and television use
  • developmental milestones

Infant sleep was assessed using the Brief Screening Questionnaire for Infant Sleep problems. This tool covered different sleep-related areas and asked parents about the following:

  • night-time sleep duration (7pm to 7am)
  • day-time sleep duration (7am to 7pm)
  • number of night awakenings
  • how long it takes for the child to go to sleep

The data was analysed using statistical methods to check for associations, adjusting for the possible effect of confounding factors such as socioeconomic status.

 

What were the basic results?

The researchers asked 715 parents questions about their child's touchscreen use. Around 75% of toddlers used touchscreen devices on a daily basis for an average of 24 minutes per day.

Usage increased with age, from 51% in the youngest category (6 to 11 months) for an average of 8.53 minutes a day, to 93% in toddlers (25 to 36 months) who spent around 45 minutes using touchscreen devices.

There was a significant association between the frequency of touchscreen use and sleep quality, as measured by looking at total sleep duration, duration of night-time sleep and daytime sleep.

Each additional hour of touchscreen use was associated with 15.6 minutes less total sleep. This was 26.4 minutes less night-time sleep, but 10.8 minutes more daytime sleep.

There was no association between touchscreen use and the number of times a night a child wakes up.

 

How did the researchers interpret the results?

The researchers concluded that, when controlled for the possible confounding effects of age, sex, TV exposure and maternal education, there was a significant association between touchscreen use and night-time sleep, daytime sleep and how quickly infants fell asleep. However there was no effect seen for the number of night awakenings.

They went on to say that future longitudinal studies are needed to clarify the long-term effects of touchscreen use and the underlying reasons for these effects using detailed sleep tracking.

 

Conclusion

This survey aimed to assess whether touchscreen use in infants and toddlers aged between 6 and 36 months has an impact on the quality of their sleep.

Sleep is very important for young children as it has a role in development, and if environmental influences are identified that reduce the quality of sleep, they should be limited.

This UK study has strengths in its good sample size and its attempts to control for the effects of other confounding variables – however, these weren't all explicitly listed. While a link between levels of touchscreen use and daily sleep was found, this cross-sectional study is not able to prove causation. We don't know that one thing has directly and independently caused the other and there may be many other unmeasured environmental factors involved.

Also, as highlighted above, parents may not have had full knowledge of their child's sleep quality or measured use of media devices accurately. Another point worth noting is that parents chose to take part in this study. There may be differences between the households of those who did and did not respond to advertisements to take part, and the children in this study may not be representative of all children.

There was also no assessment of the effect reduced sleep might have on developmental milestones, despite having asked about this. This would be an area for further research.

Despite limitations of this study, it is well known that sleep is important for young children as it has a role in development. Any issues found to reduce the quality of sleep should be limited to reduce the risk.

At six months of age a child is expected to have three hours of daytime sleep and 11 hours at night. By 36 months the amount of daytime sleep might reduce to as little as 45 minutes, although 11.5 to 12 hours are still needed at night. There is no indication in this study of how much sleep touchscreen users were found to have and whether this was less than the recommended amount.

Recent US guidelines recommend that children aged between 2 to 5 years should be restricted to one hour of any type of "screen time" per day.

If your child is not getting enough sleep there are sleep tips for children, such as relaxation techniques and avoiding screens in the bedroom, which can help.

Read more advice about sleep in children.

Links To The Headlines

'Touchscreen-toddlers' sleep less, researchers say. BBC News, April 13 2017

Touchscreen use by toddlers linked to poor sleep patterns. The Independent, April 13 2017

Ipads could hinder babies' sleep and brain development, study suggests. The Daily Telegraph, April 13 2017

Babies and toddlers lose 16 minutes of sleep for every one hour they spend using a touchscreen, putting them at risk of doing badly in school in later life. Mail Online,  April 13 2017

Links To Science

Cheung CHM, Bedford R, de Urabain IRS, et al. Daily touchscreen use in infants and toddlers is associated with reduced sleep and delayed sleep onset. Scientific Reports. Published online April 13 2017

Being either under or overweight may increase migraine risk

NHS Choices - Behind the Headlines -

"People who are too fat or too thin are 'more likely to suffer from migraines'," reports The Sun.

Researchers reviewed data from 12 studies involving 288,981 people and concluded obese people have a 21% increased risk of migraines, compared to those of healthy weight.

Migraines are moderate to severe headaches that are more common in women. People who are underweight also have a small increased risk.

Researchers don't know exactly how weight affects migraine risk, but it may be to do with chemicals released by fatty tissue. Researchers found that both age and sex affected people's chances of the condition, as well as their weight.

This type of research can't tell us whether migraine is caused directly by weight. And we don't know whether obese people with migraine can lower their chances of having the painful headaches by losing weight.

Still, trying to achieve a healthy weight should help lower your risk of a range of chronic diseases such as heart disease and type 2 diabetes.

Read more about how to lose weight safely with the NHS Weight Loss Plan.

 

Where did the story come from?

The study was carried out by researchers from Harvard TH Chan School of Public Health and Johns Hopkins University School of Medicine in the US, the University of L'Aquila in Italy, and the University of Queensland in Australia.

The researchers reported no direct funding. The study was published in the peer-reviewed journal Neurology.

The Sun gave an accurate overview of the study. The Mail Online's rather odd headline claimed that: "Being a healthy weight is the only way to beat migraine," ignoring the fact that many people of healthy weight get migraines, and there are plenty of migraine treatments around.

The Mail also said that "migraine sufferers could prevent the misery of migraine headaches by staying at a healthy weight," when the research does not show that changing weight affects migraine.

Both newspapers use the researchers' figure that obesity leads to a 27% greater risk of migraine, based on an analysis adjusted for age and sex. However, the fully-adjusted figure, taking into account multiple risk factors for migraine, is 21%.

 

What kind of research was this?

This is a meta-analysis, which pooled results from previously-published studies looking at links between weight and migraine. Meta-analyses are a good way of summarising all the existing research about a topic. However, they are only as good as the studies that they report.

All of the studies in this case were observational in nature, and so are not able to show that being over- or underweight causes migraines.

 

What did the research involve?

Researchers looked for previously-published observational studies on migraine and weight. They pooled the data to look for links between migraine risk and different categories of weight – underweight, healthy weight, overweight or obese. They adjusted their figures to take account of confounding factors known to affect migraine risk, such as age and sex.

The studies included were assessed to be of fairly good quality (all ranking seven or above on a 10-point quality scale).

The researchers conducted sensitivity analyses to ensure the pooled results were not skewed by any individual study. They also asked the original study authors for additional information, meaning they were able to include data not used in previous meta-analyses.

 

What were the basic results?

The study found that obese people and underweight people, but not overweight people, were more likely to report having migraines.

Compared to people of healthy weight:

  • obese people were 21% more likely to have migraines (odds ratio [OR] 1.21, 95% confidence interval [CI] 1.08 to 1.34)
  • underweight people were 12% more likely to have migraines (OR 1.12, 95% CI 1.03 to 1.21)

Both the chances of having migraines, and the link between migraines and obesity, were strongest in younger people and lessened with age.

 

How did the researchers interpret the results?

The researchers say their findings show a potential "moderate" increased risk of migraine from being obese. They say this finding "supports the need for research to determine whether interventions to reduce obesity decrease the risk of migraine".

They suggest this will help scientists understand the causes of migraine better, and possibly develop treatments based on people's weight. 

 

Conclusion

The study results are clear: people who are obese have a moderately increased chance of getting migraine headaches, and people who are underweight have a small increased chance. However, the results don't tell us why that is.

There are a few limitations to be aware of:

  • More than half the studies used people's self-reported height and weight to calculate body mass index, which may have under-estimated the proportion of people who were overweight.
  • Half the studies used people's self-report of migraine, rather than a medical diagnosis, which could have affected the accuracy of the results.
  • There were substantial differences between the included studies, this reduces the reliability of the combined results.

The link to weight is likely to be only one factor contributing to whether someone gets migraine, including genes inherited from parents. Lots of things have been identified as possible triggers for migraine headaches in those susceptible, including:

  • hormonal changes (many women find they are more likely to get migraine around the time of their period)
  • diet (some people report migraines after eating specific food such as cheese, or when they skip meals)
  • emotional states such as anxiety, depression or shock
  • tiredness and lack of sleep, or shift work
  • environmental factors such as bright lights or changes in the weather

While it's always a good idea to keep to a healthy weight (it's not called a healthy weight for nothing), we don't know from this study if losing weight (for obese people) or gaining weight (for underweight people) will affect their chances of getting migraines.

Avoiding the triggers listed above, when possible, should also help.

Read more about migraine prevention.

Links To The Headlines

Why being a healthy weight is ONLY way to beat migraine: Being under or over raises risk by 27% - and women with chubby tummies are most at-risk. Mail Online, April 12 2017

People who are too fat or too thin are ‘more likely to suffer from migraines’. The Sun, April 13 2017

Links To Science

Gelaye B, Sacco S, Brown WJ, et al. Body composition status and the risk of migraine - A meta-analysis. Neurology. Published online April 12 2017

Could your tattoos put you at risk of heat stroke?

NHS Choices - Behind the Headlines -

"Do you have a tattoo? You may be at-risk of heat stroke as inked skin produces significantly less sweat than normal," the Mail Online reports.

A small US study, involving 10 men, found tattooed skin produced less sweat, which could lead to over-heating.

The drug pilocarpine was used to induce sweating on the participants' tattooed skin and then on non-inked skin on the opposite side of the body. The researchers found less sweating in the tattooed skin and the level of sodium was higher (sweat was more concentrated).

Sweat serves an important role as part of the body's "thermostat", by helping regulate the body's temperature, as it cools you off when it evaporates from your skin.

The authors suggest the possibility that high temperatures combined with a large proportion of tattooed skin would limit heat loss and so could increase risk of heat exhaustion and heatstroke. However, this has not been explored.

As a general health point – tattoos aside – if you notice someone has signs of heat exhaustion, such as tiredness, feeling faint, headache, feeling sick, or is very thirsty, you should get them to lie down in a cool place, remove unnecessary clothing, cool their skin and get them to drink fluids.

Read more advice about treating heat exhaustion.

 

Where did the story come from?

The study was carried out by researchers from Alma College, Michigan in the US and was funded by Alma College.

The study was published in the peer-reviewed journal Medicine & Science in Sports & Exercise and the authors declare there were no conflicts of interest.

The Mail Online reported the study accurately, saying that it is currently unknown whether long term health would be affected by the finding that tattooed skin produces less sweat. However its headline suggesting that if you have a tattoo you may be "at-risk of HEAT STROKE," (in full caps) is jumping ahead of what the study actually showed, as the effects of heat were not actually studied.

 

What kind of research was this?

This was an experimental study that aimed to look at differences in sweat secretion and amount of sodium in the sweat between tattooed and non-tattooed skin. It involved use of a medical device designed to induce sweating and participants were tested twice, once on their tattooed skin and once on their non-tattooed skin.

The tattooing process involves puncturing the skin with needles loaded with dye into the dermal layer. The dermal layer is made up of collagen fibres, nerves, blood vessels and glands, including sweat glands that produce sweat when the body heats up and exceeds regular temperature levels.

Researchers wanted to see if the tattooing process impaired the function of the sweat glands, and if so, by how much.

This study is useful to look into this as it is analysing skin from the same person twice and therefore everything other than the tattooed/non-tattooed skin remains the same. However, the extremely small sample size and lack of any further investigation into potential effects on body temperature make it quite limited.

 

What did the research involve?

Researchers took 10 healthy males who had a tattoo on one side of their body, and compared their sweat rates and the level of sodium in their sweat to the same (non-tattooed) area on the other side of their body.

The tattoos were on the upper back, shoulder, upper body, upper arm or lower arm and completely covered a circular area of at least 5.2cm2. The patch of skin with the highest density of ink was used as the tattooed area. The unmarked skin in the exact opposite position on the other side of their body represented the non-tattooed skin.

Sweat was induced using gel disks containing pilocarpine, a substance used to induce sweating. The disks were attached to electrodes that were used to deliver pilocarpine into the skin in two five minute sessions.

After the second session, sweat was drawn into tubing that was modified to allow sweat collection into a disk. The sweat rate was measured by looking at the change in weight of the collection disk before and after sweat collection.

Sweat was then diluted and the sodium concentration of each sample was measured.

Sweat rate and sodium concentration were compared for the tattooed and non-tattooed skin of each participant.

What were the basic results?
  • All 10 participants generated less sweat from tattooed skin than non-tattooed skin.
  • The mean ratio of sweat rates from tattooed to non-tattooed skin was 0.53 (±0.12), therefore the average sweat rate from tattooed skin was about half the sweat rate from non-tattooed skin.
  • Nine of 10 participants had higher sodium concentration in their sweat from tattooed skin than non-tattooed skin.
  • The mean sodium concentration from tattooed skin was 1.73 times higher than non-tattooed skin.
  • Age of tattoo did not seem to have an effect.

 

How did the researchers interpret the results?

The researchers conclude that tattooed skin has a lower sweat rate and a higher sweat sodium concentration than non-tattooed skin. They say: "Additional studies need to be conducted to determine the mechanism associated with these changes in sweat function and the extent that they may affect thermal balance."

 

Conclusion

The study showed that artificially stimulating sweat glands in a tattooed area of skin in 10 men produced a lower sweat rate than stimulating sweat glands in a non-tattooed area of skin in the same person.

The authors suggest a number of possible explanations for this, including that it may be because tattooing skin starts an inflammatory response that may cause damage to normal tissue including sweat glands. However, these are only theories and need to be investigated further.

While this is interesting preliminary research, there are some important things to remember:

  • There were only 10 male participants involved in the study. A much larger study would be needed to see if the findings still hold true.
  • 7 out of 10 participants had their tattooed skin tested first. This might have had an effect on their sweat rate, for example if their body continued producing sweat from the first round and this was included when their non-tattooed skin was later tested.
  • The sweat glands were artificially stimulated in an environment where the level of heat was kept constant. We don't know if this represents the sweat response caused by over-heating in the real-life situation. We certainly don't know whether it could have effects in terms of making you more likely to over-heat and develop heat exhaustion or heat stroke, as with the media's rather bold assumption.

In any case, even if tattoos do impair sweating, the odd couple of tattoos scattered on your skin are unlikely to have much of an effect on your temperature regulation. It could be more of an issue if you had large portions of your body covered with tattoos. But even then as said, this tiny study proves little and the findings need confirmation.

The Mail's reporting of the study, slightly over-hyped as it was, highlights the fact that all of us should be aware of the signs of heat exhaustion and the subsequent steps – get the person to lie down in a cool place, cool their skin remove unnecessary clothing, and get them to drink fluids – that should be taken.  

Links To The Headlines

Do you have a tattoo? You may be at-risk of HEAT STROKE as inked skin produces significantly less sweat than normal. Mail Online, April 12 2017

Links To Science

Luetkemeier MJ, Hanisko JM, Aho KM. Skin Tattoos Alter Sweat Rate and Na+ Concentration. Medicine & Science in Sports & Exercise. Published online February 25 2017

Daily diet of fresh fruit linked to lower diabetes risk

NHS Choices - Behind the Headlines -

"Eating fresh fruit daily could cut risk of diabetes by 12%," the Mail Online reports.

A study of half a million people in China found those who ate fruit daily were 12% less likely to get type 2 diabetes than those who never or rarely ate it.

It was also found that people with diabetes at the start of the study who ate fruit regularly were slightly less likely to die, or to get complications of diabetes, such as eye problems (diabetic retinopathy), during the study than those who ate fruit rarely or never.

Many people with diabetes in China avoid eating fruit, because they are told it raises blood sugar. However, the study suggests fresh fruit may actually be beneficial for people with and without diabetes.

Fruits which release sugars more slowly into the blood, such as apples, pears and oranges, are the most popular in China, according to the researchers. So this may be the preferred option if you are worried about diabetes risk, or have been diagnosed with diabetes.

The study doesn't show that fruit directly prevents diabetes or diabetes complications, as an inherent limitation of this type of study is that other factors could be involved. And it doesn't tell us how much fruit might be too much.

Overall, the research suggests fresh fruit can be part of a healthy diet for everyone.

 

Where did the story come from?

The study was carried out by researchers from the University of Oxford, and Peking University, Chinese Academy of Medical Sciences, China National Center for Food Safety Risk Assessment, Non-communicable Disease Prevention and Control Department, and Pengzhou Center for Disease Control and Prevention, all in China. It was funded by the Kadoorie Charitable Foundation.

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

The Mail's report was basically accurate, although it did not point out that this type of study cannot prove cause and effect. The report confused some readers by saying that fruit does not raise blood sugar because it is metabolised differently to refined sugar.

However, what the study found was that fruit-eaters' blood sugar was not on average higher than that of non-fruit eaters. Like most food, the rise in sugar levels after eating fruit is usually temporary.

The Sun's report was poorly written and contained some basic grammatical errors.

 

What kind of research was this?

This was a large-scale prospective cohort study. Researchers wanted to look for associations between fruit eating, diabetes and complications of diabetes.

However, while this type of study is good for spotting links, it cannot prove that one factor causes another.

 

What did the research involve?

Researchers used information from a big ongoing cohort study called the China Kadoorie Biobank Study, which recruited half a million adults aged 30 to 79 between 2004 and 2008.

Participants filled in questionnaires about their health, diet and lifestyle and had measurements taken of their blood sugar, blood pressure, cholesterol and other health-related factors. The diet questionnaires were repeated over the course of the study. After an average seven years of follow-up, researchers looked to see how fruit consumption related to diabetes.

Some people in the study (almost 6%) had diabetes at the start of the study. While not actually specified in the study, we assume the majority of these cases were type 2 diabetes. Type 1 diabetes usually begins in childhood and is less common than type 2.

About half of them had previously been diagnosed, and half were diagnosed due to their blood sugar readings taken during the study. China's Disease Surveillance Points system was used to identify any deaths and cause of death during the study. Disease registries and health insurance claims were used to look into diabetes-related health complications.

The researchers took the average responses from the diet questionnaires to establish how regularly people ate fruit, to account for possible changes in dietary habits.

They adjusted the figures to take account of potential confounding factors including age, age at diabetes diagnosis, gender, smoking, alcohol consumption, physical activity and body mass index. 

 

What were the basic results?

Only 18.8% of people surveyed reported eating fruit daily, and 6.4% said they never or rarely ate fruit. Some 30,300 people had diabetes at the start of the study, and there were 9,504 new cases of diabetes in the seven years of follow up, or 2.8 for each 1,000 people each year.

  • People who ate fresh fruit daily were 12% less likely to develop diabetes than those who never or rarely ate fresh fruit (hazard ratio (HR) 0.88, 95% confidence interval (CI) 0.83 to 0.93).
  • Of the people with diabetes at the start of the study, 11.2% died during follow up (16.5 for every 1,000 people each year).
  • People with diabetes who ate fresh fruit on three days a week or more were 14% less likely to die of any cause, compared to those who ate fresh fruit less than one day a week (HR 0.86, 95% CI 0.80 to 0.94). They were also less likely to die from diabetes-related causes or cardiovascular disease, specifically.
  • People with diabetes who ate fresh fruit daily were also 14% less likely to have complications of damage to their large blood vessels (such as heart attack or stroke) than those who ate fresh fruit never or rarely (HR 0.86, 95% CI 0.82 to 0.90). They were also 28% less likely to have small blood vessel complications, such as eye or kidney disease (HR 0.72, 95% CI 0.63 to 0.83).

 

How did the researchers interpret the results?

The researchers say their results "provide strong evidence in support of current dietary guidelines that fresh fruit consumption should be recommended for all, including those with diabetes."

They say that people with diabetes in China eat much less fruit than people without diabetes, because of concerns about sugar in fruit. They say the study shows that better health education is "urgently needed" in China and other Asian countries where diabetes is common, and many people misunderstand the effects of eating fresh fruit.

They speculate that "natural sugars in fruit may not be metabolised in the same way as refined sugars," although their paper did not investigate this.

 

Conclusion

The study findings – that eating fresh fruit every day does not raise the risk of diabetes, and may reduce it – are reassuring and in line with dietary advice in the UK. It's also helpful to see evidence that people who already have diabetes are likely to benefit from fresh fruit as well, because there has not been much research into fruit-eating for people with diabetes.

However, it's a step too far to say that fresh fruit prevents diabetes or diabetes complications. Fresh fruit is just one part of a healthy diet, and diet is just one of the things that may affect someone's risk of getting diabetes. This type of study can't tell us whether fresh fruit actually protects against diabetes, because it can't account for all the other health and lifestyle factors involved.

Though it would be expected that the results of this large scale study should be applicable to other populations, there may be differences between people from China and other populations. This could include differences in prevalence of diabetes and its risk factors, differences in healthcare (for example, diagnostic criteria and methods for coding health outcomes in databases), and other environmental and lifestyle differences, including fruit consumption.

The study didn't ask people which types of fruit they ate, but the researchers say the most commonly eaten fruits in China are apples, pears and oranges, which release sugars more slowly into the blood stream than bananas, grapes and tropical fruits.

It's important to make a distinction between whole fresh fruit, which contains lots of fibre, and fruit juice, which is very high in sugar. Previous research that we reported on in 2013 found that fruit may lower diabetes risk, but fruit juice may raise it.

The most effective method of reducing your diabetes risk is to achieve or maintain a healthy weight, through a combination of regular exercise and healthy eating. Read more about preventing diabetes.   

Links To The Headlines

Eating fresh fruit daily could cut risk of diabetes by 12%: New research reduces fears it is unhealthy because of high sugar content. Mail Online, April 12 2017

Eating fresh fruit every day and making lifestyle changes lower the risk of diabetes, study says. The Sun, April 12 2017

Links To Science

Du H, Li L, Bennett D, et al. Fresh fruit consumption in relation to incident diabetes and diabetic vascular complications: A 7-y prospective study of 0.5 million Chinese adults. PloS Medicine. Published online April 11 2017

Brain cell reprogramming therapy shows promise for Parkinson's

NHS Choices - Behind the Headlines -

"New technique in which brain cells are reprogrammed could one day provide a cure for Parkinson's disease," The Independent reports.

Researchers, using mice with Parkinson's disease, "reprogrammed" cells to replace the nerves lost in the condition. These nerves produce the messenger chemical dopamine, and help to coordinate body movements.

Parkinson's is a neurological condition, of unknown cause, where there is a progressive loss of dopamine-producing nerve cells in the brain. The gradual loss of these nerves leads to the symptoms of Parkinson's, such as tremor and muscle stiffness.

In this study researchers used an injection of a specially engineered virus to introduce a combination of genes into the brains of the mice. These genes were designed to target a type of cell known as astrocytes. These cells serve a wide range of functions, but crucially they do not carry electrical signals like nerve cells or produce dopamine.

This virus was also able to convert astrocytes within the brains of the mice into dopamine-producing cells (which the researchers called induced dopamine neurons (iDANs)). They saw improvement in some aspects of walking in these mice when they exercised on a treadmill.

Researchers hope their methods could eventually be used to treat humans with Parkinson's.

While these are promising findings, it may be premature to call this a breakthrough, as BBC News put it. As yet, we do not know whether this approach could be used to reverse symptoms in people with Parkinson's disease.

The effectiveness, and more importantly the safety of this approach in humans is currently uncertain.

 

Where did the story come from?

The study was carried out by researchers from the Karolinska Institutet, Medical University of Vienna, Malaga University and Stanford University. Funding was provided by a large number of institutions, including the Swedish Research Council, Swedish Foundation for Strategic Research and the Karolinska Institutet. There were no reported conflicts of interest.

The study was published in the peer-reviewed journal Nature Biotechnology.

The UK media's reporting of the study, aside from a slightly over-optimistic tone, was accurate and included useful commentary from independent experts.

 

What kind of research was this?

This was a laboratory experiment and animal study in mice and human brain cells. It aimed to investigate whether it is possible to modify cells commonly found in the brain (called glial cells – specifically a type called astrocytes) to replace those lost through Parkinson's disease. The researchers hope this approach could reduce or reverse symptoms.

The nerve cells lost in Parkinson's disease are in a part of the brain called the substantia nigra. They produce a chemical called dopamine, which transmits signals from these cells to other nerve cells. Dopamine belongs to the class of chemicals known as neurotransmitters.

Researchers have been studying different ways to replace these cells. In the past they have been able to convert adult mouse and human skin cells into dopamine-producing nerve cells in the laboratory.

However, these cells would need to be transplanted into the brain, a procedure which could pose a number of serious risks.

In the current study, researchers wanted to assess whether they could get cells already in the brain to convert into dopamine producing nerve cells, to avoid the need for transplantation.

Animal studies such as this are a useful way to carry out early stage research which can then be refined before testing in human trials. In this case human cells were also modified in the laboratory, which increases confidence that the technique might work in humans.

 

What did the research involve?

The researchers used genetic engineering to get the glial cells to switch on genes needed to become dopamine producing nerve cells. Researchers tested the effect of switching on a number of genes in human glial cells in the laboratory under a number of different conditions. They aimed to identify the combination that was most effective at getting the glial cells to become dopamine producing nerve cells.

Mice were engineered to have symptoms of Parkinson's by destroying their dopamine-producing nerve cells. Their brains were then injected with the combination of genes, contained within a virus, which had been identified in the first set of experiments, to see if this would convert their glial cells.

They were then analysed five weeks later to see if this modification had resulted in improvements to their motor (movement) skills.

 

What were the basic results?

The researchers found that they were able to get human glial cells in the laboratory to convert into dopamine producing nerve cells. They got the best results when they used a specific combination of four genes important in the development of these cells. They could get up to 16% of the glial cells to develop the characteristics of dopamine-producing nerve cells.

They then injected this specific combination of four genes into the brains of some mice with Parkinson's-like symptoms. After five weeks, the treated mice appeared to walk better on a treadmill compared to control mice.

 

How did the researchers interpret the results?

The researchers conclude their findings show that in mice it was possible to re-programme cells in the brain to replace the dopamine-producing nerve cells lost in Parkinson's disease. As a result of this they were able to reverse some of the symptoms of Parkinson's in a mouse model of the disease.

The researchers conclude: "The next steps to be taken toward achieving this goal include improving reprogramming efficiency, demonstrating the approach on human adult striatal astrocytes … in vivo [in an actual human, as opposed to a lab experiment], and ensuring safety and efficacy in humans."

 

Conclusion

This laboratory and animal study aimed to see whether it is possible to modify a type of cell commonly found in the brain, called glial cells, to become dopamine-producing nerve cells. These dopamine-producing nerve cells are the ones lost in people with Parkinson's disease. If a method could be found to replace these cells, it could potentially be used to treat the condition.

Previous research has shown that mouse and human skin cells can be converted to dopamine-producing cells in the laboratory. However, this is the first study to develop a way to convert a different type of cell already in the brain into dopamine-producing nerve cells. It has also shown that this can produce improvements in Parkinson's-like symptoms in a mouse model of the disease.

These findings are promising, particularly as the researchers have shown that it is possible to use this technique to modify human cells as well as mouse cells. However, the approach has not yet been tested in people with Parkinson's and it is not possible to know whether the cells would function as expected or whether the change would be long lasting.

Even before human studies can be carried out, it is likely that more animal experiments would be needed to ensure the approach is effective and safe in the long-term. 

Links To The Headlines

New neuron reprogramming technique could hold key to curing Parkinson's disease, say scientists. The Independent, April 11 2017

Brain cell therapy 'promising' for Parkinson's disease. BBC News, April 11 2017

Parkinson's breakthrough as experiments show brain cells killed by the disease can be replaced. Daily Mirror, April 11 2017

Links To Science

Di Val Cervo PR, Romanov RA, Spigolon G, et al. Induction of functional dopamine neurons from human astrocytes in vitro and mouse astrocytes in a Parkinson's disease model. Nature Biotechnology. Published online April 10 2017

Growing up with a pet may boost a baby's bacterial health

NHS Choices - Behind the Headlines -

"Having a pet dog…can help reduce the child's chances of developing allergies and becoming obese in later years," claims the Daily Mirror, in a somewhat misleading report.

Researchers did find a link between pet ownership and an increased diversity of "healthy bacteria" in infants, but didn't look at long-term outcomes such as the development of allergies or obesity.

The researchers carried out a range of tests on faecal (poo) samples taken from infants to assess the levels and composition of the bacteria in their guts.

Gut bacteria is widely known to play an important role in future health. Infant gut bacteria is thought to be influenced by several factors including the method of birth delivery, drinking breast milk versus formula, and treatment of the mother with antibiotics. So the hypothesis that furry pets could boost infant immunity has increasingly been discussed.

Overall, the study found that the composition of gut bacteria was richer and more diverse in infants who had been exposed to pets both in the womb and after birth. But whether or not this observation actually has any effect on health outcomes wasn't explored.

Proven methods you can use to reduce your child's risk of allergies include breastfeeding and ensuring they are never exposed to tobacco smoke, including in the womb.

 

Where did the story come from?

This Canadian study was carried out by researchers from several institutes including the University of Toronto, the University of Alberta and the University of British Columbia. It was funded by a grant from the CIHR Canadian Microbiome Initiative.

The study was published in the peer-reviewed scientific journal Microbiome. It is available on an open-access basis and is free to read online.

Both the Mirror's and the Mail Online's headlines were misleading, wrongly giving the impression that researchers had looked at allergy and obesity rates in later life. This was not the case.

The body of reporting in both sources was much more balanced and had greater focus on the gut bacteria.

 

What kind of research was this?

This was an analysis of a subgroup of infants from a larger prospective cohort study: the Canadian Healthy Infant Longitudinal Development Study (CHILD). It wanted to assess whether a baby's exposure to pets while in the womb and after birth has any impact on their gut bacteria.

Giving antibiotics to a mother during labour can disrupt her baby's gut bacteria, so antibiotic use was also analysed – as well as the method of delivery: caesarean (elective versus emergency) and vaginal delivery (with or without antibiotics).

Prospective cohort studies such as this are useful for understanding whether a link between an exposure (in this case, pets) and an outcome (a change in infant gut bacteria) exists. However, the challenge with this study design is that it isn't able to fully rule out the involvement of other confounding environmental and lifestyle factors, such as diet.

Although a randomised controlled trial (RCT) is the best way to validate any findings, it certainly wouldn't be practical (let alone ethical) to expose parents and their infants to pets against their will. The study also doesn't explore whether levels of infant gut bacteria have any effect on long-term outcomes.

 

What did the research involve?

This study analysed a subsample of 753 infants from the CHILD study, which enrolled pregnant women between 2009 and 2011.

The mothers were given a questionnaire about pet ownership during their second or third trimester of pregnancy, and three months after birth.

Exposure to pets was categorised into:

  • no pet exposure in the prenatal and postnatal periods
  • only prenatal pet exposure
  • both prenatal and postnatal pet exposure

The category assessing "only postnatal pet exposure" was found to only include seven mothers, so it was excluded from subsequent analysis.

Gut bacteria in faecal samples was analysed for infants with complete data on prenatal and postnatal pet exposure (n=746).

Data on a range of potential confounding factors was also collected:

  • mode of delivery
  • use of antibiotics during delivery
  • maternal race
  • maternal asthma and allergy status during pregnancy
  • type of home
  • size of household
  • type of floor
  • presence of siblings
  • breastfeeding status
  • infant antibiotic exposure before three months

The data was analysed to test for any links between pet exposure and the composition of gut bacteria.

Statistical analysis was carried out to compare four different birth scenarios:

  • vaginal without antibiotics
  • vaginal with antibiotics
  • elected caesarean
  • emergency caesarean

 The analysis was adjusted to take into account the confounders.

 

What were the basic results?

Out of the 746 infants, 46.8% of households owned furry pets during and after pregnancy. The majority of pet owners had dogs, closely followed by cats.

Overall, the composition of gut bacteria was richer and more diverse in infants who had been exposed to pets during both the prenatal and postnatal period. In particular, there was an abundance of two bacteria, ruminococcus and oscillospira. Previous research has linked each of these strains to improved "gut health".

The researchers add that previous studies have found an association between lower levels of these bacteria and a greater likelihood of childhood allergies and obesity. But this hypothesis was not investigated in this study.

The study also found that a baby's exposure to pets while in the womb resulted in lower levels of streptococcal bacteria in their gut.

 

How did the researchers interpret the results?

The researchers concluded: "Our findings highlighted the differential impact of pet exposure on infant gut microbiota following variant birth scenarios; however, in common, the abundance of ruminococcus and oscillospira were found to be increased independent of other factors.

"In addition, our finding of reduced streptococcal colonization with prenatal pet ownership may lower the risk for childhood metabolic and [allergic] disease. Further research is needed to link the pet-related microbiota changes with health outcomes of infants in the CHILD cohort, as well as in other populations."

 

Conclusion

This subgroup analysis of babies from a large Canadian birth cohort assessed whether exposure to furry pets before and after birth has any impact on infant gut bacteria. Overall it found that exposure to pets while in the womb and after birth was linked with richer and more diverse gut bacteria.

The researchers say that several studies in the past, including their own, have found a link between richness of gut bacteria and both the development of allergies and the development of obesity. Therefore these findings may be taken to imply that pet exposure could protect against allergy and obesity in infants – as in media reports. However, later child health outcomes, including the development of allergy or obesity, were not investigated in this study.

This short term study only looked at the composition of gut bacteria in infants at three months of age. It would be useful to see how long-term exposure to pets affects gut bacteria in individuals and whether the same results are observed, and to see whether there is any link with other health outcomes.

The study also found that pre-natal exposure to pets resulted in lower levels of streptococcal bacteria. Many women carry group B streptococcus without symptoms, and this can sometimes cause infection in newborns, hence the relevance of this link. However, again this has not been investigated further.

There is also the possibility that any links between pet ownership and bacterial levels are being influenced by other environmental and health-related confounders. Bacterial levels may not necessarily be a direct result of the pets. Also, bear in mind that the results of this Canadian study may not necessarily apply to the UK or other countries.

These findings pave the way for future research around pet exposure and health outcomes in individuals, especially around allergies. However, this research is too early in stage to recommend that parents-to-be have a pet to protect their children against allergies, and certainly not against obesity (although walking your dog could be good exercise!).

Breastfeeding children and minimising their exposure to tobacco smoke will also reduce their allergy risks. And regular exercise and a healthy diet should prevent a child from becoming obese.

Read more healthy weight advice for parents.

Links To The Headlines

Why owning a pet dog can help parents have a healthy baby. Daily Mirror, April 7 2017

Why loving dogs is good for your health: People exposed to pets from an early age are less likely to be obese and have fewer allergies. Mail Online, April 7 2017

Links To Science

Tun HM, Konya T, Takaro TK, et al. Exposure to household furry pets influences the gut microbiota of infant at 3–4 months following various birth scenarios. Microbiome. Published online April 6 2017

Tea not proven to 'shield you against dementia'

NHS Choices - Behind the Headlines -

"It's tea time! How at least two cups a day can shield you from dementia," reports the Mail Online. This rather optimistic headline reports on a Singaporean study of around 900 Chinese people aged 55 and above.

The study searched for a potential link between tea consumption and development of dementia. It found the risks of dementia were halved in tea-drinkers. However, when breaking the results down further, the links were only significant for women who drank three to four cups a day and in drinkers who carry a particular dementia-risk gene.

Despite the relatively large sample size, only 72 people developed dementia. But breaking down this number further according to tea intake leaves only small groups for analysis. And the smaller the sample size, the bigger the risk that pure chance affected the results.

Also, despite adjusting for other health and lifestyle factors that could be influencing the link, it is always difficult to isolate the direct effect of tea drinking.

The researchers suggest that promotion of tea drinking could have benefits for the brain but they also point out that further studies are needed to confirm the results found in their study.

There is currently no guaranteed method(s) of preventing dementia, but a useful maxim is "what is good for the heart is also good for the brain". Regular exercise, a healthy diet, moderate alcohol consumption and avoiding smoking can help lower dementia risk.

 

Where did the story come from?

The study was carried out by researchers from the National University of Singapore. It was funded by the Biomedical Research Council; the Agency for Science, Technology and Research; the Virtual Institute for the Study of Ageing; and the Alice Lim Memorial Fund.

The study was published in the peer-reviewed Journal of Nutrition, Health and Aging.

The Mail Online's headline was overly optimistic: it took the 50% figure at face value. The website noted the small sample size, but the limitations of the study were not discussed.

 

What kind of research was this?

This was an analysis of data from a prospective cohort study of Chinese older adults, which aimed to investigate whether there's a link between tea consumption and dementia.

In Chinese culture, the consumption of strong tea is considered to enhance brain-based skills such as memory and alertness in the short-term. However, the regular consumption is also thought to have long-term benefits, which several studies have previously looked into.

With this background, the authors of this research wanted to further test the hypothesis that tea drinkers are less likely to develop brain disorders such as dementia, when compared to non-drinkers.

The researchers also wanted to see whether the association was different between males and females, and in people carrying a high-risk variant of the apolipoprotein (APOE) gene – studies have suggested that people are more likely to develop Alzheimer's if they carry this gene type.

Cohort studies are valuable for testing the association between an exposure and outcome, and although they aren't always able to prove cause and effect, can give a good indication of any potential links.

As mentioned by the study authors, a randomised-controlled trial (RCT) would be one of the best ways to further test a hypothesis such as this. However, it is not easy to recruit sufficient people, randomise them to a tea drinking pattern they have to stick to, and then follow them for long enough to look at the effect on cognitive outcomes.

 

What did the research involve?

This analysis used data from the Singapore Longitudinal Ageing Studies (SLAS), which studied ageing and health in Singaporeans aged 55 years and above. It recruited 2,808 participants. Baseline data was collected from 2003 to 2005, and follow-up of neurocognitive disorders was conducted from 2006 to 2010.

The SLAS study collected information on cognitive function, having assessed this using a version of the Mini-Mental State Examination (MMSE) at baseline and during follow-up assessments. The MMSE is a well respected method of testing a range of cognitive abilities.

An MMSE score of 26 and above was defined as being "normal". During follow-up, adults who had a score of less than 26 or a decline in the MMSE score of one or more were further assessed using the Clinical Dementia Rating (CDR).

Participants were asked about their tea consumption habits through a questionnaire given at baseline and during follow-up. The survey categorised tea into: "Ceylon/English" tea; "Chinese" tea and "Green" tea.

Frequency of tea consumption was coded as:

  • 0 – never or rarely
  • 1 – less than one cup/week
  • 2 – more than one cup/week but less than one cup/day
  • 3 – one-two cups/day
  • 4 – three or more cups/day

The level of tea consumption was categorised into four groups:

  • 0 – none
  • 1-2 – low
  • 3-4 – medium
  • 5 or more – high

This study assessed data from a group of 957 SLAS participants who had an MMSE score of 26 or more at baseline. Among these people, 72 (7.5%) developed a neurocognitive disorder (dementia) during follow-up.

The researchers analysed the data for differences between tea drinkers and non-drinkers. The model was adjusted for numerous potential confounders, including:

  • age
  • gender
  • smoking
  • alcohol consumption
  • body mass index (BMI)
  • diabetes
  • heart diseases
  • depression
  • dietary intake
  • presence of the APOE ε4 gene (the high risk variant)

 

What were the basic results?

69% of participants in this analysis were tea consumers at baseline. Out of the 660 tea drinkers, 39 individuals (5.9%) developed dementia; out of the 297 non-drinkers, there were 33 incident cases (11.1%).

The analysis indicated that tea drinkers had a 50% reduced chance of developing dementia during follow-up (odds ratio [OR] 0.50, 95% confidence interval [CI]: 0.28 to 0.87). Those who drank a medium amount of tea had 64% reduced risk (OR 0.36, 95% CI: 0.16 to 0.78). Results were not statistically significant for either low and high levels of tea intake, which slightly confuses the picture.

By gender, tea drinking gave reduced risk in women (OR 0.32, 95% CI: 0.15 to 0.69) but links were not statistically significant in men.

Tea drinking appeared to give protection in high-risk APOE carriers (OR 0.14, 95% CI: 0.02 to 0.93), but did not have a significant effect in non-carriers (OR 0.56, 95% CI: 0.30 to 1.04).

 

How did the researchers interpret the results?

The researchers concluded: "Our data suggest that a simple lifestyle measure such as tea drinking can reduce a person's risk of developing neurocognitive disorders in late life.

"Together with earlier reports on cognitive benefits of tea drinking, our study supports the promotion of tea drinking as a simple, culturally acceptable and cheap preventive measure among other known protective interventions such as participating in physical, social and cognitive activities."

 

Conclusion

This analysis of data from a prospective cohort study of Chinese older adults looked at a potential link between tea consumption and development of dementia. It found that tea drinkers who took part in the study were less likely to develop dementia compared to non-drinkers. The links were observed specifically in women tea drinkers, and in drinkers who carry the APOE ε4 gene that has been linked with Alzheimer's development.

This was a well-designed cohort study which controlled for numerous potential confounders in its analysis. However, there are a number of things to bear in mind, many of which have been pointed out by the authors:

  • Not all of the links with tea consumption were significant. When analysed by intake, only those drinking three or four cups a day had apparent protection, with no link for greater or lesser amounts. However, as they say, this could be down to the small number of people who developed dementia during the study. Breaking down this number according to tea intake leaves only small samples for analysis. Large scale studies would need to be conducted to confirm these findings.
  • While significant links were found specifically for women and for carriers of the high-risk variant of the APOE gene, we shouldn't draw strong conclusions at this stage. We don't know the reason for this link – it could be influenced by other health and lifestyle factors that haven't been taken into account.
  • This study was conducted in people of Chinese ethnicity and therefore cannot necessarily be generalised to other populations. People of different cultures and ethnicities could have different susceptibilities to medical conditions, and could also have different tea drinking patterns.
  • The study defined development of dementia as scoring above a particular level on the Clinical Dementia Scale, but we cannot necessarily apply the findings to particular types of dementia, like Alzheimer’s or vascular dementia.

The findings of this study warrant further exploration, although high quality randomised controlled trials may be difficult. This study, on its own, does not prove that drinking tea will stop you from getting dementia.

To reduce your risk of developing dementia and other serious health conditions, it's recommended that you:

Links To The Headlines

It's tea time! How at least two cups a day can shield you from dementia. Mail Online, April 7 2017

Links To Science

Feng L, Chong MS, Lim WS, et al. Tea consumption reduces the incidence of neurocognitive disorders: Findings from the Singapore longitudinal aging study. The Journal of Nutrition, Health and Aging. Published online January 15 2016

Antibiotic use linked to 'pre-cancerous' bowel changes

NHS Choices - Behind the Headlines -

"Taking antibiotics for more than two weeks increases your risk of bowel cancer by 73 per cent," reports the Daily Mail.

However, the study it reports on did not look at rates of bowel cancer. What it did find is an increased risk of bowel polyps for women who took antibiotics for two months or more.

Bowel polyps are small growths that develop on the lining of the colon or rectum. The majority of these growths are benign (non-cancerous), though it is estimated that without treatment to remove them, a small minority will turn cancerous.

This study included 16,642 women aged over 60, who'd had a colonoscopy, a test used to screen for bowel cancer in the US (not routinely used for screening in the UK). They were asked to remember how much they'd used antibiotics earlier in life.

Those who said they'd used antibiotics for a period of at least two months from the age of 20 to 60 were more likely to have been diagnosed with a colorectal adenoma (more commonly known as a bowel polyp) during colonoscopy.

Antibiotics kill off some of the diverse bacteria that live in the gut, which may lead to an imbalance of bacteria. It's been suggested that this could make the gut more vulnerable to cancerous growths.

However, the study doesn't prove antibiotics directly cause bowel cancer, or even bowel polyps. If you've been prescribed antibiotics, you shouldn't stop taking them because of this study.

 

Where did the story come from?

The study was carried out by researchers from Harvard Medical School, Harvard TH Chan School of Public Health, the University of Nebraska and Yale School of Medicine. It was funded by grants from the US National Institutes of Health and various charitable bodies. The study was published in the peer-reviewed medical journal Gut.

BBC News covers the study in a balanced and accurate fashion, and includes useful information on known bowel cancer risk factors. In contrast, the Mail Online used a scaremongering headline, based on the subgroup of women found to be at highest risk. But this figure did not take into account multiple risk factors for bowel cancer, so we do not know if it is accurate. The story also downplays the fact that more than 90% of this type of polyp (adenoma) does not become cancerous.

 

What kind of research was this?

This was a prospective cohort study in which a large number of women where followed up over a long period of time. The intention was to make links between lifestyle and health outcomes. But this type of study cannot prove that one factor (antibiotic use) causes an outcome (bowel polyps). It can only show that they are linked.

 

What did the research involve?

The researchers gave women aged 60 or over questionnaires asking about their lifestyle and health. They were asked about use of antibiotics during their younger life, as well as more recently. They were also asked if they'd had a colonoscopy and been diagnosed with polyps as a result.

After adjusting for potential confounding factors, the researchers looked to see whether women who'd been diagnosed with polyps were more likely to have taken antibiotics for long periods in earlier life.

The women were all taking part in the Nurses' Health Study, a long-running study in the US that started in 1976. Women were asked to fill in questionnaires every two years.

For this study, researchers included only women:

  • aged 60 or over in 2004
  • without a history of cancer or polyp before 2004
  • who reported their use of antibiotics up to age 59 in the 2004 questionnaire
    who'd had at least one colonoscopy
  • between 2004 and 2010

They adjusted their figures to take account of many factors linked to an increased risk of colorectal cancer, including poor diet, increasing age, family history of colorectal cancer, diabetes, body mass index (BMI), smoking and lack of exercise. They also adjusted the results for aspirin and hormone replacement therapy (HRT) which are linked to a reduced risk of colorectal cancer.

Researchers followed up the medical records of women who reported having been diagnosed with a polyp, to see where in the bowel it was found, and whether it was high or low risk in terms of how likely it was to turn cancerous. However, they did not report how many women developed bowel cancer.

They designed the study so the figures would not be affected by certain people having multiple colonoscopies. They looked separately at women's antibiotic use in their 20s and 30s, in their 40s and 50s, and more recently.

 

What were the basic results?

Of the 16,642 women in the study, 1,195 (7%) had a polyp diagnosed during a colonoscopy.

Compared to women who'd never taken antibiotics:

  • Women who took antibiotics for two months or more aged 20 to 39 had a 36% increased risk of a polyp (odds ratio [OR] 1.36, 95% confidence interval [CI] 1.03 to 1.79).
  • Women who took antibiotics for two months or more aged 40 to 59 had a 69% increased risk of a polyp (OR 1.69, 95% CI 1.24 to 2.31).
  • The women had no increased risk of polyps attached to having taken antibiotics more recently (within the previous four years).
  • Compared to women who did not report any use of antibiotics between the ages of 20 to 39 and 40 to 59, women who had 15 or more days of antibiotics during both of these periods of time had a 73% increased risk of polyps (OR 1.73, 95% CI 1.19 to 2.51). This result was only adjusted for age, not the other potential confounding factors.

The chance of having high or low risk polpys was about the same as having any polyps. The chance of having a polyp in the upper region of the colon (called the proximal region) seemed more strongly linked to antibiotic use than the chances of having a lower colon polyp.

 

How did the researchers interpret the results?

The researchers said their results "provide additional support" for linking antibiotic use to bowel cancer, and that – if the findings are confirmed by other studies – they "suggest the potential need to limit the use of antibiotics".

However, they admit that the bacteria being treated by the antibiotics might also have raised inflammation in the body. Inflammation is another risk factor for cancer, so the problem might be the infection, not the treatment.

 

Conclusion

Antibiotics, like all drugs, have side effects. We know that they affect the composition of bacteria that live in a healthy gut. This study suggests that might possibly be linked to future development of bowel cancer.

However, there are some major limitations to keep in mind. Bowel polyps are very common, and they're not cancerous. Most people who have them won't know they're there, unless they have a colonoscopy. Some polyps do develop into bowel cancer, but we don't know if any of these women got bowel cancer, or how many of their polyps would have become cancerous if not treated.

It's highly possible that women aged 60 might not remember accurately how often they used antibiotics in their 20s, or for how long. So we can't be sure whether women were over-estimating or under-estimating their antibiotics use.

Observational studies such as this cannot show that one factor directly causes another. As the researchers say, antibiotics are used to treat bacterial infections. Infections cause inflammation, and that's a risk factor for cancer. So the study may have measured the effect of repeated exposure to bacterial infection, rather than use of antibiotics.

The study was only carried out in women, so we don't know if the results apply to men.

The study did a good job of controlling for other potential confounding risk factors, but no study can control for everything. It's possible there are other factors involved which we don't know about.

Antibiotics have been over-used in the past and this study is a reminder that they should only be used when necessary. But it doesn't show that they cause bowel cancer. If you're taking antibiotics prescribed by your doctor to treat an infection, you should carry on taking them. Not doing so could contribute towards the ongoing problem of antibiotic resistance.

Known risk factors for bowel cancer include:

  • red and processed meat
  • smoking
  • drinking too much alcohol
  • being overweight
  • being inactive

Avoiding these risk factors should help lower your risk of bowel cancer.

Links To The Headlines

Taking antibiotics for more than two weeks increases your risk of bowel cancer by 73 per cent. Mail Online, April 5 2017

Antibiotic 'link to bowel cancer precursor'. BBC News, April 5 2017

Links To Science

Cao Y, Wu K, Mehta R, et al. Long-term use of antibiotics and risk of colorectal adenoma. Gut. Published online April 4, 2017

Reports that Marmite prevents dementia are laying it on a bit thick

NHS Choices - Behind the Headlines -

"A daily slice of Marmite on toast may help prevent you getting dementia," the Daily Mail reports, with little justification.

A small study did find that Marmite had an effect on electrical activity in the brain, but there is no evidence this would prevent dementia.

The study involved 28 people in their early 20s. Researchers looked to see whether eating Marmite affected the brain's response to watching flickering images on a screen, measured by electroencephalogram (EEG) scans. This test is used as a measure of "brain cell excitability" in the visual cortex area.

Marmite contains vitamin B12 and glutamate which are thought necessary for the brain to produce GABA, which is thought to reduce brain cell excitability. Too little GABA may be a factor in epilepsy.

The study compared the effect of eating a teaspoon of Marmite each day for one month with eating peanut butter. Healthy volunteers were tested before and after the trial of Marmite or peanut butter. After a month, scans on the Marmite-eaters' brains showed lower levels of excitability.

The researchers suggest that boosting GABA levels through diet might contribute to treating epilepsy. However, there's no clinical evidence to support this indication, never mind the media speculation about dementia.

For those who fall into the "hate camp" when it comes to Marmite, other sources of vitamin B12 include meat and cheese.

 

Where did the story come from?

The study was carried out by researchers from the University of York and was funded by the Wellcome Trust and the Leverhulme Trust.

The Leverhulme Trust was set up by the founder of Lever Brothers (William Hesketh Lever) now Unilever, which manufactures Marmite. However, the trust says it does not seek to influence the topic or study design of research when it provides grants.

The study was published in the peer-reviewed Journal of Psychopharmacology.

Predictably, the UK media loved this story. The Daily Telegraph and Daily Mirror referred to Marmite "giving a boost" to the brain. Sky News said it "keeps the brain healthy" and The Sun said it "may prevent dementia."

The Daily Mirror's report is the most balanced and was the only one to point out the link between funding and Unilever. It concludes that: "an analysis by the Daily Mirror of the nine-page study [ie reading it] found zero references to dementia or Alzheimer’s disease".

Several media outlets reported that the study was done in men only; however the study makes clear that more than half of the participants were women. 

 

What kind of research was this?

This was a randomised controlled trial, which is a good way to see the effect of an intervention. Researchers wanted to see if the yeast extract reduced the brain's response to visual stimuli.

 

What did the research involve?

Researchers measured brain response to visual stimuli (flickering images on a screen) using EEGs, in 28 volunteers. They were randomly allocated to take a teaspoon of either Marmite or peanut butter a day, in addition to their usual diet. After a month they were tested again, and the results compared between the two groups.

The volunteers (10 men and 18 women) were all in their 20s. None had epilepsy (in case flickering images triggered a seizure), smoked, had nut allergies or used controlled substances.

The experiment used flickering images with a "control" task, in which volunteers had to estimate the difference in contrast between two wave forms. This allowed researchers to check the groups were concentrating on the screen equally.

Researchers used several variations of the task, including a "mask" variation which should reduce the effect on an area of the brain called the visual cortex.

Volunteers were asked to take a teaspoon of their allocated spread each day and record that they had done so. Statistical models were used to look for differences between the EEGs for those who'd eaten Marmite and those who'd eaten peanut butter.

The researchers also tested both spreads for levels of glutamate and B vitamins. A sub-group of Marmite-eaters was tested again two months later.

 

What were the basic results?

Researchers say that on average the people who ate Marmite had reduced levels of "evoked response" – activity in response to images – compared to their baseline results. The average response didn't change for those eating peanut butter.

Only evoked responses were changed – response to background levels of activity when viewing a blank screen were not affected. The volunteers' performance on the attention test was no different between the two groups, suggesting that Marmite-eaters and peanut butter eaters had concentrated on the screen to the same degree.

In the group of Marmite-eaters retested after two months, response levels were still lower than at baseline, but not as low as immediately after the month-long trial.

In the chemical analysis of the spreads, Marmite had three times as much vitamin B6, almost twice as much glutamate and 116 times as much vitamin B12 than the peanut butter.

 

How did the researchers interpret the results?

The researchers said their results were "consistent with an increase in the availability of GABA in visual areas of the brain."

They said that previous research has shown that people with epilepsy showed increased visual responses when tested using the same visual stimuli as used in this experiment. "This raises the possibility that dietary interventions geared towards increasing GABA concentration might reduce excitability to normal levels, and potentially alleviate some symptoms of the disorder," they say.

They suggest it could reduce the number of seizures and be particularly useful for people who can't take anti-epilepsy drugs, or whose medicines haven't controlled their seizures.

They conclude that additional studies would be required to determine which substance in Marmite might be responsible for the results.

 

Conclusion

This is an early investigative research study, and while some of the findings are interesting, it's a long way from showing that yeast extract spreads can help with conditions like epilepsy or other neurological disorders.

The study's strength is that it was carried out as a randomised controlled trial. However, its small size means we need to see the results replicated in larger studies to be sure they are not down to chance. We also need to see longer-term studies into the actual clinical effects of the changes measured. At this point, we don't know what effect – if any – the changes in brain response have on the people involved.

The study has no implications for people with dementia, or at risk of dementia. The lead researcher told NHS Choices: "We're a bit puzzled as to where the idea [that dementia is involved] has come from. Our study didn't test any patients and we don't have any reason to expect that Marmite would have any effect on dementia at this time."

It's also important to be aware that the suggested effects on epilepsy have not been tested on people with epilepsy. No-one with epilepsy should be tempted to stop taking their medicines in favour of Marmite.  

Links To The Headlines

Time to start loving it? How a daily slice of Marmite on toast may help prevent you getting dementia. Daily Mail, April 5 2017

Marmite could help improve healthy brain function, scientists claim. ITV News, April 5 2017

Marmite may boost brain and help stave off dementia. The Daily Telegraph, April 5 2017

Marmite is good for the brain, study finds. The Independent, April 5 2017

Love it or hate it, Marmite could boost brain power, say scientists. Daily Mirror, April 5 2017

Links To Science

Smith AK, Wade AR, Penkman KEH, Baker DH. Dietary modulation of cortical excitation and inhibition. Journal of Psychopharmacology. Published online April 4 2017

Firefighters warned about heart attack risk

NHS Choices - Behind the Headlines -

"Working in hot temperatures increases the risk of suffering a heart attack," BBC News reports.

It has been known for some time that the leading cause of death amongst serving firefighters is heart attacks and not fire-related injuries as some people might assume. Researchers wanted to establish why this is the case.

The new study featured 19 healthy firefighters who either took part in a "fire suppression simulation" (putting out an actual fire in a simulation facility) or light, non-emergency activities.

The researchers looked at blood samples and measurements of core body temperature after these activities. They found that the simulation of putting out a fire increased the "stickiness" of the firefighters' blood – making it more likely to clot – in part due to them being dehydrated. It also resulted in the blood vessel walls being less elastic, and in signs of some minor injury to the heart muscle due to lack of oxygen.

All of these factors, as well as the added stress of dealing with an emergency, may combine to increase heart attack risk. The findings are important, but further larger studies are needed to confirm the results and establish useful precautions that can be taken to reduce the risk.

In the meantime, current advice is that firefighters stay well hydrated and take time to cool down after putting out a fire. 

Similar advice applies to anyone exposed to a high temperature environment, especially if they are taking part in a strenuous activity, such as endurance running.

 

Where did the story come from?

The study was carried out by researchers from the University of Edinburgh and was funded by the British Heart Foundation and the Colt Foundation. A number of authors also received grants from the British Heart Foundation, the Wellcome Trust and the Fire Brigade Union.

The study was published in the peer-reviewed medical journal Circulation. The UK media's coverage of the study was accurate.

 

What kind of research was this?

This was a randomised controlled crossover trial in healthy firefighters which assessed the effects of a standard training exercise to put out a fire on cardiovascular health.

In the US, around 45% of firefighter on-duty deaths are due to cardiovascular events such as heart attack. It is believed the risk increases when they are required to put out fires as they experience increased physical exertion, high temperatures, and exposure to air pollution.

The researchers wanted to look at whether they could identify any biological effects of putting out a fire that might cause an increase in risk.

This type of trial is the best way of testing whether a factor or situation – in this case fighting a fire – definitely has an effect. In this case it might have been difficult (and possibly dangerous) to assess the firefighters while putting out a real fire, so they were assessed during a training exercise.

 

What did the research involve?

The study included 19 healthy firefighters. They all took part in a fire simulation exercise and also a set of light, non-emergency activities on two different days.

The researchers took various measurements, such as their heart rate, core body temperature and blood tests during and after these exercises to see how the firefighters' cardiovascular systems responded.

The firefighters were selected at random from the Scottish Fire and Rescue Service to be invited to participate. To join the trial they could not be:

  • smokers
  • on regular medication

or have any of the following:

  • cardiovascular disease
  • irregular heartbeat
  • diabetes
  • high blood pressure
  • asthma
  • kidney or liver conditions
  • infectious illness
  • respiratory tract infection within the four weeks before the study

The firefighters had to attend for each activity after 48 hours off duty to reduce the risk that their recent regular work activities might affect the results. They were also required to not drink any alcohol for 24 hours before each test day and not have food, tobacco, and caffeinated drinks for at least four hours before each test.

The firefighters all took part in both a standard simulated firefighting exercise (exposure) and light duties similar to those undertaken during a shift free of an emergency (control), on different days.

The simulated firefighting exercise was carried out in a special training facility and lasted on average about 20 minutes (median). The firefighters entered the facility as part of a four person team, went up the stairs carrying a water filled hose, finding and putting out a fire on the first floor, and identifying and rescuing a 80kg dummy "casualty".

A number of measurements were taken before, during and after the activities. Blood was taken at four different time points:

  • before exposure or control
  • immediately after exposure or control
  • four hours after
  • 12 hours after

The blood samples were tested for various different markers that indicate level of cardiovascular risk. For example, they tested how prone to clotting the blood was (as blood clots can lead to heart attack or stroke), whether the proteins in the blood indicated that the heart muscle was experiencing damage, and how elastic the blood vessel walls were.

The firefighters were fitted with portable heart (ECG) and blood pressure monitors at least half an hour before each activity and for the following 24 hours. They also swallowed an ingestible temperature monitor the evening before which measured core body temperature before, during and for six hours after each activity.

Sweat loss was determined using body mass before and after each activity and the firefighters were also asked to rank their perceived level of exertion immediately after each activity. 

 

What were the basic results?

The trial featured 19 healthy non-smoking firefighters (16 men and three women) who were 41 years old on average. Only 17 of them completed both activities.

The average core body temperature of the firefighters was 37.4C at the start of the study, increasing to 38.4C at its peak. There was an increase in core body temperature (1.0C) and reduction in weight (by 0.46 kg) among the firefighters following the fire simulation training, due to dehydration. 

When compared to the control non-emergency activity, one to two hours after the fire simulation activity the firefighters' blood samples showed an increased tendency to form clots (was more "sticky") in tests in the laboratory.

Immediately after the fire simulation exercise the firefighters' blood samples also showed increases in other factors such as haemoglobin, volume of red blood cells, platelets (fragments of cells found in the blood that are involved in clotting), and white blood cells, in comparison with the control activity.

Blood flow through the firefighters' forearms increased after the fire simulation exercise, but the blood vessels were less responsive to certain drugs which widen the blood vessels.

A marker protein (called cardiac troponin)which indicates heart muscle injury due to the muscle not receiving enough oxygen showed small increases in the hour following the fire simulation compared with after the control activity. The levels of this protein were still within normal ranges, suggesting that the extent of lack of oxygen in the heart muscle was relatively small.

The firefighters themselves did not experience any symptoms of cardiovascular injury during the study.

 

How did the researchers interpret the results?

The researchers conclude that exposure to extreme heat and physical exertion during firefighting increases tendency for clot formation, impairs blood vessel function, and results in reduction in oxygen in the heart muscle and heart muscle injury in healthy firefighters.

They say: "Our findings provide pathogenic mechanisms to explain the association between fire suppression activity and [heart attacks] in firefighters."

 

Conclusion

This randomised crossover trial aimed to assess whether putting out a fire has an effect on the biological signs of cardiovascular health of firefighters. 

By simulating a fire fighting scenario the researchers found that exposure to these conditions increased tendency of the blood to clot, reduced the stretchiness of the blood vessel walls, and caused a slight increase in a marker of heart muscle damage.

This trial is thought to be the first assessing this link. Whilst a randomised controlled trial is the best way of investigating this link, there are some limitations to consider.

  • The trial included a controlled scenario with much of the risk of removed, in a real life situation the level of exertion and stress may be greater.
  • This was also carried out in healthy firefighters under specific conditions which is not a true reflection of all firefighters attending firefighting activities.
  • Whilst the firefighters had to be off duty for 48 hours to avoid their work in the previous 48 hours affecting results, we do not know if other non-work related exposures may have altered findings.
  • While the study was reported as a randomised crossover trial it wasn't clearly stated that the firefighters undertook the fire simulation exercise and the control activity in random order, which is important for making sure the participants' characteristics on the day were as well balanced as possible.

This is a small study, and whilst the findings do suggest ways in which firefighting might affect cardiovascular risk, further larger studies would be required to confirm the results and also establish any precautions that can be taken to reduce the risk.

Current advice to firefighters is to make sure that they stay well hydrated. Dr Mike Knapton, The British Heart Foundation's associate medical director, said: "It's essential that firefighters are aware of this risk and take simple steps such as taking time to cool down and rehydrate after tackling a blaze. It's also important for them to be aware of the early warning signs of a heart attack so that, if the worst should happen, they can receive medical attention as soon as possible."

While the research involves firefighters, the results do highlight the fact that even people who assume that they are in perfect health can suddenly develop a heart attack.

Read more about the early warning signs and symptoms of a heart attack.

Links To The Headlines

Firefighters have higher heart attack risk 'because of heat'. BBC News, April 3 2017

Firefighters are more likely to suffer a heart attack because they are exposed to extreme HEAT, study finds. Daily Mail, April 3 2017

Fighting fires is bad for the heart: new study finds exposure to heat causes blood clots. The Daily Telegraph, April 3 2017

Links To Science

Hunter Al, Shah ASV, Langrish JP, et al. Fire Simulation and Cardiovascular Health in Firefighters. Circulation. Published online April 3 2017

British babies 'among the world's biggest criers' claim unproven

NHS Choices - Behind the Headlines -

"Babies in Britain, Canada and Italy cry more than elsewhere," The Guardian reports. But the review the newspaper is reporting on only found reliable data from a handful of nations so the accuracy of the claim is unclear.

Researchers looked at previously gathered data on colic patterns. Colic is a common, yet poorly understood condition associated with excessive, frequent crying in babies who appears to be otherwise healthy. The condition is not serious but can be distressing for parents.

Researchers found that colic was most common in the first six weeks of life, and became less common over the next six weeks. It was most common in the UK, Canada and Italy, with Denmark, Germany and Japan having the lowest rates.

Both the researchers and the media speculate why this is the case. The researchers discuss the fact that Danish parents tend to be in closer physical contact with their baby on a daily basis than UK parents. While The Guardian discusses the fact that breastfeeding rates are far higher in Denmark compared to the UK. Both claims are unproven – and the review actually found some data to suggest bottle-fed babies were less likely to cry.

If your baby has colic, it is important to remember that it is not your fault and your baby will get better eventually. There is no single proven method to treat colic, but you could try holding your baby during a crying episode, burping your baby after feeds, gently rocking your baby over your shoulder or bathing your baby in a warm bath. Read more advice about colic.

 

Where did the story come from?

The study was carried out by researchers from the University of Warwick and Kingston University in the UK. The study was published in the peer-reviewed The Journal of Pediatrics.

One of the authors is supported by a PhD scholarship from the Republic of Turkey Ministry of Education, but they report no other sources of funding. The authors declare no conflict of interest.

While the UK media's reporting of the study was generally accurate, the majority of the headlines, such as the Metro's "British newborn babies cry more than in any other country on the planet," provided a distorted view of the research. It suggests researchers gathered data from around the world. In fact, they only found reliable data from nine countries; all of which were developed nations.

 

What kind of research was this?

This was a systematic review and meta-analysis aiming to find out the mean length of fussing and crying and the prevalence of colic in infants from various countries in the first three months of their life.

While this type of review and meta-analysis is good for showing an overall picture of research in a certain area – in this case, prevalence of colic and crying in babies – it is only as good as the studies it includes.

 

What did the research involve?

The authors searched literature databases to identify observational studies (published up to December 2015) that included general population samples of infants aged one to 13 weeks, and measured fussing or crying in 24 hour behaviour diaries and reported average cry duration.

Researchers assessed the studies for quality, looking at specific features such as whether the sample size was adequate, and whether the study accounted for other factors like socioeconomic and household circumstances. In particular they also looked to see whether studies assessed colic according to the modified Wessel criteria. This is a well-validated definition, also known as the "rule of threes", where colic is defined as the baby fussing/crying for more than three hours a day, on at least three days in any one week.

The authors identified 28 relevant diary studies including a total of 8,690 babies from the UK, Canada, the US, Italy, the Netherlands, Germany, Australia, Denmark and Japan.

They grouped the studies according to the age babies were assessed: 1-2 weeks, 3-4 weeks, 5-6 weeks, 8-9 weeks and 10-12 weeks. They looked to see if cry duration changed over the first 12 weeks of life, varied according to country, and varied by feeding type or study quality.

 

What were the basic results?

The average time fussing or crying across studies was:

  • 117 minutes (standard deviation [SD] 67) at 1-2 weeks of age
  • 118 minutes (SD 69) at 3-4 weeks of age
  • 133 minutes (SD 70) at 5-6 weeks of age
  • 68 minutes (SD 46) by 10-12 weeks of age

Crying and fussing durations were higher than average in Canada (150 minutes at 3-4 weeks) and The Netherlands (150 minutes at 5-6 weeks) and lower than average in Germany (69 minutes at 1-2 weeks), Japan (107 minutes at 5-6 weeks) and in Denmark at all ages other than 8-9 weeks.

The prevalence of colic in the first six weeks ranged from 17% to 25% and decreased to 11% by 8-9 weeks and to 0.6% by 10-12 weeks.

Prevalence of colic was high in the UK (28% at 1-2 weeks), in Canada (34% at 3-4 weeks) and in Italy (21% at 8-9 weeks), compared with Denmark (6% at 3-4 weeks) and Germany (7% at 3 to 4 weeks) and Japan (2% at 5 to 6 weeks).

The researchers found some evidence that bottle-fed and mixed feeding babies had lower colic prevalence than breastfed babies at 5-6 weeks. Studies that did not report on feeding type had higher prevalence of crying at the 10-12 mark than studies that did; which further complicates the picture.

 

How did the researchers interpret the results?

The researchers concluded that they "found no evidence for a 'universal' increase of fuss/cry duration over the first 6 weeks of life culminating in a 'crying peak' at 5-6 weeks of age as proposed previously".

However, they did find that fuss/cry durations were high across the first six weeks of life, followed by a "universal" reduction in fuss/cry duration between six and 12 weeks of age.

They further add that "colic or excessive fuss/cry may be more accurately identified by defining fuss/cry above the 90th percentile in the chart provided based on the review."

 

Conclusion

This study suggests the prevalence of colic is highest in the first six weeks of a child's life and then decreases over the next six weeks. Colic seems to be less common in babies in Denmark, Germany and Japan and more common in babies from Canada, the UK and Italy.

This study is valuable in demonstrating the pattern of fussing and crying over the first 12 weeks of a baby's life and how this varies across countries, but there are limitations to the research:

  • There was a varied number of studies from the different countries. For example, there were seven studies from the UK, but only one study from Canada, Germany and Japan. Similarly the included studies varied in the age groups assessed. For example, the UK studies reported colic prevalence data at both 1-2 weeks and 5-6 weeks of age, whereas the Canadian study only looked at 3-4 weeks. Overall this variability in the quantity of data available from the different countries may weaken the strength of the findings.
  • Also, relatively few countries were represented by this review, including no studies from developing countries for comparison. Therefore it cannot be said if the pattern of crying will be consistent across all countries globally.
  • Mothers might interpret fussing/crying differently in different cultures so some might have reported fussing/crying more readily than others. Colic may have been more stringently defined in some studies than others. There may also be differences in how accurately the diaries were kept between studies. All of these things may lead to under- or over-reporting of colic which might affect accuracy of the findings.
  • Studies also varied regarding the different factors taken into account – like household factors, number of children in the house, and method of feeding.

All of these factors could have an influence on colic, and as the studies weren't consistent in their quality and measurements, care should be taken before concluding too firmly from these results.

Colic remains a poorly understood condition and there is no proven method to treat or prevent it.

Caring for a baby with colic can be very difficult for parents, particularly first-time parents. Support groups, such as Cry-sis, offer help and advice if you need it. You can contact the Cry-sis helpline for advice on 0845 122 8669 (9am-10pm, seven days a week). 

Links To The Headlines

Babies in Britain, Canada and Italy cry more than elsewhere – study. The Guardian, April 3 2017

British babies cry the most, Danish babies the least. Why? The Guardian, April 3 2017

Why anxious British parents' babies are among the greatest criers in the world. The Daily Telegraph, April 3 2017

British babies cry more than almost anywhere else in the world. ITV News, April 3 2017

British babies are among the best in the world... at CRYING. Daily Mirror, April 3 2017

British babies cry more than almost anywhere else in the world, study finds. Sky News, April 3 2017

British children are the biggest cry babies in the world: Infants thought to bawl more because their parents are 'quicker to respond'. Daily Mail, April 3 2017

British newborn babies cry more than in any other country on the planet. Metro, April 3 2017

Links To Science

Wolke D, Bilgin A, Samara M. Systematic Review and Meta-Analysis: Fussing and Crying Durations and Prevalence of Colic in Infants. The Journal of Pediatrics. Published online April 3 2017

Morning after pill 'less reliable' for women over 11 stone

NHS Choices - Behind the Headlines -

"Women who take morning-after pill could still fall pregnant if they weigh more than 11 stone," the Daily Mirror warns.

New guidelines on emergency contraception discuss recent evidence that body mass index (BMI) and overall body weight may impact on the effectiveness of oral emergency contraception.

The guideline – produced by the Faculty of Sexual Reproductive Healthcare – covers various recommendations around the type of emergency contraception that should be used in different circumstances. The aspect that has caught the media attention is that there is some uncertainty about the effectiveness of the commonly used morning after pill, Levonelle One in women who are overweight.

 

Who produced the guideline?

The Faculty of Sexual Reproductive Healthcare (FSRH) is a professional organisation of the Royal College of Obstetricians and Gynaecologists. It produces guidelines and training support for healthcare professionals to help them deliver the highest quality of sexual and reproductive healthcare.

The new guideline, Emergency Contraception, gives recommendations based on a systematic review of the available evidence, along with input from experts and the guideline development group.

 

What are the currently available forms of emergency contraception?

There are currently two forms of emergency contraception available – oral hormone tablets and the copper-containing intrauterine device or coil.

There are two hormone tablets. Levonorgestrel (brand name Levonelle One) is a single tablet that should ideally be taken within 12 hours of unprotected intercourse, but is effective up to 72 hours (three days). Levonorgestrel is also available over the counter.

The newer tablet, ulipristal acetate (brand name ellaOne), available on prescription only, can be taken up to five days (120 hours) after unprotected intercourse.

The copper coil is believed to be more effective than the hormone methods and can be inserted into the womb up to five days after unprotected sex. It can also be used as an ongoing method of contraception.

However, if there's a chance the woman could have a sexually transmitted infection (STI) from having unprotected sex there can be a risk from inserting the coil, so antibiotics are usually given.

 

What does the new guideline recommend?

The guideline gives recommendations covering circumstances when emergency contraception may be needed (e.g. unprotected sex or possible failure or incorrect use of contraception) and the professional responsibilities of providers of emergency contraception (e.g. advising on need for ongoing contraception).

They then give data on the effectiveness of the different methods, confirming much of what is already known:

  • the copper coil is the most effective method
  • ellaOne is effective up to 120 hours
  • Levonelle One is effective up to 72 hours (evidence has shown it's ineffective after 96 hours)
  • ellaOne has been shown to be more effective than Levonelle One
  • the two hormone tablets are less likely to be effective if taken after suspected ovulation – in which case the copper coil is the preferred method

 

What do they say about weight or BMI

This is the main focus of the media coverage. The guideline covers two points on this:

  • Women should be informed that the effectiveness of the copper coil is not known to be affected by weight or BMI.
  • Women should be informed that it is possible that higher weight or BMI could reduce the effectiveness of oral emergency contraception, particularly Levonelle One.

If the woman weighs more than 70kg (11 stone) or has a BMI above 26kg/m2 (just above the 25 "threshold" for being overweight) and wants an oral method ellaOne is the recommended method. Ongoing hormonal contraception should then start after five days.

If Levonelle One is taken the new guideline recommends a double dose (3mg) as well as that the woman should start ongoing contraception immediately.

This is based on a systematic review of studies that have suggested that both hormone methods could be less effective in women who are overweight, obese or have higher body weight than those with normal or underweight BMI or lower body weight. Weight is thought to have a greater effect on Levonelle One than on ellaOne, hence the latter is recommended in preference. 

 

Other reasons oral emergency contraception may be ineffective

The FSRH also states that hormone tablets may not work if the woman is taking drugs that induce liver enzymes, such as epilepsy drugs. This warning also applies for the herbal remedy St John's Wort, which some people use to treat depression. In these cases women should use the copper coil in preference, or if not, a double dose of Levonelle One (though its effectiveness is unknown for this specific indication), ellaOne should not be used.

ellaOne can also be ineffective if progestogen-based contraception, such as the mini pill, is taken within five days of taking the tablet, and possibly if it was also taken in the seven days before ellaOne. ellaOne is also unsuitable for women who take steroids for severe asthma, and breastfeeding women should avoid breastfeeding or expressing for a week after taking ellaOne.

 

Conclusion

Overall the FSRH guideline gives additional clarity around the different types of emergency contraception that should be selected in different circumstances.

These recommendations are based on the best level of evidence and expert understanding to date. However, they may change in the future as more evidence comes to light.

In particular, related to the issue of weight on the effectiveness of oral emergency contraception, the European Medicines Agency (EMA) concluded in 2014 that the available evidence "was limited and not robust enough to support with certainty a conclusion that oral emergency contraception is less effective in women with higher body weight or BMI."

Still, as quoted in the Daily Mirror, the conclusion of Dr Asha Kasliwal, FSRH president, would seem a sensible one: "we hope its publication [the guidelines] will further awareness amongst healthcare professionals and women alike that the copper IUD is the most effective form of emergency contraception."

Read more about emergency contraception.

Links To The Headlines

Women who take morning-after pill could still fall pregnant if they weigh more than 11 stone. Daily Mirror, April 1 2017

Morning-after pill could fail if you weigh over 11 stone, new study warns. The Daily Telegraph, March 31 2017

Morning-after pill could FAIL if you weigh 11 stone or more, new guidelines warn. Mail Online, March 31 2017

Morning-after pill may fail the overweight. The Times, April 1 2017 (subscription required)

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