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

Moderate drinking may reduce heart disease risk

NHS Choices - Behind the Headlines -

"A daily pint or glass of wine can slash the chances of a suffering heart attack by a third," reports The Sun.

Researchers found that people who drank alcohol within moderate drinking guidelines were less likely to have a first episode of a range of heart and vascular diseases than those who never drank alcohol.

This four-year study looked at health records of almost 2 million adults without any cardiovascular disease at the start of the study.

It found that non-drinkers were more likely to need treatment for many diseases such as heart attack, heart failure and angina, compared to people who drank alcohol within the previous recommended guidelines, which were 21 units per week for men and 14 units for women.

There was less difference between the groups for circulation diseases such as stroke and bleeding in the brain.

However, heavy drinkers, consuming above guideline limits, were also at higher risk compared with moderate drinkers. Former and occasional drinkers also had increased risk of several outcomes.

Along with other study limitations, like the possible influence of other health and lifestyle factors, we can't be certain that moderate drinking directly decreases risk.

And at the risk of sounding like killjoys, there are far healthier and more effective methods of reducing cardiovascular disease, such as regular exercise. Regular drinking, can increase your risks of a number of cancers.

Alcohol guidelines changed at the start of 2016 to recommend that both men and women should drink no more than 14 units per week. This was to reflect the point that there is no such thing as a "safe amount" of alcohol.

 

Where did the story come from?

The study was carried out by researchers from Cambridge University and University College London and was funded by organisations including the National Institute for Health Research, Wellcome Trust and Medical Research Council.

The study was published in the peer-reviewed British Medical Journal (BMJ) on an open-access basis so it is free to read online.

The study was received with enthusiasm by the UK media. The Sun's exhortation to readers to drink "a pint a day," accompanied by a photograph of a man sinking a beer, was typical of the tone of much of the coverage. However, the headline oversimplifies the study.

The Daily Mirror does a more balanced job, warning readers that "There's a catch" and quoting experts warning of the link between alcohol and cancer.

The Mirror also carries a statement from Dave Roberts, director general of the Alcohol Information Partnership, who claims that "the anti-alcohol campaigners' mantra that there is no safe limit just doesn't stack up".

But as the Alcohol Information Partnership is funded by drinks firms including Diageo, Pernod Ricard, Campari and Bacardi (as the Mirror helpfully points out) there may be a potential conflict of interest.

The media reporting also fails to point out that this study was basing the definition of moderate drinking on the old, pre-2016, recommendations (21 units per week for a man, 14 per week for a woman).

 

What kind of research was this?

This was a cohort study using population-based records. Researchers wanted to see how alcohol consumption at different levels was linked to a wide range of cardiovascular conditions.

Cohort studies can show links between factors, such as alcohol consumption and cardiovascular disease risk. But they can't show that one factor causes another. Confounding factors (such as diet and physical activity) might distort the results.

 

What did the research involve?

Researchers used anonymised electronic patient records from a GP database, which included people's reported alcohol consumption. They included 1,937,360 patients aged 30 or over, and tracked their illnesses, hospital admissions and deaths over an average six years.

They divided people into groups based on their drinking, then (after adjusting for confounding factors) looked to see what their chances were of having had one of 12 cardiovascular conditions, or having died from any cause.

The researchers only looked at people's first record of a cardiovascular disease. So, for example, someone might have had treatment for unstable angina, then later go on to have a heart attack, but only the unstable angina would be recorded.

The researchers used three linked databases, to give them a better chance of including all necessary detail. As well as the GP database they used the Myocardial Ischaemia National Audit Registry Project, hospital episode statistics and the Office of National Statistics.

The researchers divided people into five groups: non-drinkers (who never drank alcohol), former drinkers, occasional drinkers, moderate drinkers (who drank within the then-current guidelines of 21 units per week for men and 14 units for women) and heavy drinkers (who exceeded this).

Potential confounding factors included in the analysis were:

  • age
  • sex
  • socioeconomic deprivation
  • smoking status
  • diabetes
  • blood pressure
  • body mass index (BMI)
  • cholesterol
  • use of antihypertensive or statin medicines
  • whether the patient had received dietary advice

 

What were the basic results?

About 5% of people in the study had a first diagnosis of a cardiovascular disease during the study. As in previous studies, this was more common among non-drinkers, former drinkers, occasional drinkers and heavy drinkers, compared to moderate drinkers.

Compared to moderate drinkers, non-drinkers had a higher risk of a first report of:

  • heart attack (32% higher risk, hazard ratio [HR] 1.32, 95% confidence interval [CI] 1.24 to 1.41)
  • unexpected death from heart disease (56% higher risk, HR 1.56, 95% CI 1.38 to 1.76)
  • heart failure (24% higher risk, HR 1.24, 95% CI 1.11 to 1.38)
  • unstable angina (33% higher risk, HR 1.33, 95% CI 1.21 to 1.45)
  • stable angina (15% higher risk, HR 1.15, 95% CI 1.09 to 1.21)
  • stroke (12% higher risk, HR 1.12, 95% CI 1.01 to 1.24)
  • peripheral artery disease (22% increased risk, HR 1.22, 95% CI 1.13 to 1.32)
  • abdominal aortic aneurysm (32% increased risk, HR 1.32, 95% CI 1.17 to 1.49)
  • death from any cause (24% increased risk, HR 1.20 to 1.28)

There was no significantly increased risk of bleeding in the brain, transient ischaemic attack ("mini-stroke"), or sudden cardiac death.

Heavy drinkers also had an increased risk of death from any cause or from heart disease, of cardiac arrest, heart failure, stroke from blood clot or bleed and peripheral artery disease, with risk increases ranging between 11% and 50%.

Former drinkers and occasional drinks also had increased risk of most outcomes compared with moderate drinkers.

The researchers also noted that all non-drinkers were more likely to belong to the most deprived socioeconomic group, to have diabetes, and to be obese.

The results were similar for women, although there was less difference in risk levels between non-drinkers and moderate drinkers.

 

How did the researchers interpret the results?

The researchers say their study showed that "moderate alcohol consumption is associated with a lower risk of initially presenting with several, but not all, cardiovascular diseases." They go on to say that "heavy drinking is differentially associated with a range of diseases."

While the research found that heavy drinkers were less likely to have a heart attack as a first presentation, the researchers warn that could be because "they die from other causes before they are able to develop a cardiovascular disease."

 

Conclusion

This study paints a more complicated picture than the "Pint a day keeps the doctor away" story proffered by The Sun.

It seems to confirm the findings of other studies, which have shown that non-drinkers tend to have a higher risk of cardiovascular diseases than people who drink moderately.

It suggests that some cardiovascular diseases (mainly those directly affecting the heart) seem to have a stronger link to a possible protective effect from alcohol than other vascular diseases, such as mini-strokes and bleeding in the brain. However, this can't be concluded with certainty due to the study design.

We need to remember that cohort studies like this cannot prove that alcohol consumption or lack of it is a direct cause of cardiovascular disease. Many health and lifestyle factors may be having an influence. For example, non-drinkers were more likely to be from deprived areas, to have diabetes or be obese, factors which the analysis didn't adjust for.

We also have no information about other factors such as diet or exercise, which could also affect the results.

Also, the researchers' decision only to include people's first diagnosis of a cardiovascular disease complicates matters. For example, if a person had a Transient ischaemic attack (TIA) (also known as a "mini-stroke") and then went onto have a full stroke, only the TIA would be recorded. Therefore it is difficult to be certain of a person's overall cardiovascular disease status. We can't be sure that the figures around how much a person's risk of a particular disease outcome is increased by a particular consumption level are accurate.

As a result, we really shouldn't conclude, for example, that people who drink heavily are less likely to have a heart attack than those who don't drink. They may have a stroke first, and then a heart attack, or die of another cause.

The study isn't a green light for people to drink more alcohol, without worrying about it. However, it does suggest that drinking alcohol within the lower-risk drinking guidelines may not raise the risk of cardiovascular disease, and may lower it. Remember that alcohol does contribute to other diseases.

Check whether you're drinking within low-risk levels with our introduction to alcohol units.

Far more effective, safer, and usually cheaper, methods of reducing your heart disease risk include regular exercisehealthy eating and quitting smoking if you smoke.

Links To The Headlines

Reduce your chances of having a heart attack by a THIRD with a daily pint or glass of wine. The Sun, March 23 2017

An alcoholic tipple a day could PREVENT you having a heart attack - but there's a catch. Daily Mirror, March 23 2017

Moderate drinking can lower risk of heart attack, says study. The Guardian, March 23 2017

Cheers! Drinkers who have one glass of wine a night 'are at less risk of heart failure than teetotallers'. Mail Online, March 23 2017

Drinking pint of beer a day linked to reduced risk of heart attack. The Independent, March 23 2017

Moderate drinkers have lower risk of heart attack. The Times, March 23 2017 (subscription required)

Links To Science

Bell S, Daskalopoulou M, Rapsomanki E, et al. Association between clinically recorded alcohol consumption and initial presentation of 12 cardiovascular diseases: population based cohort study using linked health records. BMJ. Published online March 22 2017

Mixing alcohol and energy drinks 'may be a risky cocktail'

NHS Choices - Behind the Headlines -

"Mixing energy drinks with alcohol could be a risky combination, leading to a greater risk of accidents and injuries," BBC News report.

A review of evidence found a number of potential risks, but the picture was not as clear-cut as reported.

Energy drinks are drinks that contain high amounts of caffeine. Some people mix them with spirits such as vodka.

Canadian researchers aimed to look at the published evidence on whether mixing alcohol with energy drinks is linked to an increased risk of harm or injury.

The researchers identified 13 studies – overall, 10 of them reported an increased risk of injury when drinking the mixture compared with alcohol on its own.

One possible factor discussed in the review is that the stimulant effects of caffeine could combine with the inhibition-lowering effects of alcohol, making people more prone to taking risks.

Caffeine could also mask the sedative effects of alcohol, so people become less aware of how much alcohol they've drunk – a phenomenon referred to as being "wide-awake drunk". 

However, the studies included in the review varied considerably in their methods, including the lifestyle factors they took into account, such as alcohol or drug use.

This review can't quantify risks or link them with particular combinations of drink, or specific quantities.

But it does serve as a general reminder that so-called "social drinking" is not without risk, both in terms of how much alcohol is consumed and potentially making yourself vulnerable to harm.

Where did the story come from?

The study was carried out by two researchers from the Centre for Addictions Research at the University of Victoria in British Columbia, Canada.

It was funded by the Canadian Institute of Health Research. No conflicts of interest were reported by the researchers.

The study was published in the peer-reviewed Journal of Studies on Alcohol and Drugs on an open access basis, so it's free to read the study online (PDF, 208kb).

The way the study was reported, while generally accurate, in some cases made the links between risks and drinking alcohol combined with energy drinks appear to be much better established than is actually the case.

And The Sun's headline, "Bingeing on vodka Red Bull or Jagerbombs 'as bad as taking cocaine'," is an opinion, not a proven fact. 

What kind of research was this?

This systematic review aimed to examine the published literature to identify studies that have assessed the link between mixing alcohol with energy drinks and the potential risk of injury. 

The researchers say in 2007-11, 13-16% of emergency department visits in North America involved people who had drunk alcohol combined with energy drinks.

This is said to be the first review to date to look at the association. A systematic review is the best way of compiling the available literature.

However, the findings of reviews are only as good as the pooled studies included.

Studies assessing links between food and drink and health outcomes are usually observational, so they aren't able to prove cause and effect because many other factors could have had an influence.

And if the studies included in a review are very different in terms of methodology, as was the case with this review, it isn't possible to carry out a meta-analysis of the results.

This means any conclusions provided by the review carry less weight of evidence.

What did the research involve?

The reviewers searched two literature databases to identify studies published between 1981 and January 2016.

The studies included must have looked at the link between consuming alcohol mixed with energy drinks and the risk of harm or injury, and compared this with the risk from just drinking alcohol.

Energy drinks and alcohol could be either consumed in a mixed drink or separately, but on the same occasion.

A total of 13 studies met the inclusion criteria – 10 of which came from the US and Canada, and the remainder from New Zealand, Australia and Taiwan.

Eight of the studies included students – high school, college or university. They all date from 2011-15.

All of the studies were cross-sectional, mostly online surveys reviewing reports of drinking injuries.

The timeframe of alcohol or energy drink consumption was questioned ranged from the past month to the past year, while the timeframe for self-reported injuries ranged from the past month to a lifetime.

Eight of the studies asked whether injuries were actually related to drink consumption, while the other five studies just asked about reports of the two, which may not necessarily have been related.

What were the basic results?

The reviewers give an overall narrative summary of the findings.

Ten of the 13 studies reported a link between drinking alcohol and energy drinks and an increased risk of injury, though there were no consistent links with the type of injury.

Three studies didn't find this link – in fact, one study actually found the risk was higher with alcohol on its own. The researchers feel the differences could have been down to the design of the studies.

Three studies reported that when the links between the two are assessed, you need to consider risk-taking tendencies or behaviours, as well as sensation seeking.

When the researchers controlled for these variables, they still found links between alcohol and energy drinks and injury.

Most studies also controlled for general alcohol consumption or binge drinking. Two studies also controlled for drug use and one for caffeine.

Studies also reported more alcohol tended to be consumed during mixed drinking sessions than when drinking alcohol on its own.

How did the researchers interpret the results?

The researchers concluded: "There is significant need for further examination of the role of [alcohol and energy drink] use in the risk of injury.

"A better understanding of the relationship … and of the potential underlying mechanisms is crucial for informing effective preventive intervention strategies."

They go on to say the review could be used to inform the public, health professionals and policy makers of the possible risks.

Conclusion

This systematic review aimed to try to better establish whether drinking alcohol mixed with energy drinks is linked with risk of injury.

Although the majority of studies generally supported a link between consumption and increased risk of injury, as the researchers acknowledge, the high variability in the methods of the individual studies and assessment of harms "makes it difficult to determine the extent of this risk".

Nearly all the studies were online surveys that asked questions about alcohol and energy drink consumption, and self-reported injury.

But the temporal relationship between the two, and whether the drink was actually the direct cause of the reported injury, is very difficult to be sure of, especially if the timeframe of reported injuries could extend to up to a lifetime, while drink consumption was relatively recent.

For example, one of the studies was even questioning reports of injury or disease in the past year as a result of participants' work.

It's also possible confounding lifestyle factors influenced any links seen. The individual studies varied considerably in the different factors they adjusted for, such as socioeconomic factors, drug use, and normal alcohol drinking behaviours.  

The studies are also mostly representative of young student populations, and none were conducted in the UK. A link may be found if college or university students in the UK were surveyed, but we can't know this for sure.

Overall, although this study is of interest and supports a plausible theory, it can't definitively tell us whether drinking alcohol combined with energy drinks will put you at greater risk of injury or harm than if you drink alcohol alone.

But the study does reinforce the fact alcohol can be a common contributing factor to injury.

Read more about the risks associated with social drinking

Links To The Headlines

'Wide awake drunk' on energy drinks and alcohol mix. BBC News, March 21 2017

Mixing alcohol and energy drinks can make nights out more dangerous, researchers warn. The Independent, March 21 2017

Bingeing on vodka Red Bull or Jagerbombs 'as bad as taking cocaine' because it masks tiredness, experts warn. The Sun, March 21 2017

Links To Science

Roemer A, Stockwell T, et al. Alcohol Mixed With Energy Drinks and Risk of Injury: A Systematic Review. Journal of Studies on Alcohol and Drugs. Published online March 21 2017

The pill provides 'lifelong protection against some cancers'

NHS Choices - Behind the Headlines -

"The pill can protect women from cancer for 30 years," is the front page headline in the Daily Mirror.

The paper reports on a landmark study that followed more than 46,000 women in the UK for up to 44 years.

The study found women who'd used the combined oral contraceptive pill – commonly known as "the pill" – were less likely to get bowel (colorectal) cancerwomb (endometrial) cancer and ovarian cancer many years after they'd stopped taking the medicine.

Although women had a higher risk of breast cancer and ovarian cancer while taking the pill, the researchers say this raised risk "appeared to be lost" within about five years of having stopped taking it.

Researchers concluded the overall effect of taking the contraceptive pill was "neutral" when taking into account the balance of higher risks and lower risks. 

But there are a number of uncertainties to consider with this research.

The study began in 1969, only a few years after the pill was first made available in the UK in 1961. Doses of oestrogen and progestogen were higher than many of the pills available now.

And the women in the study used the pill for an average of 3.5 years, which may be different from how women use the pill today.

Because of the type of study, we don't know for certain whether the change in cancer risk is because of the effects of the pill or whether other health or lifestyle factors had an influence.

Still, women who took the pill can be reassured it's unlikely to have had a long-term effect on their cancer risk.

Where did the story come from?

The study was carried out by researchers from the University of Aberdeen, and was funded by the Royal College of General Practitioners, the Medical Research Council, Imperial Cancer Research Fund (now part of Cancer Research UK), the British Heart Foundation, and several pharmaceutical companies that manufacture oral contraceptive pills (Schering, Wyeth Ayerst, Ortho Cilag and Searle). 

It was published in the peer-reviewed American Journal of Obstetrics and Gynaecology.

The study was widely covered in the UK media, and the reporting was broadly accurate.

However, several headlines and stories failed to warn readers this type of study can't prove the pill was the reason for lower rates of certain cancers among women who took it.

For example, weight and alcohol are linked to cancer risk, but weren't measured in the study. We don't know whether women who took the pill were more or less likely to drink alcohol or be overweight.

What kind of research was this?

This long-term prospective cohort study aimed to look at whether the use of the combined oral contraceptive pill has an effect on long-term cancer risks.

One concern related to use of the pill is that as it uses hormones, it could have an effect on the risk of developing certain cancers known to be related to hormones, such as breast and ovarian cancers.

Observational studies like this are good ways to track patterns of risk, especially over the long term.

But they can't prove that one factor (in this case, taking the contraceptive pill) directly causes another (cancer or protection against cancer).

What did the research involve?

The study involved women taking part in the UK Royal College of General Practitioners' Oral Contraception Study in 1968-69.

Researchers followed-up 23,000 women who were using combined oral contraceptive pills at the start of the study, and 23,000 who hadn't used them at that point.

The women's GPs were required to fill in reports every six months on their hormone use, pregnancies, illnesses or deaths. This continued until 1996.

In the 1970s, three-quarters of the women were "flagged" in cancer registries so the study would be notified about any subsequent cancer diagnosis. This information provided the post-1996 data.

The study results have been reported at various times since it began. This paper looks at the longest period of follow-up.

Researchers had already seen a reduction in rates of ovarian, endometrial and colorectal cancers, and wanted to see if these reductions persisted into older age.

They also wanted to see if using the pill during childbearing years could produce new cancer risks in later life, and look at the overall balance of cancer risk among older women who used the pill in the past.

The researchers used the data to calculate the incidence rate of cancers in women who'd ever or never taken the pill.

They presented the results as the difference between the two incident rates (number of cancer cases per 100,000 women per year) and the percentage of cancers that might have been attributable to taking or not taking the pill.

Researchers adjusted their figures to account for the women's age, whether they smoked at the start of the study, whether they had children, and their social class.

What were the basic results?

There was very little difference in the chances of getting cancer overall. There were 542.44 cancers per 100,000 women per year among those who took the pill, and 566.09 among those who didn't take the pill.

This overall difference is small enough to be down to chance – in other words, it's not statistically significant.

Overall:

  • ovarian cancer risk was 22.1 per 100,000 women per year for pill users and 33.27 for non-pill users – women who took the pill were 33% less likely to get ovarian cancer (the difference between the incident rate for the two groups in the study [incident rate ratio, or IRR] 0.67, 99% confidence interval [CI] 0.5 to 0.89) 
  • cancer of the womb lining (endometrial cancer) risk was 19.42 per 100,000 women per year for pill users and 29.56 for non-pill users – women who took the pill were 34% less likely to get ovarian cancer (IRR 0.66, 99% CI 0.48 to 0.89)
  • bowel (colorectal) cancer risk was 47.85 per 100,000 per year for pill users and 59.16 for non-pill users – women who took the pill were 19% less likely to get colorectal cancer (IRR 0.81, 99% CI 0.66 to 0.99)

Women who took the pill were 48% more likely to get breast cancer while they were taking it and for five years afterwards, but the difference in risk disappeared five years after stopping treatment.

The researchers concluded there was no overall increase in risk when the whole period of the study was considered.

How did the researchers interpret the results?

The researchers said: "Our results suggest that users of oral contraceptives are protected from colorectal, endometrial and ovarian cancer for many years after stopping, perhaps for more than 35 years for colorectal and ovarian cancer.

"Most women who choose to use oral contraceptives do not expose themselves to long-term cancer harms." 

Conclusion

The research is in line with other studies that have reported on cancer risk and the pill.

This study had the advantage of being both very large and having the longest follow-up period of any study of the effects of the pill on cancer.

But we shouldn't lose sight of this study's limitations.

It's not possible to say that taking the pill prevented women from getting certain cancers. It may be the case, but other confounding factors could be involved.

The researchers took account of some basic factors that affect cancer risk, but not others like diet, physical exercise, weight and alcohol use.

Many of the women in the study were lost to follow-up, mainly because they moved away or otherwise lost touch with their GP before they could be flagged for the cancer registries. But it's unlikely that this would affect pill users or non-pill users differently.

Hormonal contraception – and women's use of it – has changed a lot since the study began in 1968.

The composition and dose of hormones used in the combined oral contraceptive pill has changed considerably since they were first introduced.

This means we can't be sure the effects of the contraceptive pills of almost 50 years ago would be the same as those of today's pills.

This study didn't assess other types of combined contraception, such as the contraceptive patch, and didn't look at progestogen-only contraceptives, such as the "mini-pill", implants, injections and intrauterine systems. This means the results can't be applied to "hormonal contraception" in general.

These uncertainties aside, this study provides reassuring news for older women, who may wonder whether the oral contraception they used in their younger years has increased the risk of getting cancer.

There's no evidence from this study of an increase in cancer risk – and the reverse may be true for certain types of cancer.

If you're looking for alternatives to hormonal contraception, condoms are 98% effective when used correctly.

Read more about contraception.

Links To The Headlines

The Pill can protect women from cancer for 30 years as breakthrough research gives new hope. Daily Mirror, March 22 2017

Contraceptive pill can slash the risk of ovarian, womb and bowel cancer for up to 35 YEARS after a woman stops taking it. Daily Mail, March 22 2017

Contraceptive pill protects women against cancer for 35 years, major study suggests. The Daily Telegraph, March 22 2017

Contraceptive pill 'can protect against some cancer types for 30 years'. The Independent, March 22 2017

Using the pill can protect women from certain cancers 'for up to 30 years'. The Guardian, March 22 2017

Women who take the contraceptive pill are 'a third less likely' to develop these cancers. The Sun, March 22 2017

Oral contraceptive pill can protect against cancers for 30 years. The Times, March 22 2017 (subscription required)

Links To Science

Iversen L, Sivasubramaniam S, Lee AJ, et al. Lifetime cancer risk and combined oral contraceptives: the Royal College of General Practitioners' Oral Contraception Study. American Journal of Obstetrics and Gynecology. Published online February 8 2017

Overweight young men 'more likely to get severe liver disease'

NHS Choices - Behind the Headlines -

"Men who are overweight in their late teens have a higher risk of developing liver cancer in later life, new research suggests," reports ITV News. Swedish researchers also found a link to other serious types of liver disease.

The researchers assessed the link between body mass index (BMI) and risk of liver disease in later life in 17-19-year-old Swedish men conscripted into national service, which was compulsory in Sweden until 2010.

More than one million teenage boys were included in the study. Researchers found a higher BMI in late adolescence was associated with an increased risk of severe liver disease, including liver cancer, in later life.

Being diagnosed with type 2 diabetes during follow-up also increased the risk of liver disease, irrespective of weight. 

But the main limitation of this study is it isn't able to prove BMI is responsible for the increased risk. Various unmeasured factors could also be having an influence.

Nevertheless, the relationship is in line with current thinking around the risks of excess fat. Fat cells can directly damage the liver in the same way as alcohol (non-alcoholic fatty liver disease).

Obesity can also raise the risk of secondary conditions that can impair the liver, such as diabetes and high blood pressure.

Women shouldn't assume that a similar risk doesn't apply to them. This study only focused on men simply because the Swedish national service system made data on men more easily available for study.

Maintaining a healthy weight will help reduce the risk of a wide range of long-term, often serious, conditions.

Where did the story come from?

The study was carried out by researchers from the Karolinska Institutet and Lund University, both in Sweden.

Funding was provided by grants from the Royal Swedish Academy of Sciences. There were no conflicts of interest declared by the authors.

The study was published in the peer-reviewed journal Gut on an open access basis, so it's free to read online or download as a PDF.

ITV News' reporting of the study was accurate.

What kind of research was this?

This population-based cohort study aimed to assess whether a high BMI is associated with an increased risk of severe liver disease and liver cancer.

Liver disease is a common illness and cause of death around the world. In the past, many cases of liver disease were related to alcohol misuse or viral infection from hepatitis B or C.

Now, in the developed world, obesity is an increasing underlying cause of severe liver disease and liver cancer.

Previous studies haven't specifically assessed how the risk may differ across BMI categories, and whether there could be an association with type 2 diabetes.

This study design is not able to prove cause and effect – it can only find possible links for further investigation.

What did the research involve?

The researchers used data of 1,220,261 Swedish men who did their military national service between 1969 and 1996, when they were aged 17-19 years.

Baseline data was collected on the following possible confounding factors:

  • BMI
  • blood pressure
  • cognitive ability
  • cardiovascular fitness 
  • muscular strength
  • parental socioeconomic status
  • parental and own education 

Men were followed up using the personal identification number (PIN) given to all Swedish citizens after birth.

This PIN was used to link the men to three national population-based registers:

  • National Patient Register of Hospital Discharges
  • Cause of Death Register
  • Swedish Cancer Register

Severe liver disease included diagnoses of:

  • liver cirrhosis
  • liver cancer
  • decompensated liver disease – when people develop signs and symptoms their liver isn't working
  • liver failure
  • cancer of the bile ducts and gallbladder
  • high blood pressure in the portal vein, which drains blood from the digestive tract into the liver
  • liver transplant
  • paracentesis – a procedure to drain fluid from the abdomen

The researchers also looked at whether the association between BMI and severe liver disease was different in those diagnosed with type 2 diabetes during the study period.

What were the basic results?

Men were followed up for an average period of 28.5 years, during which there were 5,281 cases of severe liver disease and 251 cases of liver cancer.

Severe liver disease

All men with a BMI over 22.5 had a significant increased risk of severe liver disease compared with men with a BMI of 18.5-22.5:

  • overweight men (BMI 25-30) – 49% increased risk (hazard ratio [HR] 1.49, 95% confidence interval [CI] 1.35 to 1.64)
  • obese men – (BMI: ≥30) more than double (217%) increased risk (HR 2.17, 95% CI 1.82 to 2.59)
  • healthy weight men (BMI 22.5-24.9) – 17% increased risk (HR 1.17, 95% CI 1.09 to 1.26)

The result for healthy weight men is somewhat surprising. A BMI of between 22.5 and 24.9, even though it's at the top end of the healthy weight range (18-24.9), wasn't previously considered to be a significant risk factor for liver disease.

Risk of severe liver disease on diabetes diagnosis

Type 2 diabetes was diagnosed in 16,451 men during the follow-up period.

Compared with men with type 2 diabetes and a BMI of 18.5 to 22.5, there was an increase in risk of severe liver disease in all BMI categories:

  • underweight men (BMI less than 18.5) – more than four times (429%) the risk (HR 4.29, 95% CI 3.17 to 5.81)
  • normal weight men (BMI 22.5-24.9) – more than triple (350%) increased risk (HR 3.50, 95% CI 2.85 to 4.30)
  • overweight men – more than triple increased (325%) risk (HR 3.25, 95% CI 2.59 to 14.08)
  • obese men – more than triple (328%) increased risk (HR 3.28, 95% CI 2.27 to 4.74)
Liver carcinoma

An increased risk of liver cancer was associated with a higher BMI, but this was only for overweight and obese men. 

  • overweight men (BMI 25-30) – 57% increased risk (HR 1.57 95% CI 1.01 to 2.45)
  • obese men (BMI greater than 30) – more than triple (359%) increased risk (HR 3.59, 95% CI 1.85 to 6.99)
How did the researchers interpret the results?

The researchers concluded that, "A high BMI in late adolescent men was associated with an increased risk of future severe liver disease, including liver cancer.

"Development of T2DM [type 2 diabetes] during follow-up was associated with a further increased risk of severe liver disease, independent of baseline BMI."

Conclusion

This cohort study aimed to assess whether a high BMI in late adolescence is associated with an increased risk of severe liver disease and liver cancer in later life.

The researchers generally found a higher BMI was associated with an increased risk of severe liver disease, including liver cancer.

A diagnosis of type 2 diabetes during follow-up was associated with a further increased risk of severe liver disease, regardless of BMI at the start of the study.

This study included a very large population, and has used reliable sources of data for medical diagnoses and cause of death.

But there are limitations to address:

  • A study like this isn't able to prove higher BMI in late adolescence is the cause of severe liver disease – it can only suggest this as a possible explanation.
  • The researchers adjusted their analyses for various health and lifestyle factors measured at baseline. But these things – such as cardiovascular fitness – may not have remained consistent during life. There are also a number of possible contributing factors, such as alcohol consumption, smoking and diet, which weren't considered that could have had an influence.
  • BMI was only measured at the start of the study. It's highly likely this varied during the course of the follow-up period.
  • The links also aren't entirely linear – that is, there's not a consistent pattern of increasing risk with increasing BMI across the results. This means the relationship isn't completely clear, and further raises the possibility other factors are having an influence.
  • This study involved a specific population sample of Swedish men conscripted to national service. We don't know the outcomes for the exempt population (such as men with an illness or disability), women, or populations from other countries and cultures. That said, from what we know about the link between obesity and liver disease, it would be surprising if women weren't subject to the same risks as men.

Being overweight or obese is a known risk factor for a number of health conditions. While this study isn't able to prove this is responsible for an increased risk of severe liver disease, the results are in line with previous research.

Maintaining a healthy weight will help reduce your risk of a number of serious conditions, including type 2 diabeteshigh blood pressure, and several types of cancer.  

Links To The Headlines

Overweight male teenagers 'more likely to develop liver cancer'. ITV News, March 21 2017

Fat chance of being healthy! Men who are overweight as teens have a 50 per cent higher risk of developing liver cancer in later life. Mail Online, March 21 2017

Links To Science

Hagström H, Tynelius P, Rasmussen F. High BMI in late adolescence predicts future severe liver disease and hepatocellular carcinoma: a national, population-based cohort study in 1.2 million men. Gut. Published online March 20 2017

New drug shows promise in preventing heart attacks

NHS Choices - Behind the Headlines -

"The cholesterol drug that outperforms statins: Patients on the medication are '27% less likely to suffer a heart attack'," the Daily Mail reports.

The drug, evolocumab, makes the liver more effective at removing "bad" cholesterol from the blood.

But the Mail's headline is somewhat misleading, as evolocumab was given along with statins and not as a replacement for them.

The paper reports on a large trial of more than 27,000 participants at high risk of cardiovascular disease, some of whom had a previous history of events like a heart attack, who were already taking statins to reduce their cholesterol.

Participants across 49 countries were given either injections of evolocumab or an identical dummy injection (placebo) alongside their current statin.

They were followed up for two years. Researchers found evolocumab reduced the risk of cardiovascular death, heart attack or stroke by 20% compared with those taking placebo. There were no serious side effects.

There were signs of a greater benefit over time, so longer follow-up would be useful to provide stronger evidence of an effect, and to also check there are no harms associated with taking the drug over a long period of time.

Overall, however, this research gives hope that this new drug has the potential to reduce cardiovascular events in people who have had an inadequate response to statins.

Current UK guidelines say evolocumab treatment should only be funded by the NHS if a person is at high risk of cardiovascular disease and has persistently high blood cholesterol levels.

Other ways of reducing your cholesterol include eating a healthy, balanced diet low in saturated fats.

Where did the story come from?

The study was carried out by researchers from multiple institutions across the globe, including Harvard Medical School, Brigham and Women's Hospital, and Amgen in the US, the University of Sydney in Australia, Imperial College London in the UK, and the University of Oslo in Norway.

It was funded by Amgen, a pharmaceutical company, who also had a role in the design of the trial. Many of the study's authors are working for Amgen or have worked for them in the past.

The study was published in the peer-reviewed New England Journal of Medicine and is open access, so it's freely available to read online.

The media reporting of this story was generally accurate, although the Mail's comparison of evolocumab with statins is unhelpful.

What kind of research was this?

This randomised controlled trial (RCT) was conducted across 49 countries. Researchers aimed to look at the effectiveness of evolocumab on cardiovascular outcomes compared with placebo in people already taking statins.

Evolocumab is a drug given by injection that lowers low-density lipoprotein (LDL) "bad" cholesterol levels by inhibiting an enzyme called PCSK9.

This enzyme hinders the liver's ability to remove LDL cholesterol from the body – stopping it working increases the liver's effectiveness.

The drug has already been found to reduce LDL cholesterol levels by around 60%. It's currently licensed for use in people with high cholesterol who are either intolerant of statins or haven't achieved sufficient reduction in LDL cholesterol with statins alone.

As it's a relatively new drug, its use and potential adverse effects are still being monitored. To date, it's not yet been established whether the drug prevents cardiovascular outcomes.

An RCT is the best way of testing how effective a drug is, as it reduces the chance of other factors being responsible for any differences seen in the results.

This trial also had the benefit of being double-blinded, meaning that neither patient nor doctor knew whether the person was being given evolocumab or a placebo.

A double-blinded RCT is seen as the gold standard in evaluating a treatment or intervention.

What did the research involve?

The trial included 27,564 participants from 49 countries aged between 40 and 85. Half were randomised to evolocumab, and the other half to placebo.

Evolocumab injections were given either 140mg every two weeks or 420mg every month depending on which the participant preferred. Control participants received matching placebo injections.

All participants had evidence of cardiovascular disease with previous heart attack, a stroke caused by a blood clot, or symptomatic artery disease, along with other risk factors for cardiovascular events.

They were all on some form of lipid-lowering therapy. More than two-thirds were taking a high-dose statin, but those taking a lower dose (for example, at least a daily 20mg dose of atorvastatin) or alternative cholesterol treatment were also included.

Participants all had a fasting LDL cholesterol level of 70mg per decilitre or higher, or otherwise non-high-density lipoprotein (HDL) cholesterol level of 100mg per decilitre or higher, at the start of the study.

The researchers followed participants for an average of 26 months. The main outcome of interest was any major cardiovascular events, which included cardiovascular death, heart attack, stroke, hospitalisation for unstable angina, or coronary revascularisation procedures.

The other outcome of interest was the overall number of cardiovascular deaths, heart attacks or strokes, but not including unstable angina and revascularisation.

What were the basic results?

Evolocumab reduced the risk of the main combined outcomes of cardiovascular death, heart attack, stroke, hospitalisation for unstable angina or coronary revascularisation by 15% (hazard ratio [HR] 0.85, 95% confidence interval [CI] 0.79 to 0.92).

To put this in absolute terms, 9.8% of the evolocumab group experienced any of these outcomes compared with 11.3% of the placebo group.

Evolocumab was more effective over time. Compared with placebo, people receiving evolocumab had 16% (95% CI 4 to 26) reduced risk in the first year, increasing to 25% (95% CI 15 to 34) beyond 12 months.

Evolocumab also reduced the risk of the secondary end point (heart attacks) by 20% (HR 0.8, 95% CI 0.73 to 0.88) just looking at cardiovascular death, heart attack or stroke alone.

In actual numbers, 5.9% of the evolocumab group experienced any of these three outcomes, compared with 7.4% of the placebo group.

Similarly, the extent of risk reduction for this outcome increased over time from 12% (95% CI 3 to 20) in the first year to 19% (95%CI 11 to 27) beyond 12 months.

The only adverse events associated with evolocumab were injection site reactions, but these were rare (2.1% of the intervention group versus 1.6% receiving placebo).

How did the researchers interpret the results?

The researchers concluded that, "In our trial, inhibition of PCSK9 with evolocumab on a background of statin therapy lowered LDL cholesterol levels … and reduced the risk of cardiovascular events.

"These findings show that patients with cardiovascular disease benefit from lowering of LDL cholesterol levels below current targets." 

Conclusion

This is a high-quality, well-conducted randomised controlled trial conducted in a very large number of people across multiple countries.

To date, it's remained uncertain whether evolocumab reduces the risk of cardiovascular events.

This study provides good evidence that the drug reduces the risk of major cardiovascular events in people with high LDL cholesterol levels, and with a high risk of having a cardiovascular event, who are already taking statins.

The follow-up is limited to around two years, during which roughly 1 in 10 people experienced a cardiovascular event.

The reduction in risk was shown to increase over time. Longer follow-up time could allow for further events and so give stronger evidence of whether there's a clear effect.

Other long-term effects of having evolocumab injections still need to be established – this means ongoing follow-up and monitoring is still needed.

The added burden of having regular injections as well as taking statins is another consideration.

Nevertheless, this study provides hope that evolocumab can further lower cholesterol, and reduce the risk of adverse cardiovascular events, in high-risk patients who have had an inadequate response to statins.

Current UK guidelines published by the National Institute for Health and Care Excellence (NICE) recommend that evolocumab treatment should only be funded by the NHS for people with a high risk of cardiovascular disease who also have persistently high cholesterol levels.

You can also reduce your cholesterol levels by eating a healthy, balanced diet low in saturated fats, and by taking regular exercise.  

Links To The Headlines

The cholesterol drug that outperforms statins: Patients on the medication are '27% less likely to suffer a heart attack', landmark trial shows. Daily Mail, March 17 2017

New drug cuts 'bad' cholesterol by 60% on average, reducing heart attack risk. The Guardian, March 18 2017

'Huge advance' in fighting world's biggest killer. BBC News, March 17 2017

Radical gene silencer drug could cut cholesterol by half. Daily Telegraph, March 17 2017

Links To Science

Sabatine MC, Giugliano RP, Keech AC, et al. Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease. New England Journal of Medicine. Published online March 17 2017

Grandparents 'may be first to spot autism in a child'

NHS Choices - Behind the Headlines -

"Grandmas are usually the first to spot autism in children," the Mail Online reports.

The headline was prompted by a US online survey of parents and family members of children with autism spectrum disorder (ASD).

Researchers wanted to explore the factors linked to early or late diagnosis. They found several factors were linked, one of which was time spent with grandparents, particularly grandmothers.

More than half of parents who said another person recognised the diagnosis said this was a grandparent, and a quarter said it was the maternal grandmother.

The likelihood that grandmothers recognised a problem increased with the amount of contact they had with the child.

The findings are arguably not that surprising. People who have frequent close contact with a child often recognise things others may not – and it just happens that these close family members are often grandparents, particularly grandmothers. 

The researchers offer a number of speculations about why this effect occurs, such as grandparents having more experience in child raising, or possibly having a more objective, less emotionally engaged, viewpoint.

The findings are interesting, but need to be followed up in further studies. This was also a US sample and the findings may not be replicated in other surveys.

If you have concerns about your child's development or interactions with others, it's important to raise this with health professionals so your child can get the support they need.

Read more advice on how to request a diagnosis if you're concerned about ASD.

Where did the story come from?

The study was carried out by researchers from Columbia University, Carnegie Mellon University, and the Ichan School of Medicine at Mount Sinai, all in the US, and was supported by grants from the Organization for Autism Research and the Seaver Foundation.

It was published in the peer-reviewed journal Autism.

The Mail Online story generally reflects the findings of this study accurately, but without discussing the logical reasons why these survey findings may have come about.

What kind of research was this?

This was a cross-sectional survey of parents of children with ASD, which also included follow-up surveys of friends and family mentioned by the parents.

The aim was to explore the effect family structure can have on diagnoses of autism, and investigate the factors that may be involved in early or late diagnosis.

Autism spectrum disorders (ASD) are lifelong developmental conditions characterised by problems with social interaction and communication, often with a preference for rigid set routines and patterns.

Children with autism usually have a lower than normal IQ, though children with Asperger's can often have heightened intellect in particular areas.

As the researchers say, ideally children would be diagnosed before the age of two, but diagnosis is often delayed until around school entry.

Earlier diagnosis means children get the support they need as they begin learning and interacting with others, a "crunch time" in terms of development.

What did the researchers do?

The first survey included 477 parents of children diagnosed with ASD. In most cases (86%), the survey was completed by the mother.

A second survey included 196 friends and family whose contact details were provided by the parent.

Researchers found 80% of the children with ASD were male and average age at diagnosis was 33 months.

The researchers don't provide details of the questions asked in the survey. They say they carried out analyses to look at the effects of different variables on the age of diagnosis.

What did they find?

The factors associated with diagnosis were as follows:

Siblings

The researchers first examined the effect of siblings. Overall, they found only children were diagnosed on average six to eight months earlier than those with siblings.

This was reported to be consistent with the theory that new parents pay more attention to their only child and are especially cautious or risk averse.

Other family members

A quarter of parents reported that others who have close contact with their child thought the child may have a serious condition before they were aware themselves. The two most common people identifying this were maternal grandmothers (27%) and teachers (24%).

However, 59% of parents who said someone else had voiced concerns reported it was a grandparent (maternal or paternal).

The likelihood of the grandparent raising concerns was linked with their frequency of contact. Frequent interactions with grandparents, especially the grandmother, were found to lead to diagnosis about five months earlier.

Friends and family survey

More than half of respondents to this survey were either grandparents or aunts or uncles, and 58% saw the child at least weekly.

Just under half of all respondents (48%) reported that they suspected a condition before they were aware that the parents had any concerns themselves. Of those who did suspect a problem early on, only half told the parents of this, with about a quarter "hinting".  

What did the researchers conclude?

The researchers said that, "While this pilot study requires replication, the results identify potential causes for accelerated or delayed diagnosis, which if better understood, could ultimately improve age of diagnosis and treatment, and hence outcomes." 

Conclusions

These cross-sectional parent and family surveys explore the factors that may be associated with the timing of diagnosis of autism spectrum disorders.

It's important to put these findings into the right context. The surveys found grandparents, particularly maternal grandmothers, were often the first to recognise the signs of ASD.

But this doesn't necessarily mean grandmothers have some sort of "superpower" for recognising developmental conditions.

The fact that in a quarter of cases close family members suspected a problem before the parents themselves may reveal that people slightly removed from a family's day-to-day life may notice things people who spend constant time with a child may not.

But this study doesn't prove cause and effect – that is, though it found grandparents often recognised the diagnosis, or were linked with slightly earlier diagnosis, it didn't explore the process by which each child was diagnosed.

And it hasn't proved that the grandparent was actually instrumental in leading to the confirmed diagnosis.

Other limitations of this study include the fact the methods the researchers used aren't completely clear.

They don't say how they identified their study sample, or give details of the surveys the parents and family members were given.

This also appears to be a US sample, though location is unclear, so the findings may not be representative of people in the UK. 

Overall, the intricacies of people's feelings, and how and why they recognise things, are quite difficult to pull apart. This pilot study doesn't provide the whole answer.

If you have concerns about your child's (or grandchild's) development or interactions with others, it's important to raise this with health professionals so the child can get the support they need as soon as possible.

Read more about the early signs and symptoms of autism.

Links To The Headlines

Grandmothers are usually the first to spot autism in children – before parents realize something is wrong. Mail Online, March 16 2017

Links To Science

Sicherman N, Lowenstein G, Tavassoli T, Buxbaum JD. Grandma knows best: Family structure and age of diagnosis of autism spectrum disorder. Autism. Published online February 8 2017

Can yoga and breathing really help 'cure' depression?

NHS Choices - Behind the Headlines -

"Taking yoga classes can help ease depressive symptoms, a new study says," reports the Mail Online.

A small study from the US found yoga was associated with a clinically significant improvement in depression symptoms.

Researchers recruited 32 people with moderate to severe depression. They were allocated to either a low- or high-dose group for yoga. The high-dose group spent more time in classes and doing yoga and other exercises at home.

Average depression scores fell over the course of the 12-week study, with no differences seen between the two groups.

But the Mail failed to mention there was no comparison group, so it's hard to assess the specific effect yoga had.

It could be the case that simply taking part in a regular group activity was beneficial. And, in some cases, symptoms may have improved anyway.

This study doesn't add much to the evidence. The researchers say they plan another study with a walking group for comparison, which might help us see whether yoga is an effective therapy for depression.

The researchers say they don't intend for yoga to be a substitute for the treatment of depression by trained healthcare professionals.

See your GP if you think you may have depression. Exercise for depression can be useful, but you may also benefit from other treatments.

Where did the story come from?

The study was carried out by researchers from Boston University School of Medicine, Harvard School of Medicine, Boston Medical Centre, McLean Hospital, Memorial Veterans Hospital, New York Medical College, Massachusetts General Hospital, and Columbia University, all in the US.

It was funded by grants from Boston University.

The study was published in the peer-reviewed Journal of Alternative and Complementary Medicine and is free to read online (PDF, 376kb).

The Mail Online story reports the facts of the study accurately, but inflates their importance, stating that the study "proves" yoga can "cure" depression, and saying the practice "could even be a replacement for antidepressant drugs".

But the researchers don't make such a claim themselves, and the story fails to point out that the lack of a comparison group means we can't assume the reduction in depression was caused by yoga.

What kind of research was this?

This was a randomised dosing trial. This design is different from a traditional randomised controlled trial (RCT) as the intervention was the same in both groups but, as the name suggests, the dosage was different. 

Usually, randomised studies include a control group, where people in that group don't get the intervention, so researchers are able to judge how successful the intervention was.

However, in this study, the investigators looked at two groups who did different amounts of yoga. That means we can't tell whether the improvements in their mental health were because of yoga or another reason.

What did the research involve?

Researchers screened 265 people with depression for the study, and eventually recruited 32 to take part in classes.

Half were randomly assigned to attend three 90-minute classes each week, with four 30-minute sessions at home. The other half were asked to attend two 90-minute classes, with three 30-minute sessions at home.

Everyone had their depression scores measured at the start, then after four weeks, eight weeks and 12 weeks. The researchers looked at average reductions in depression scores for the two groups.

Depression scores were measured by the Beck Depression Inventory, a self-completed 21-item questionnaire that scores depression symptoms as minimal (0-13), mild (14-19), moderate (20-28) or severe (29-63).

Researchers looked at whether changes in average depression scores differed between the two groups. They also considered whether the number of people with minimal symptom scores was different by the end of the study.

What were the basic results?

Both groups saw big drops in their average depression scores from the start to the end of the study:

  • in the high-dose group, the average score fell from 24.6 to 6, a drop of 18.6 points (95% confidence interval [CI] 22.3 to 14.9)
  • in the low-dose group, the average score fell from 27.7 to 10, a drop of 17.7 (95% CI 22.8 to 12.5)

This is the equivalent of a change from moderate depression to minimal depression symptoms. There was no difference between the groups in terms of how many people had only minimal symptoms at the end of the study.

One person dropped out of the study from each group. Nobody reported severe adverse effects from taking part in the classes, although 13 people reported muscle soreness.

How did the researchers interpret the results?

The researchers say their study "provides evidence that participation in an intervention composed of Iyengar yoga and coherent breathing is associated with a significant reduction in depressive symptoms for individuals with major depressive disorder."

They note that people taking three classes a week said it "entailed a demanding time commitment" and concluded that, "Although the thrice-weekly classes (plus home practice) had significantly more subjects with BDI-II scores ≤10 at week 12, the twice-weekly classes (plus home practice) may constitute a less burdensome but still effective way to gain the mood benefits from the intervention." 

Conclusion

Many people report finding yoga and breathing exercises to be relaxing and helpful for their mental health. This study provides some evidence the practice might help people with symptoms of depression.

But flaws in the study mean we can't be sure this is the case. The lack of a control group is the big problem.

For some people, depression simply gets better over time. For others, taking part in a class, being able to talk about their mental health, or getting out and doing some gentle physical exercise may improve their symptoms.

We don't know whether yoga specifically made a difference because the study doesn't tell us this.

Other problems include the study's relatively small size. Also, the cut-off point of 10 on the depression score seems to have been randomly chosen, rather than being of any clinical significance.

The large number of people who dropped out of the study or lost touch with organisers before the study began (approximately 63) also points to the practical difficulty with the intervention.

Attending two or three yoga classes a week, plus three or four home practice sessions, may be difficult for many people with moderate to severe depression to fit into their lives.

And some people may have felt they were unable to cope with the experience of interacting with others in a group activity.  

But it's encouraging that most people in the study saw big improvements in their mental health over the 12-week period.

There are many treatments for depression, including antidepressant medicines and talking therapies, as well as relaxation therapies like yoga. An important first step is to talk to your GP.

Read more about treatments for depression.

Links To The Headlines

Why yoga beats depression: Harvard and Columbia study 'prove' how the relaxing workout eases symptoms. Mail Online, March 15 2017

Links To Science

Streeter CC, Gerbarg PL, Whitfield TH, et al. Treatment of Major Depressive Disorder with Iyengar Yoga and Coherent Breathing: A Randomized Controlled Dosing Study. Journal of Alternative and Complementary Medicine. Published online February 16 2017

Ibuprofen claimed to raise cardiac arrest risk by a third

NHS Choices - Behind the Headlines -

"Taking common painkillers like ibuprofen 'increases your risk of cardiac arrest by a THIRD'," The Sun reports.

Researchers found a link between the potentially fatal heart problem and ibuprofen use, as well as another type of non-steroidal anti-inflammatory drug (NSAID) called diclofenac. A cardiac arrest is a serious emergency where the heart stops pumping blood around the body.

The Danish study looked at 29,000 people who experienced a cardiac arrest, and then at whether these people had taken NSAIDs.

The researchers found the risk of a cardiac arrest was increased by a third for those who took ibuprofen in the 30 days leading up to cardiac arrest.

The risk was doubled for those taking diclofenac, which is only available on prescription in the UK. There was no evidence of an increased risk for other NSAIDs.

But the underlying biological reasons for this link weren't discussed in the study, so it's not clear what might cause this increased risk of cardiac arrest.

It's also possible some people were taking NSAIDs because they had symptoms of a pre-existing (possibly undiagnosed) condition that could increase the risk of cardiac arrest, such as heart disease.

An alternative painkiller to try is paracetamol, or you could try physiotherapy for things like joint and muscle pain. Get advice from your pharmacist or GP on the most suitable treatment for your symptoms.

Where did the story come from?

The study was carried out by researchers from institutions in Denmark, including Copenhagen University Hospital, Aalborg University and the University of Southern Denmark.

It was funded by the European Regional Development Fund, the Novo Nordisk Foundation, and TrygFonden, a foundation that promotes public health. The authors declared no conflict of interest.

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

Generally, the media coverage of the study was accurate, although The Sun inaccurately claimed that, "Ibuprofen – the most common NSAID – increased that risk by a staggering 50 per cent".

This isn't actually the case – ibuprofen accounted for 51% of total NSAID use, but was found to increase risk by 31%, not 50%.

What kind of research was this?

This observational case-time-control study looked at data from the Danish nationwide registries to find out if there's a link between using NSAIDs and an increased risk of having a cardiac arrest outside of hospital.

A cardiac arrest is when the heart suddenly stops pumping blood around the body. The person will usually fall unconscious and stop breathing. It's not the same as a heart attack, although a heart attack can lead to cardiac arrest.

A case-time-control study is good because the same individual is both the case and the control in two different periods of time. This means confounding variables like pre-existing illnesses remain the same when comparing the two groups.

What did the research involve?

This study involved a case-time-control design, including all people aged 10 and above who had a cardiac arrest outside hospital where efforts were made to resuscitate them between 2001 and 2010, as identified by the Danish Cardiac Arrest Registry.

The case-time-control design meant each person was both the case and the control in different time periods. Their exposure to NSAIDs was assessed in both the case and control periods.

They were in the case period in the 30 days before their cardiac arrest and the control period was a preceding 30-day period, when they didn't experience a cardiac arrest event. There was a 30-day "wash out period" in between the control and the case times.

NSAID exposure was assessed by looking at prescribing patterns for the most commonly used NSAIDs in Denmark. These were diclofenac, naproxen and ibuprofen, as well as two COX-2 selective inhibitors, rofecoxib and celecoxib.

The researchers only included people in the analysis who requested a prescription in the case period, but not during the control period.

Information on other existing illnesses was obtained from discharge diagnoses from hospital admissions up to five years before the cardiac arrest.

One problem is that prescribing patterns change over time in the general population, but the study accounted for this by using a control group from the general population to adjust for these changes.

What were the basic results?

The analysis identified 28,947 people who experienced an out-of-hospital cardiac arrest between 2001 and 2010.

In the case period, 3,376 people had been treated with an NSAID in the 30 days leading up to cardiac arrest.

Ibuprofen was the most commonly prescribed NSAID, accounting for 51% of total NSAID use, followed by diclofenac, which accounted for 21.8% of total use.

The main findings were:

  • use of any NSAID increased risk of cardiac arrest by 31% (odds ratio [OR] 1.31, 95% confidence interval [CI] 1.17 to 1.46)
  • use of ibuprofen increased risk of cardiac arrest by 31% (OR 1.31, 95% CI 1.14 to 1.51)
  • use of diclofenac increased risk of cardiac arrest by 50% (OR 1.50, 95% CI 1.23 to 1.82)
  • use of naproxen was not associated with cardiac arrest, nor was use of COX-2 inhibitors

NSAID users were more likely to be women, have less cardiovascular disease, but be more likely to have cancer and rheumatic diseases. They were also more likely to be treated with psychiatric medication, diuretics and morphine.

How did the researchers interpret the results?

The researchers concluded that, "In a nationwide cohort of persons with OHCA [out-of-hospital cardiac arrest], we found that short-term treatment with non-selective NSAIDs, particularly ibuprofen and diclofenac, was associated with an increased early risk of cardiac arrest.

"We found no association between cardiac arrest and use of the COX-2 selective inhibitors, rofecoxib and celecoxib, nor the non-selective NSAID naproxen."

They went on to say: "Our findings support the accumulating evidence of an unfavourable cardiovascular risk profile associated with use of the non-selective NSAIDs. This calls for special awareness in order to balance risks against benefits in treatment with NSAIDs."

Conclusion

This study showed an association between taking ibuprofen or diclofenac and an increased risk of a cardiac arrest in the following 30 days, but no association was found with the other NSAIDs investigated.

But this study does have its limitations:

  • Although the researchers used the same people to avoid confounding variables, the same person will differ in certain aspects over time – for example, certain diseases may get better or worse, which might have affected the results.
  • The study only looked at prescribed drugs and not over-the-counter drugs. In Denmark, ibuprofen was the only over-the-counter drug sold at the time of the study and therefore a large number of people taking ibuprofen might have been missed.
  • It could be that people are taking NSAIDs for other underlying problems that increase the risk of cardiac arrest, so it might be these problems increasing risk of cardiac arrest, not the NSAIDs.
  • The dose and duration of NSAIDs might have varied across participants. It's not clear whether the greater the dose or duration, the higher the risk of cardiac arrest.
  • The study was carried out in Denmark – the findings might not be as relevant to other populations, who have different lifestyles.

The Guardian carries a quote from the lead author of the study, Professor Gunnar Gislason, warning: "The findings are a stark reminder that NSAIDs are not harmless … [and] should be used with caution and for a valid indication.

"They should probably be avoided in patients with cardiovascular disease or many cardiovascular risk factors."

If you're unclear about whether you should be taking NSAIDs, ask your GP or pharmacist for advice.

Links To The Headlines

Taking common painkillers like ibuprofen 'increases your risk of cardiac arrest by a THIRD'. The Sun, March 15 2017

Heart attack fears over use of common painkillers: Drugs including ibuprofen found to raise the risk by up to 50%. Mail Online, March 15 2017

Ibuprofen may be linked to potentially fatal cardiac arrests. Metro, March 15 2017

Links To Science

Sondergaard KB, Weeke P, Wissenberg M, et al. Non-steroidal anti-inflammatory drug use is associated with increased risk of out-of-hospital cardiac arrest: a nationwide case–time–control study. European Heart Journal – Cardiovascular Pharmacotherapy. Published online December 24 2016

New breast cancer drugs could help more than previously thought

NHS Choices - Behind the Headlines -

"Up to one in five women with breast cancer could benefit from a type of treatment currently only given to patients with a rare form of the disease," The Independent reports.

Research suggests around 20% of women with breast cancer may benefit from a new class of drug known as PARP inhibitors.

PARP (poly ADP ribose polymerase) inhibitors were designed to treat women with breast cancer related to inherited mutations in the BRCA1 and BRCA2 genes (the so-called "Angelina Jolie mutation", because of the film star's history of the mutation) which are thought to account for up to 5% of breast cancers.

But this latest research suggests that as many as one in five women with breast cancer could benefit from PARP inhibitors.

In the study, researchers designed a computer programme to recognise genetic "signatures" associated with problems in the body's ability to defend itself against cancer. These problems are linked to the BRCA1 and BRCA2 mutations.

The software looked for non-inherited genetic problems that were similar to the problems caused by inherited BRCA1 and BRCA2 mutations, which might mean they could be treated in the same way. Of the 560 people tested, the model found 90 people – around 20% of the group – had genetic problems similar to those caused by BRCA1 and BRCA2 mutations, suggesting they might also benefit from PARP inhibitors.

The next step would be to see whether using PARP inhibitors in these types of cases would be helpful.

 

Where did the story come from?

The study was carried out by researchers from more than 30 medical institutions, led by the Wellcome Trust Sanger Institute in the UK. It was funded by the European Community, the Wellcome Trust, Institut National du Cancer in France and the Ministry of Health and Welfare in Korea.

There are potential conflicts of interest as three of the researchers have a patent for the code and intellectual property rights of the algorithm used to identify BRCA1 and BRCA2 deficiency. Another researcher was involved in the invention of PARP inhibitors.

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

The Independent, The Sun and BBC News all gave accurate overviews of the research. However, reading the headlines, you would not realise that the drugs have not yet been tested in the groups that might benefit.

Also, The Independent's headline: "One in five breast cancer patients not receiving new treatment that could benefit them," suggests the drugs are being deliberately withheld, when in fact there had not previously been any suggestion they could help, and we still don't know whether they are helpful.

 

What kind of research was this?

This was laboratory research using whole genome analysis of tissue in the laboratory, and feeding it through computer algorithms. This sort of research is good at generating theories, but clinical trials are needed before we know the practical application of the results.

 

What did the research involve?

Researchers took DNA from breast cancer tumours removed from 560 people and did whole genome sequencing. They used DNA from people known to have inherited BRCA1 or BRCA2 mutations to develop a computer programme to recognise signature features linked to the mutations. The programme then compared these results with results from people with non-inherited breast cancer.

The programme created a model, called HRDetect, to spot people who didn't have the inherited BRCA1 or BRCA2 mutation, but did have DNA changes that made them deficient in BRCA proteins. HR refers to homologous recombination repair, a method by which BRCA1 and BRCA2 proteins defend cells against cancer.

They tested HRDetect on several groups, and looked to see if it could be used on biopsy samples, rather than large tissue samples from removed tumours. They tested it on ovarian and pancreatic cancers, as well as the initial breast cancer group.

 

What were the basic results?

The HRDetect model found that, in women with non-inherited breast cancer:

  • 69 out of 538 breast tumours were BRCA1 or BRCA2 deficient
  • 16 out of 73 ovarian cancer tumours were BRCA1 or BRCA2 deficient
  • 5 out of 96 pancreatic cancer tumours were BRCA1 or BRCA2 deficient

The researchers say the model showed 98.7% sensitivity (meaning that it missed less than 2% of tumours which were BRCA1/BRCA2 deficient). This is very high. They don't report on specificity – how many might have been wrongly identified as deficient (also known as a false positive result).

The model performed as well on samples of tumours from small needle biopsies as on large specimens removed during surgery. This suggests that the model could be used early in the clinical process, from the patient's first biopsy. This might help direct treatment from an early stage.

 

How did the researchers interpret the results?

The researchers said the model was "extraordinarily effective" as a predictive tool.

"If the tumours with predicted BRCA1/BRCA2 deficiency also demonstrate sensitivity to PARP inhibitors, this would unearth a substantial cohort of patients who could be responsive to selective therapeutic agents," they add. They say that this is "potentially transformative" of treatment and recommend use of their model in trials of PARP inhibitors.

 

Conclusion

Advances in genetic technology are happening fast, improving our knowledge about which treatments may be most suitable for which types of cancer. However, testing these theories takes time, which can be frustrating for researchers, when newspaper headlines suggest people should already be receiving new treatments.

This study potentially widens the pool of people who may benefit from targeted cancer treatment with PARP inhibitors, from around 5% to around 20%. That's clearly good news, but the potential for benefit needs to be tested in clinical trials.

The researchers express a great deal of confidence in the accuracy of their model. It would still be useful to see it externally validated in other groups of people, before we can know how well it performs in the real world. It would also be useful to see how specific the test is, as well as how sensitive it is.

One question remains about the 20% figure. It's not clear how the researchers selected people to take part in the study. They deliberately selected 22 patients who were known to have BRCA mutations. But we don't know whether the others in the study were randomly selected and representative of all people with breast cancer. If they were not randomly selected, then the 20% figure may not hold true for the wider population of people with breast cancer.

Most people with breast cancer don't have inherited gene mutations. Find out more about predictive genetic tests for cancer risk genes

Links To The Headlines

One in five breast cancer patients not receiving new treatment that could benefit them, scientists say. The Independent, March 14 2017

New drug for one in five breast cancers. BBC News, March 14 2017

Drugs to treat breast cancer patients with 'Angelina Jolie gene' may help thousands without faulty DNA. March 13 2017

Links To Science

Davies H, Glodzik D, Morganella S, et al. HRDetect is a predictor of BRCA1 and BRCA2deficiency based on mutational signatures. Nature Medicine. Published online March 13 2017

Children's screen time linked to diabetes risk factors

NHS Choices - Behind the Headlines -

"Children who are allowed more than three hours of screentime a day are at greater risk of developing diabetes," The Guardian reports.

In a new study, UK researchers found a link between three hours or more of screen time and risk factors for type 2 diabetes, such as higher body fat.

The study used data from almost 4,500 children aged around 10 years collected between 2004 and 2007. They found that children with more than three hours of screen time per day had higher body fat and insulin resistance compared to children with an hour or less per day. Screen time was defined as time spent watching television and using computers or games consoles.

It is unlikely that the screen time itself is causing an increase in risk; more that this could indicate a more sedentary lifestyle.

One concern is that the data was collected before the use of smartphones and tablets became widespread in children. So it could be the case that screen time use has now increased among children, but we would need further research to confirm this.

Recent US guidelines (there are currently no UK guidelines) recommend no screen time for infants under 18 months, one hour for children aged 2-5, and then older children should be assessed on a case by case basis by their parents.

The study supports current physical activity recommendations for children which say they should do at least an hour's exercise every day. Sticking to this will help reduce the risk of chronic diseases such as type 2 diabetes in later life.

 

Where did the story come from?

The study was carried out by researchers from the University of London and the University of Glasgow. Funding was provided by the National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care (CLAHRC). Data collection was funded by grants from the Wellcome Trust, the British Heart Foundation and the National Prevention Research Initiative.

The study was published in the peer-reviewed medical journal Archives of Disease in Childhood.

There were no conflicts of interest reported by the research team.

The UK media generally reported on this study accurately, though none of the media outlets really explains why this link may have been seen or that the study can't prove that screen time itself increases risk.

The Mail Online provided a number of figures from other sources to add context to the study findings. We are unable to comment on the accuracy of these sources. 

 

What kind of research was this?

This is a cross-sectional survey looking into association between daily screen time and risk markers for type 2 diabetes and cardiovascular disease in children aged nine and 10 years.

Type 2 diabetes and obesity are increasing in adults and children. The effect of sedentary behaviour such as watching television and using computers, known as "screen time", are a cause for concern and associations have been seen between prolonged screen time and body fatness in children.

Using data from this survey the researchers were able to identify potential risk factors, however due to the nature of this study design they would not be able to prove that one thing causes the other. The researchers say they can use their findings to design further studies to prove causation.

randomised controlled trial would be required to prove such a link. However, a trial that randomises children to different amounts of sedentary time or physical activity and then follows them for sufficient time to observe outcomes may be neither feasible nor ethical.

 

What did the research involve?

This was a cross-sectional study known as The Child Heart and Health Study in England.

Researchers carried out a survey of primary school children aged nine and 10 years from London, Birmingham and Leicester. A single research team collected key information between October 2004 and February 2007. Some of the information recorded was as follows:

  • ethnic origin (based on the ethnicity of both parents)
  • socioeconomic status
  • height
  • weight
  • skin fold measurements
  • fat mass
  • blood glucose and insulin levels
  • insulin resistance – a measurement of how the body's cells respond to insulin
  • cholesterol
  • blood pressure
  • pubertal status measured in girls (girls tend to start puberty earlier than boys)

On the same day as the physical measurements were taken, children completed a questionnaire asking "How many hours each day do you spend watching television or video and playing computer games?"

The children had to tick the most appropriate response, the options were:

  • none
  • an hour or less
  • one to two hours
  • two to three hours
  • more than three hours

In a sub-group of children, activity was measured using a monitor worn around the waist.

When analysing the findings the researchers attempted to account for the effects of confounding factors such as socioeconomic status, physical activity and pubertal status.

 

What were the basic results?

The analysis focused on the 4,495 children (2,337 girls and 2,158 boys) who had screen time data, all physical measurements and a fasting blood sample. More than 2,000 children had physical activity data collected from the waist monitor.

The most commonly reported screen time duration was one hour or less (37%), with 18% reporting more than three hours and 4% reporting no screen time at all.

Boys were more likely to have more than three hours of screen time a day, 22% compared to 14% of girls.

Differences were seen between ethnic groups, a higher proportion of black African-Caribbean children (23%) had more than three hours of daily screen time compared with white Europeans (16%) and South Asians (16%).

Children reporting more than three hours of screen time were found to have a higher level of body fat than those with an hour or less screen time.

This was as measured by ponderal index (ponderal means related to weight – the index is a measure of kg/m3; which was on average 1.9% higher), skinfold thickness (4.5% greater), fat mass index (3.3% higher) and leptin (a hormone that controls hunger – 9.2% higher).

They also had higher levels of blood insulin and insulin resistance compared to children taking one hour or less, though there was little link with blood glucose control.

 

How did the researchers interpret the results?

The researchers conclude: "Strong graded associations between screen time, adiposity and insulin resistance suggest that reducing screen time could facilitate early T2D [type 2 diabetes] prevention. While these observations are of considerable public health interest, evidence from randomised controlled trials is needed to suggest causality."

 

Conclusion

This cross sectional study aimed to investigate the association between markers for type 2 diabetes and the amount of screen time a child has.

The study found an association between higher levels of screen time and higher body fat and insulin resistance. However, as mentioned, this type of study is not able to prove cause and effect. It is most likely not the screen time itself that is the cause of these factors, more that this could indicate a generally less healthy and more sedentary lifestyle. A similar link might be found for children who spend more time reading books instead of taking physical activity.

The researchers have tried to adjust for physical activity and socioeconomic status that could be influencing the link. However, it is possible that some confounding remains in the model or that other important factors were missed – diet being a notable possibility. It's also possible that children who reported more screen time may have had other health conditions which were not accounted for in the analysis that could have increased their risk.

Other important limitations are that the amount of screen time was self-reported and children may not have remembered or reported this accurately. The measures of body fat and blood glucose control were also one-off measurements taken at single point in time. They don't tell us that the child will go on to develop type 2 diabetes.

Nevertheless the study suggests a reduction in screen time could be beneficial in improving health and possibly reducing the risk of type 2 diabetes and other obesity-related diseases in later life.

One pressing concern is that the data gathered in the study was taken before the use of smartphones and tablets became widespread in older children. Smartphones became commonly used around 2008 to 2010 and the first tablet (the iPad) was released in 2010. So it could well be the case that screen time has now increased in older children.

With these concerns in mind it is important that children are taught to compensate for time spent "gawping at gadgets" (as the Mail puts it) with time spent being physically active.

Guidelines for children and young people recommend that to maintain a basic level of health at least 60 minutes of physical activity every day should be taken; this could be cycling, playground activities or more vigorous activity, such as running and tennis. Exercises for strong muscles and bones are recommended three days a week such as push-ups, jumping and running.

Read more advice about encouraging children to be more physically active.

Links To The Headlines

Screentime linked to greater diabetes risk among children. The Guardian, March 13 2017

Watching TV three hours a day linked to child diabetes. The Independent, March 13 2017

Children's risk of developing Type 2 diabetes soars with just three hours of screen time a day. Mail Online, March 13 2017

Kids who spend three hours a day watching telly or playing video games ‘flirting with diabetes’. The Sun, March 13 2017

Links To Science

Nightingale CM, Rudnicka AR, Donin AS, et al. Screen time is associated with adiposity and insulin resistance in children. Archives in Disease for Childhood. Published online March 13 2017

Children's screen time linked to diabetes risk factors

NHS Choices - Behind the Headlines -

"Children who are allowed more than three hours of screentime a day are at greater risk of developing diabetes," The Guardian reports.

In a new study, UK researchers found a link between three hours or more of screen time and risk factors for type 2 diabetes, such as higher body fat.

The study used data from almost 4,500 children aged around 10 years collected between 2004 and 2007. They found that children with more than three hours of screen time per day had higher body fat and insulin resistance compared to children with an hour or less per day. Screen time was defined as time spent watching television and using computers or games consoles.

It is unlikely that the screen time itself is causing an increase in risk; more that this could indicate a more sedentary lifestyle.

One concern is that the data was collected before the use of smartphones and tablets became widespread in children. So it could be the case that screen time use has now increased among children, but we would need further research to confirm this.

Recent US guidelines (the are currently no UK guidelines) recommend no screen time for infants under 18 months, one hour for children aged 2-5, and then older children should be assessed on a case by case basis by their parents.

The study supports current physical activity recommendations for children which say they should do at least an hour's exercise every day. Sticking to this will help reduce the risk of chronic diseases such as type 2 diabetes in later life.

 

Where did the story come from?

The study was carried out by researchers from the University of London and the University of Glasgow. Funding was provided by the National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care (CLAHRC). Data collection was funded by grants from the Wellcome Trust, the British Heart Foundation and the National Prevention Research Initiative.

The study was published in the peer-reviewed medical journal Archives of Disease in Childhood.

There were no conflicts of interest reported by the research team.

The UK media generally reported on this study accurately, though none of the media outlets really explains why this link may have been seen or that the study can't prove that screen time itself increases risk.

The Mail Online provided a number of figures from other sources to add context to the study findings. We are unable to comment on the accuracy of these sources. 

 

What kind of research was this?

This is a cross-sectional survey looking into association between daily screen time and risk markers for type 2 diabetes and cardiovascular disease in children aged nine and 10 years.

Type 2 diabetes and obesity are increasing in adults and children. The effect of sedentary behaviour such as watching television and using computers, known as "screen time", are a cause for concern and associations have been seen between prolonged screen time and body fatness in children.

Using data from this survey the researchers were able to identify potential risk factors, however due to the nature of this study design they would not be able to prove that one thing causes the other. The researchers say they can use their findings to design further studies to prove causation.

randomised controlled trial would be required to prove such a link. However, a trial that randomises children to different amounts of sedentary time or physical activity and then follows them for sufficient time to observe outcomes may be neither feasible nor ethical.

 

What did the research involve?

This was a cross-sectional study known as The Child Heart and Health Study in England.

Researchers carried out a survey of primary school children aged nine and 10 years from London, Birmingham and Leicester. A single research team collected key information between October 2004 and February 2007. Some of the information recorded was as follows:

  • ethnic origin (based on the ethnicity of both parents)
  • socioeconomic status
  • height
  • weight
  • skin fold measurements
  • fat mass
  • blood glucose and insulin levels
  • insulin resistance – a measurement of how the body's cells respond to insulin
  • cholesterol
  • blood pressure
  • pubertal status measured in girls (girls tend to start puberty earlier than boys)

On the same day as the physical measurements were taken, children completed a questionnaire asking "How many hours each day do you spend watching television or video and playing computer games?"

The children had to tick the most appropriate response, the options were:

  • none
  • an hour or less
  • one to two hours
  • two to three hours
  • more than three hours

In a sub-group of children, activity was measured using a monitor worn around the waist.

When analysing the findings the researchers attempted to account for the effects of confounding factors such as socioeconomic status, physical activity and pubertal status.

 

What were the basic results?

The analysis focused on the 4,495 children (2,337 girls and 2,158 boys) who had screen time data, all physical measurements and a fasting blood sample. More than 2,000 children had physical activity data collected from the waist monitor.

The most commonly reported screen time duration was one hour or less (37%), with 18% reporting more than three hours and 4% reporting no screen time at all.

Boys were more likely to have more than three hours of screen time a day, 22% compared to 14% of girls.

Differences were seen between ethnic groups, a higher proportion of black African-Caribbean children (23%) had more than three hours of daily screen time compared with white Europeans (16%) and South Asians (16%).

Children reporting more than three hours of screen time were found to have a higher level of body fat than those with an hour or less screen time.

This was as measured by ponderal index (ponderal means related to weight – the index is a measure of kg/m3; which was on average 1.9% higher), skinfold thickness (4.5% greater), fat mass index (3.3% higher) and leptin (a hormone that controls hunger – 9.2% higher).

They also had higher levels of blood insulin and insulin resistance compared to children taking one hour or less, though there was little link with blood glucose control.

 

How did the researchers interpret the results?

The researchers conclude: "Strong graded associations between screen time, adiposity and insulin resistance suggest that reducing screen time could facilitate early T2D [type 2 diabetes] prevention. While these observations are of considerable public health interest, evidence from randomised controlled trials is needed to suggest causality."

 

Conclusion

This cross sectional study aimed to investigate the association between markers for type 2 diabetes and the amount of screen time a child has.

The study found an association between higher levels of screen time and higher body fat and insulin resistance. However, as mentioned, this type of study is not able to prove cause and effect. It is most likely not the screen time itself that is the cause of these factors, more that this could indicate a generally less healthy and more sedentary lifestyle. A similar link might be found for children who spend more time reading books instead of taking physical activity.

The researchers have tried to adjust for physical activity and socioeconomic status that could be influencing the link. However, it is possible that some confounding remains in the model or that other important factors were missed – diet being a notable possibility. It's also possible that children who reported more screen time may have had other health conditions which were not accounted for in the analysis that could have increased their risk.

Other important limitations are that the amount of screen time was self-reported and children may not have remembered or reported this accurately. The measures of body fat and blood glucose control were also one-off measurements taken at single point in time. They don't tell us that the child will go on to develop type 2 diabetes.

Nevertheless the study suggests a reduction in screen time could be beneficial in improving health and possibly reducing the risk of type 2 diabetes and other obesity-related diseases in later life.

One pressing concern is that the data gathered in the study was taken before the use of smartphones and tablets became widespread in older children. Smartphones became commonly used around 2008 to 2010 and the first tablet (the iPad) was released in 2010. So it could well be the case that screen time has now increased in older children.

With these concerns in mind it is important that children are taught to compensate for time spent "gawping at gadgets" (as the Mail puts it) with time spent being physically active.

Guidelines for children and young people recommend that to maintain a basic level of health at least 60 minutes of physical activity every day should be taken; this could be cycling, playground activities or more vigorous activity, such as running and tennis. Exercises for strong muscles and bones are recommended three days a week such as push-ups, jumping and running.

Read more advice about encouraging children to be more physically active.

Links To The Headlines

Screentime linked to greater diabetes risk among children. The Guardian, March 13 2017

Watching TV three hours a day linked to child diabetes. The Independent, March 13 2017

Children's risk of developing Type 2 diabetes soars with just three hours of screen time a day. Mail Online, March 13 2017

Kids who spend three hours a day watching telly or playing video games ‘flirting with diabetes’. The Sun, March 13 2017

Links To Science

Nightingale CM, Rudnicka AR, Donin AS, et al. Screen time is associated with adiposity and insulin resistance in children. Archives in Disease for Childhood. Published online March 13 2017

Hair loss drugs linked with erectile dysfunction

NHS Choices - Behind the Headlines -

"Men who take this drug [finasteride] to combat baldness are 'five times more likely to suffer erectile dysfunction'," The Sun reports.

While this may sound hair-raising, the actual evidence the paper is reporting on is not a major cause for concern.

This US study looked at a medical records database to see how common erectile dysfunction (impotence) was among men prescribed two drugs, dutasteride and finasteride, both used to treat non-cancerous prostate enlargement. The drugs work by blocking the male hormone testosterone. A low dose of finasteride is also used to treat male pattern baldness.

Overall they found that around 1 in 17 of all men prescribed either drug for prostate enlargement had erectile dysfunction. This figure fell to 1 in 31 of those prescribed finasteride for baldness. Using the drug for longer was generally linked with a higher risk. However, in 99% of men, stopping the drugs solved the problem so it wasn't as catastrophic as the media implies.

The research highlights a known side effect of these drugs but shouldn't give too much cause for concern. If sexual problems do occur, the drug can be stopped, solving the problem in nearly all cases.

 

Where did the story come from?

The study was carried out by researchers from Northwestern University, Chicago, and the University of Catania in Italy. It was funded by grants from the National Institutes of Health. Additional funding was provided from the Post-Finasteride Syndrome Foundation.

The study was published in the peer-reviewed journal PeerJ on an open-access basis so you can read or download the study for free (PDF, 2.04Mb).

The Sun and the Mail Online are arguably guilty of exaggerating the results. While their reports of the increased risk of erectile dysfunction are largely accurate, they don't make clear that the actual risk of persistent problems once you stop the drugs is extremely small.

Also the Mail's claim that "Viagra doesn't help" is unsupported. The study only looked at whether Viagra (sildenafil) was prescribed, not whether it worked or not.

 

What kind of research was this?

This was a cohort study that aimed to investigate whether length of time taking a class of drugs known as 5a-reductase inhibitors (5α-RIs) increased risk of erectile dysfunction.

There are two 5α-RI drugs – finasteride and dutasteride – both of which effectively inhibit the male hormone testosterone by blocking the enzyme involved in its metabolism. Both are licensed to treat benign enlargement of the prostate gland, but a low dose of finasteride is also licensed to treat male pattern baldness. Both drugs are already known to have side effects of decreased libido (sex drive) and erectile dysfunction.

This study aimed to see whether the duration of exposure has an effect, and whether it persists after stopping the drugs.

 

What did the research involve?

The study included men from the Chicago region who had taken 5α-RIs.

Electronic medical records were accessed to look at the drug, dose, and duration of use. Researchers searched the database for recorded side effects of impotence or erectile dysfunction.

This was defined as the first recorded instance, which coincided with discontinuation of the 5α-RI and prescription of a phosphodiesterase -5 inhibitors (PDE5I), such as sildenafil to treat the problem.

They also looked at recorded diagnoses such as prostate disease, prostate cancer and alopecia, along with other medical conditions such as cardiovascular disease, high blood pressure, diabetes or obesity, to analyse the influence of these factors.

Researchers analysed the effect of low-dose finasteride (<1.25mg – taken for male pattern baldness) vs. higher dose (5mg – taken for prostate enlargement), and also finasteride vs. dutasteride. They also included a comparison cohort of men prescribed 5α-RIs and with no record of erectile dysfunction, and men who had not taken 5α-RIs.

 

What were the basic results?

The database included 691,268 men and 17,475 had 5α-RI exposure.

Men who had taken 5α-RIs were more likely than non-exposed men to have had a recording of erectile dysfunction in their medical records, with on average one case for every 17 men prescribed the drugs. They were also more likely to have recordings of low libido and to have been prescribed a PDE5I.

Erectile dysfunction was linked with exposure duration above 90 days. 1.4% of men also had persistent erectile dysfunction that lasted for 90 days after discontinuing the drugs.

Young men (age 16 to 42) prescribed low-dose finasteride (<1.25mg) were also more likely to have a record of erectile dysfunction recorded with 31 cases for each man prescribed the drug. Of young men on low dose, 0.8% had erectile dysfunction that persisted after stopping the drugs.

Other factors that were strong predictors of erectile dysfunction, aside from use of 5α-RIs, were records of prostate disease or prostate surgery, a greater number of medical consultations and increased age.

The four strongest predictors for erectile dysfunction that persisted after stopping 5α-RIs were prostate disease, increased age, duration of use and prescription of anti-inflammatory drugs alongside 5a-RIs.

Specifically in young men taking low-dose finasteride the strongest factor for risk of persistent erectile dysfunction was duration of use, with use above 205 days linked to increased risk.

 

How did the researchers interpret the results?

The researchers conclude: "Risk of persistent erectile dysfunction was higher in men with longer exposure to 5α-RIs. Among young men, longer exposure to finasteride posed a greater risk of PED [permanent erectile dysfunction] than all other assessed risk factors."

 

Conclusion

This review confirms what is already known, that 5α-reductase inhibitors (5α-RIs) increase risk of erectile dysfunction.

However, it also shows that even the low-dose formulation of finasteride taken by younger men for male pattern baldness is associated with increased risk.

It is important to recognise that erectile dysfunction is already a known risk of the drug. It occurred in around one in 31 young men exposed – but the vast majority of cases resolved after stopping the drug. Erectile dysfunction only persisted in less than one in 100 young men after discontinuation of 5α-RI treatment.

Even for men taking the standard higher dose for enlarged prostate, only 1.4% had persistent erectile problems after stopping the drug.

Therefore it is a slight media distortion to suggest that this is a permanent problem and "Viagra won't help". The researchers looked for prescription of drugs such as Viagra to indicate the problem in the medical records, but they haven't looked at response to this at all.

Another limitation is that this study looked at medical records from one region of the US only. This may not give a true representation of how common erectile dysfunction is among men prescribed these drugs – either for enlarged prostate or male pattern baldness. Some men may not have discussed adverse sexual effects with their doctor and it may not have been documented in the medical records.

Overall, the research highlights a known side effect of these drugs but does not give overt cause for concern. Men prescribed these drugs for male pattern baldness will have been informed of the side effects. If sexual problems do occur, the drug can be stopped and the problem will resolve in nearly all cases.   

Links To The Headlines

Men who take THIS drug to combat baldness are ‘FIVE TIMES more likely to suffer erectile dysfunction’. The Sun, March 10 2017

Bad news for bald men: Hair loss drugs cause erectile dysfunction that lasts for years (and even Viagra won’t cure the problem). Mail Online, March 10 2017

Links To Science

Kiguradze T, Temps WH, Yarnold PR, et al. Persistent erectile dysfunction in men exposed to the 5a-reductase inhibitors, finasteride, or dutasteride (PDF 2.03 MB). PeerJ. Published online March 9 2017

Parents told to use pram covers to protect babies from air pollution

NHS Choices - Behind the Headlines -

"Parents warned to use pram covers to protect babies from air pollution," reports The Daily Telegraph.

The advice is prompted by a UK study where researchers simulated a normal walk to school in Guildford, involving parents pushing a pram or carrying a younger child in their arms while accompanying an older child to school. The route went through both low traffic and high traffic zones, across four traffic intersections and past a bus stop.

It used measuring instruments to assess levels of pollution at pram height and adult height.

It found that the concentrations of fine pollutant particles were higher during morning hours, particularly around traffic intersections and bus stops, while coarser particles were more concentrated in the afternoon. Fine particles are thought to be potentially more dangerous as, due to their size, they can penetrate deeper into the body's airways.

However, there was little to no difference between levels at pram and adult height.

Importantly, this research cannot demonstrate that exposure to these particles directly causes adverse health outcomes, such as respiratory diseases.

Further studies are needed to validate these findings, and possibly investigate the potential long-term implications of exposure to pollution.

The researchers recommend using barriers such as pram covers to protect children in prams from the vehicle emissions at road level, especially at traffic intersections and other traffic hotspots, and during peak traffic times.

 

Where did the story come from?

The UK study was carried out by researchers from the University of Surrey and the Indian Institute of Technology Roorkee. It was funded by the University Global Partnership Network (UGPN) as the work was conducted as part of the project, NEST-SEAS (Next-Generation Environmental Sensing for Local To Global Scale Health Impact Assessment).

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

Coverage in the UK media was both widespread and accurate.

 

What kind of research was this?

This was an experimental study which aimed to investigate pollution particulates that babies in prams are exposed to compared with babies carried by adults along different walking routes to school.

Children are thought to be more susceptible to environmental exposures because of their developing systems, higher inhalation rates and lower body weights.

Due to their height, children are closer to traffic emissions than adults but there has been limited research looking at this in detail. This study wanted to fill this gap.

Experimental studies like this one are useful for exploring a particular hypothesis but require validation through further research, such as studies examining varying walking routes in different urban and more rural environments. Also, this type of study can't demonstrate exposure to pollution causes health outcomes such as respiratory diseases.

 

What did the research involve?

The experiment was conducted to simulate a school walking route around the town of Guildford, during morning drop-off (starting at 8am) and afternoon pick-up hours (starting at 3pm). The total length of the route was 2.7km and took an average of 37 minutes to walk.

The route was designed to go through both low traffic and high traffic zones, across four traffic intersections and past a bus stop.

Instruments were placed inside a pram to measure the level of exposure to particulates at a height of 0.7m above the ground. The instruments were also carried by adults to represent the level of exposure to children being held by their parents.

The outcomes of interest were particle mass (PMC) and particle number (PNC) concentrations.

The respiratory deposition dose (RDD) was calculated by multiplying the concentration, deposition fraction (DF) and estimated ventilation rate (VR) of young babies. In other words, an estimate of the amount of particles a baby was exposed to was calculated by multiplying the number of particles, their density in a given volume of air and the expected breathing rate of a typical baby.

The results were compared between morning drop-off and afternoon-pick up, between pram and adult height measurements, and through different pollution hotspots.

 

What were the basic results?

There was little to no difference in the concentrations of particulates at pram-level when compared with adult height.

Small sized particles were higher during the morning drop-off compared to during afternoon-pick up and coarse particles were found to be more prevalent during afternoon hours. Correspondingly the respiratory deposition dose (RDD) for coarse particles was calculated to be 41% lower in the morning, while the RDD for fine particles was 10% higher in the morning.

The results showed high levels of coarse and small sized particles were present at pollution hotspots (traffic intersections and bus stops).

The dominant elements were found to be sodium, chlorine and iron; the sodium chloride is thought to be from road salt and iron from brake abrasion.

 

How did the researchers interpret the results?

The researchers concluded: "This study provides hitherto missing knowledge on the exposure of in-pram babies during the morning and afternoon pick-up periods of children from school. The findings clearly suggest much higher concentrations of fine PMC and PNC during the morning peak hours, especially on the traffic intersections and bus stand."

 

Conclusion

This study aimed to investigate the pollution that babies and young children are exposed to, whether in the pram or carried by adults, on different school drop-off and pick-up walking routes.

It generally found that the concentrations of fine particulates (PMC and PNC) were higher during morning hours, particularly around traffic intersections and bus stops.

Experimental studies like this one are useful for testing hypotheses but there are a few points worth noting:

  • The study assessed a single town. They would need to compare their findings with many more assessments on different routes, and in different towns, cities and rural environments.
  • Despite the media emphasis on exposure in prams, the study found that there was no difference in exposure compared with if the baby/child was carried at adult height.
  • And importantly, this study has not assessed whether this exposure is actually associated with health outcomes, such as respiratory diseases. As mentioned by the authors, further studies need to assess the toxicity of particles to fully understand their effects on infants.

However, this particular study may pave the way for future research on this topic.

As lead researcher Dr Prashant Kumar suggests in an accompanying press release: "One of the simplest ways to combat this is to use a barrier between the in-pram children and the exhaust emissions, especially at pollution hotspots such as traffic intersections, so parents could use pram covers if at all possible".

Links To The Headlines

Parents warned to use pram covers to protect babies from air pollution. The Daily Telegraph, March 10 2017

Use pram covers 'to protect babies from air pollution'. BBC News, March 9 2017

Taking your baby on a school run? Use a buggy cover! Children in prams are exposed to DOUBLE the amount of pollution during the morning drop off. Mail Online, March 9 2017

Use buggy covers to combat air pollution danger, parents warned. The Guardian, March 9 2017

Cover prams to shield babies from pollution, scientists say. The Times, March 10 2017 (subscription required)

Links To Science

Kumar P, Rivas I, Sachdeva L. Exposure of in-pram babies to airborne particle during morning drop-in and afternoon pick-up of school children. Environmental Pollution. Published online March 6 2017

'Tooth loss link to increased risk of dementia'

NHS Choices - Behind the Headlines -

"Dementia breakthrough: Brushing your teeth 'can help ward off devastating condition'," reads the Daily Express.

The news is based on a study that found tooth loss was associated with an increased risk of dementia.

The study involved more than 1,500 elderly people in Japan who had their health monitored between 2007 and 2012.

The study found participants with fewer teeth had a greater chance of developing dementia within the five years of the study.

For example, people with 1-9 teeth had an 81% higher risk of dementia than those with 20 teeth or more.

There are 850,000 people with dementia in the UK, with numbers set to rise to more than a million by 2025.

Although this isn't the first study to link oral hygiene with dementia, we don't know whether tooth loss is a cause of dementia or whether it could be a sign of something else.

Poor oral hygiene might be a sign of poor overall health or unhealthy behaviour, or it might be linked to having a poor diet – it's harder to eat a full, balanced diet if you don't have many teeth.

Although the study doesn't show that tooth brushing can "ward off" dementia, there are plenty of good reasons to keep teeth healthy.

Tooth decay not only causes pain, but chronic inflammation that's been linked to risk of heart disease.

Good oral hygiene includes brushing your teeth twice a day, regular visits to the dentist, and avoiding sugary food and drink.

Where did the story come from?

The study was carried out by researchers from Kyushu University in Japan, and was funded by the Ministry for Education, Culture, Sports, Science and Technology of Japan, the Ministry of Health, Labour and Welfare of Japan, and the Japan Agency for Medical Research and Development.

It was published in the peer-reviewed Journal of the American Geriatrics Society and is free to read online.

Despite the misleading headline, the Daily Express reported on the study reasonably accurately. The i newspaper and the Daily Mirror also did a reasonable job.

But the stories also said a study we reported on last year showed tooth brushing reduced dementia risk – when in fact all the people in last year's study already had dementia, and it looked at gum disease, not whether people brushed their teeth.

What kind of research was this?

This was a prospective cohort study. Researchers wanted to compare what happened to people with different levels of tooth loss to see who was most likely to develop dementia.

These types of studies are useful for identifying links between factors, but can't tell us whether one factor (such as tooth loss) causes another (dementia).

What did the research involve?

Researchers followed 1,566 adults aged 60 or above in one region of Japan. They had their teeth checked by a dentist and were asked about many aspects of their lives.

They were followed up closely for five years (2007-12) to check for signs of dementia.

After adjusting for confounding factors, the researchers looked at whether people with less than 20 remaining teeth were more likely to have developed dementia of any type, compared with those with at least 20 teeth.

Diagnoses of dementia were made by specialist stroke physicians and psychiatrists. They aimed to differentiate between Alzheimer's disease and vascular dementia, which is caused by multiple small strokes that damage the brain.

Researchers adjusted figures to take account of a wide range of potential confounding factors, including people's age, sex, job, history of high blood pressure, stroke or diabetes, education levels, smoking and alcohol intake, tooth brushing frequency, use of dentures, and regular visits to the dentist.

They looked at the risk of getting any type of dementia, then at the risks of Alzheimer's disease and vascular dementia separately.

What were the basic results?

During the study, 180 people (11.5%) developed some type of dementia. Compared with people who had 20 teeth or more:

  • those with 10-19 teeth had a 62% higher risk of dementia (hazard ratio [HR] 1.62, 95% confidence interval [CI] 1.06 to 2.46)
  • those with 1-9 teeth had an 81% higher risk of dementia (HR 1.81, 95% CI 1.11 to 2.94)
  • those with no teeth had a 63% higher risk of dementia, although this figure could have been down to chance, probably because of the small number of people in the study with no teeth (HR 1.63, 95% CI 0.95 to 2.80) – these results could also be affected by people with no teeth wearing a full set of dentures

The researchers found no link between number of teeth and vascular dementia. Although they found a link between numbers of teeth and Alzheimer's disease, this number didn't stand up after adjusting for confounding factors.

How did the researchers interpret the results?

The researchers said: "These findings highlighted the clinical value of maintaining healthy dentition [teeth] throughout life to reduce the risk of dementia in the general population."

They suggest several ways in which tooth loss may be linked to dementia risk.

They say the act of chewing might stimulate blood flow to the brain, or people with a full set of teeth may have a healthier diet, and inflammation from long-term tooth decay or gum disease might increase the likelihood of Alzheimer's disease.

They also admit that poor oral health could be a general sign of overall poor health.

Conclusion

This study adds to the evidence that good oral health is linked to good overall health, including a reduction in the chances of developing dementia in later life.

But the research doesn't prove that regular tooth brushing will prevent dementia.

We don't know what causes dementia. From research so far, it looks as if there are a number of interlinked causes.

Brain health and ageing are likely to be affected by factors including diet, exercise, smoking, alcohol use, blood pressure and genetics.

While living a healthy lifestyle may certainly reduce the chances of dementia, there are no guarantees.

This study has a few limitations. The number of people in the study, and the number who got dementia, was relatively small.

That means we should be cautious about the results, especially when looking at Alzheimer's disease and vascular dementia separately.

Only 42 people of 1,566 people had vascular dementia, so it's hard to draw conclusions based on such small numbers. That's why we say some of the results could be down to chance.

This type of study does not allow us to say whether the factors studied (tooth loss) directly caused the outcome (dementia).

There are lots of possible confounding factors. Although the researchers tried to account for some of them, there may be others that were missed.

But don't throw away your toothbrush. Good oral health is important for many reasons, and it may play a role in reducing the risk of dementia. What we don't know is how big a role, and whether it's a direct cause and effect.

Links To The Headlines

Keeping more of your own teeth lessens the risk of getting dementia. Daily Mirror, March 8 2017

Dementia breakthrough: Brushing your teeth 'can help ward off devastating condition'. Daily Express, March 8 2017

Tooth loss linked with increased risk of dementia, study finds. The iNews, March 8 2017

Links To Science

Takeuchi K, Ohara T, Furuta M et al, Tooth Loss and Risk of Dementia in the Community: the Hisayama Study. The Journal of the American Geriatrics Society. Published online March 8 2017.

Substance found in red wine 'helps fight ageing'

NHS Choices - Behind the Headlines -

"Red wine can 'help fight the ageing process' – but how much would you have to drink?," is the question posed by The Sun, after a US study suggested resveratrol, a substance found in the skin of red grapes, may help keep our muscles and nerves healthy as we get older.

But the story might also ask "and are you a mouse?" as the research was carried out in rodents, not people.

Researchers gave mice food containing resveratrol for a year, then compared the muscle and nerve cells of those mice to cells from mice the same age who'd had a normal diet. In the mice who'd had the resveratrol-enriched diet, they found less evidence of age-related changes.

Although red wine contains resveratrol, the amount varies widely, from around 0.2mg to 12.6mg per litre. That's nothing like enough to get the amounts consumed in this study.

The mice were fed 400mg of resveratrol per kilogram of body weight each day. An average weight woman in the UK (around 70kg) would need 28g of resveratrol a day for the same effect – or more than 2,000 litres of the most resveratrol-rich wine. An average weight man would need even more.

The researchers also looked at another chemical, metformin, but found it had less effect. However, they did find that a low-calorie diet seems to slow age-related changes in muscles and nerves. Previous studies have shown that exercise may help.

So eating less and exercising more is certainly a better bet than trying to drink your way to agelessness.

Where did the story come from?

The study was carried out by researchers from Virginia Tech, Roanoke College and the National Institute on Aging, all in the US, and was funded by the National Institutes of Health. The study was published in the peer-reviewed Journals of Gerontology: Biological Sciences and is open-access, meaning it's free to read online.

While The Sun's headline might have been a bit misleading, the story did make clear that the researchers don't recommend anyone tries "blasting their bodies with resveratrol in any form" to try to replicate the findings seen in mice.

Oddly, The Independent says the study showed resveratrol could keep the brain young. But the research looked at junctions between muscles and nerves in the leg, so it's unclear where this came from.

Interestingly, the media focused on the link with red wine rather than the findings of a calorie-controlled diet.

What kind of research was this?

This was experimental research on animals. The researchers were interested in determining the effect of resveratrol, metformin and calorie restriction on ageing.

Resveratrol occurs naturally in the skins of some red fruits, including some grapes, blueberries and mulberries. Metformin is a drug used to lower blood sugar for people with type 2 diabetes. Both have been linked to speeding up the repair of nerve endings.

While animal research can suggest areas for human research, there's a big difference between humans and mice, so we can't be sure the results apply to anything other than mice.

What did the research involve?

Researchers divided laboratory-bred mice into four groups and fed them either:

  • a normal diet
  • a lower calorie diet from four months of age
  • a diet enriched with resveratrol from one year of age
  • a diet enriched with metformin from one year of age

When the mice were aged two years, they looked at their muscle and nerves, at the meeting point of the two (the neuromuscular junction, or NMJ) in a leg muscle. They also looked at the NMJs of three-month-old mice to see how they compared to the older mice.

They used tissue staining and powerful microscopes to examine the tissues. Four mice were examined for each age group and each diet condition.

To check whether the substances had a direct effect on muscle cells, the researchers also did studies where they grew cells from the mice in the laboratory and fed them with either standard nutrient mix, or a nutrient mix enriched with resveratrol or metformin.

They compared the cell cultures for differences in structure and muscle fibre size.

What were the basic results?

Compared with mice fed a regular diet, those who'd been given resveratrol or who'd had a calorie-restricted diet showed:

  • less fragmentation of tissue at the neuromuscular junction
  • fewer areas where the nerve cells had degenerated, which would have meant that the muscle no longer had input from nerves

The two-year-old mice which had calorie-restricted diets had neuromuscular junctions that were most similar to the three-month-old mice. Metformin had little effect in this experiment.

Looking at the cell cultures, the researchers found that metformin, resveratrol and calorie restriction had an effect on the cross-sectional size of the muscle fibres. The majority of the muscle fibres were small. Mice fed the calorie-restricted diet had a greater proportion of small muscle fibres.

The researchers say that this indicates less ageing as muscle fibres increase in size with ageing.

How did the researchers interpret the results?

The researchers said their findings suggest that "resveratrol preserves motor function [movement] in part by protecting NMJs [neuromuscular junctions] and muscle fibres". They point out that it was "less effective compared with a CR [calorie restricted] diet" in preventing age-related changes.

However, they say, mice were started on the calorie-restricted diet at four months of age, while resveratrol was only started at 12 months of age. They suggest introducing resveratrol earlier might increase the effect.

They said it was "surprising" that metformin had little effect and speculated that this might have been because of the dose used.

Conclusion

Resveratrol has been of interest to anti-ageing scientists for many years and researchers have previously shown it may be linked to a slowing of the decline in thinking and movement, at least in rodents. This study suggests a possible way this might happen.

But the results don't tell us anything about what happens in humans. They suggest this substance may be useful for further research in humans at some point. They certainly don't provide a reason to drink gallons of red wine, in the hope of seeing an anti-ageing effect.

Drinking too much alcohol is a sure-fire way to speed up deterioration of thinking skills, and can cause brain damage. Too much alcohol in the long term is linked to several cancers, heart diseasestroke and liver disease.

Find out whether you're drinking too much, and get tips about cutting down.

Links To The Headlines

Cheers to a long life: This is how red wine can 'help fight the ageing process' – but how much would you have to drink? The Sun, March 7 2017

Red wine compound can slow brain ageing, study finds. The Independent, March 7 2017

Links To Science

Stockinger J, Maxwell N, Shapiro D, et al. Caloric restriction mimetics slow aging of neuromuscular synapses and muscle fibers. Journals of Gerontology: Biological Sciences. Published online March 7 2017.

Mediterranean diet linked to lower risk of one type of breast cancer

NHS Choices - Behind the Headlines -

"Eating a Mediterranean diet 'cuts deadly breast cancer risk by 40%' in postmenopausal women," says the Mail Online of a widely reported study carried out by researchers in the Netherlands.

The researchers looked at data from a study involving more than 60,000 women aged 55-69 over a 20-year period.

At the start of the study, details of the women's diet, physical activity and other cancer-related risk factors were collected.

The researchers then compared the diets of more than 2,000 women who went on to develop breast cancer with a selected group of similar women who didn't develop the cancer.

Overall, there was no link between a Mediterranean diet and breast cancer risk.

However, the researchers found women whose diet was most like a Mediterranean diet were 40% less likely to develop one particular type of breast cancer: oestrogen receptor-positive breast cancer.

As with all studies of this type, it's difficult to separate out the effects of diet and other lifestyle factors, such as exercise and smoking. This makes it difficult to be certain that the differences in risk are the result of the Mediterranean diet alone.

The researchers tried to take into account other factors that could affect the risk of breast cancer, but it's difficult to identify all possible contributing factors.

The Mediterranean diet has been linked to many health benefits. Sticking to a healthy, balanced diet with plenty of fruit and vegetables, wholegrains and some fish, along with a low intake of red meat and sugary foods, is in line with current government recommendations for healthy eating, as set out in the Eatwell Guide.

Where did the story come from?

The study was carried out by researchers from Maastricht University Medical Centre in the Netherlands.

Funding was provided by the Wereld Kanker Onderzoek Fonds Nederland, as part of the World Cancer Research Fund International grant programme.

The study was published in the peer-reviewed International Journal of Cancer. A summary of the study is available to read for free online.

This study has been reported in a number of media sources, who presented the main findings of this story reasonably. But most failed to make it clear in their headline that the link was only found with one type of breast cancer.

What kind of research was this?

This study analysed data from women who had participated in the Netherlands Cohort Study to investigate the link between a Mediterranean diet and a reduced risk of postmenopausal breast cancer (ER-negative breast cancer).

The analysis was effectively a nested case control study, where women in the cohort who developed breast cancer were compared with a selected group of controls from the cohort who didn't develop breast cancer.

As well as looking at all types of breast cancer together, the researchers looked at different types of breast cancer separately.

Around 70% of breast cancers are oestrogen receptor positive (ER positive). This means there are a significant number of oestrogen receptors in the breast cancer tissue. This type of breast cancer can respond well to hormonal treatments.

If oestrogen receptors aren't present in large numbers, it's known as oestrogen receptor-negative (ER negative) breast cancer.

The Mediterranean diet has been linked to better health for a number of years. It's thought the diet may reduce the risk of cancer because of its high fibre and antioxidant content, and because it helps maintain a healthy body weight.

This type of study is good for identifying possible links between lifestyle factors and disease. But the main limitation is that groups of people who have different diets may also differ in other ways that affect their risk of disease, and it's difficult to separate out the effects of all of the contributing factors.

Researchers will often use various statistical techniques to try to take potential confounding factors into account, but it's difficult to be sure this has been completely successful.

What did the research involve?

The researchers used data from women participating in the Netherlands Cohort Study (NLCS).

At the start of the study, the women completed a questionnaire about their cancer risk factors.

The questionnaire collected data on the following:

  • dietary intake
  • smoking habits
  • physical activity
  • body measurements

Dietary information was collected using a 150-item semi-quantitative food frequency questionnaire for the year prior to joining the study. This was checked using a nine-day diet record.

This dietary data was used to calculate how close the women's diets were to the typical Mediterranean diet pattern.

Although drinking a moderate amount of alcohol is a normal part of a Mediterranean diet, the researchers didn't consider alcohol to be part of the Mediterranean diet in their analysis because alcohol consumption is a risk factor for breast cancer.

The researchers identified the women who developed cancer by looking at the Netherlands Cancer registry records and the nationwide Dutch Pathology Registry (PALGA).

Once the researchers identified the women who developed cancer during the study, they compared their diet with that of a randomly selected group of women from the cohort who had no history of cancer (except some cases of skin cancer) at the start of the study, and whose diet information was complete.

What were the basic results?

A total of 62,573 women aged 55-69 were followed for an average of 20.3 years (1986-2007). During the follow-up period, 3,354 women developed breast cancer.

Women whose diets were more like the Mediterranean diet were generally more physically active, educated to a higher level, and more likely to have taken oral contraceptives at some stage.

Those whose diets were less like the Mediterranean diet tended to be older, were less likely to have had any children, and more likely to be current smokers and have a family history of breast cancer (in some analyses).

No significant association was seen between sticking to a Mediterranean diet and overall risk of breast cancer or ER-positive breast cancer.

Women whose diets most closely resembled a Mediterranean diet were 40% less likely to develop ER-negative breast cancer than women whose diet was least like a Mediterranean diet (hazard ratio [HR] 0.60,95% confidence interval [CI] 0.39 to 0.93).

How did the researchers interpret the results?

The researchers concluded that, "Our findings support an inverse association between [Mediterranean diet] adherence and, particularly, [oestrogen] receptor-negative breast cancer.

"This may have important implications for prevention because of the poorer prognosis of these breast cancer subtypes."

Conclusion

This study aimed to assess whether sticking to a Mediterranean diet was associated with a reduction in breast cancer risk for postmenopausal women.

The researchers found following a Mediterranean diet was indeed associated with a reduction in breast cancer risk – but only for ER-negative breast cancer.

This study has both strengths and weaknesses. Its large, prospective design and long period of follow-up are strengths.

The typical weakness of this type of study is that many factors are likely to contribute to risk, and it's very difficult to be sure the factor in question – in this case, eating a Mediterranean diet – is wholly responsible for the differences seen.

The researchers did take other factors into account in their analysis, but it's possible that the effects of unknown or unmeasured factors remain.

The researchers also note other possible limitations, including: 

  • They didn't know the ER status of all of the breast cancer cases, so they had to exclude some from their analysis.
  • It's possible there's an element of inaccuracy in the responses from the food frequency questionnaires, as is often the case when participants are asked to recall information.
  • The women may have altered their diet or physical habits during the study period, meaning information collected at the start of the study no longer accurately reflected their lifestyles, and this was not accounted for.

Although this study has limitations, the Mediterranean diet has been linked to many health benefits, including a healthier heart.

A Mediterranean diet is similar to the government's healthy eating advice set out in the Eatwell Guide, which also involves eating plenty of fruit and vegetables, and not too much red meat or sugary foods.

Links To The Headlines

Mediterranean diet may reduce risk of form of breast cancer – study. The Guardian, March 6 2017

Eating a Mediterranean diet 'cuts deadly breast cancer risk by 40%' in post-menopausal women. Mail Online, March 6 2017

Mediterranean diet could slash risk of deadly breast cancer by 40pc. The Daily Telegraph, March 6 2017

Can a Mediterranean diet really stop breast cancer? We look at the facts. Daily Mirror, March 6 2017

The diet to SLASH risk of cancer in women: Breast tumours are cut by 40 per cent. Daily Express, March 6 2017

Mediterranean diet 'cuts risk of deadly form of breast cancer by 40%'. The Independent, March 6 2017

Links To Science

Van den Brandt PA, Schulpen M. Mediterranean diet adherence and risk of postmenopausal breast cancer: results of a cohort study and meta-analysis. International Journal of Cancer. Published online March 5 2017.

Is red hair gene linked to increased risk of Parkinson's?

NHS Choices - Behind the Headlines -

"Redheads are more likely to develop Parkinson's," claims the Mail Online after a study found the gene that makes people with red hair susceptible to skin cancer also increases the risk of brain disease.

But the study didn't actually look directly at redheads (human ones, anyway). Instead, it used mice to look at whether a red hair gene called MC1R might be important in the region of the brain affected by Parkinson's. The study found the MC1R gene was active in this brain region in mice.

When researchers stopped the gene working, it led to nerve cells in this region dying, resulting in the mice developing progressive problems with movement.

The researchers suggested drugs targeting MC1R might help in treating Parkinson's.

The causes of Parkinson's disease in humans are not completely understood. While this research supports the possibility this gene plays a role, there are likely to be other genetic factors involved, as well as environmental factors.

Not all studies in humans have found a link between variants in the MC1R gene and Parkinson's. Even if there is some increase in risk associated with certain forms of this gene, it's likely to be relatively small.

Where did the story come from?

The study was carried out by researchers from Massachusetts General Hospital, Harvard Medical School and the University of California in the US, and the Tongji University School of Medicine in China.

The work was funded by the National Institute of Neurological Disorders and Stroke, the National Natural Science Foundation of China, the RJG Foundation, the Michael J Fox Foundation, the Milstein Medical Asian American Partnership Foundation, and the US Department of Defense.

The news headlines fail to capture the uncertainty about whether redheads are at greater risk of Parkinson's. Some studies have suggested this may be the case, but the evidence isn't conclusive.

The current research didn't look at this question directly – it looked at whether researchers could find a biological reason why there might be a link.

What kind of research was this?

This animal research looked at how a gene that determines whether people have red hair might also play a role in Parkinson's disease.

Other studies have suggested people with malignant melanoma – a skin cancer more common in redheads and fair-skinned people – might be at greater risk of Parkinson's. Studies have also shown higher than expected rates of melanoma in people with Parkinson's.

The researchers thought the link between the two conditions might be down to a gene called the melanocortin 1 receptor (MC1R) gene. People who carry certain versions of the MCR1 gene tend to have red hair and fair skin.

Some studies – but not all – have suggested carrying certain red hair MC1R variants and having red hair are also associated with an increased risk of Parkinson's disease.

The researchers wanted to look at whether the MC1R gene has an effect on nerve cells in the brain that produce a specific signalling chemical called dopamine.

In Parkinson's, these nerve cells die off, which causes the slow movement problems characteristic of the disease. If the gene is important in these cells, this would explain why there might be a link between red hair and Parkinson's.

Humans and other animals share many of their genes, so researchers often investigate what genes do in animals to give strong pointers of their roles in humans.

What did the research involve?

The researchers studied mice with a defective form of the MC1R gene. These mice have yellow coats, the equivalent of red hair in humans. The researchers compared these with normal mice with functioning MC1R genes.

They first looked at whether the MC1R gene in normal mice was active in the dopamine-producing nerve cells in the part of the brain affected by Parkinson's disease, the substantia nigra.

They compared the abnormal mice with the non-functioning MC1R gene and the normal mice to see whether the substantia nigra looked different and whether the mice moved differently. They also looked at how the defective gene might affect brain cells.

One way of producing mice with a Parkinson's-like condition is by exposing them to chemicals that kill the dopamine nerve cells.

The researchers looked at whether the abnormal mice were more susceptible to two different chemicals that can do this.

They then looked at whether "switching on" the protein made by the MC1R gene chemically might protect normal mice against the effects of one of these Parkinson's-inducing chemicals.

What were the basic results?

The researchers found the MC1R gene was normally active in the dopamine-producing nerve cells of the substantia nigra, which are typically affected by Parkinson's disease.

Mice with an inactive MC1R gene showed progressive problems with their movement. They moved around less in an open area compared with normal mice of a similar age, and the problem got worse as they aged.

These mice appeared to be losing dopamine-producing nerve cells in the substantia nigra.

Additional experiments suggested brain cells in these mice had more DNA damage from naturally occurring chemicals called free radicals.

The abnormal mice were more susceptible than normal mice to two different Parkinson's-inducing chemicals.

The researchers also found chemically activating the protein made by the MC1R gene in normal mice reduced the effects of these toxic chemicals.

How did the researchers interpret the results?

The researchers concluded that genetically "shutting off" MC1R signalling in mice leads to the death of some dopamine-producing nerve cells.

Conversely, "switching on" MC1R signalling helps protect these cells from damage by chemicals that normally produce Parkinson's-like effects in mice.

The researchers suggest this may mean drugs that target MC1R might help in Parkinson's. It also supports the possibility that the MC1R gene plays a role in the risk of both melanoma and Parkinson's disease.

Conclusion

This study looked at the role the red hair gene MC1R plays in the brains of mice. The findings suggest the gene has a part to play in keeping certain nerve cells in the brain alive.

The cells in question are those that die off in Parkinson's disease and cause the condition's characteristic movement problems.

These findings in mice are likely to need further investigation in human cells and tissue in lab studies.

Exactly what causes brain cells to die, causing Parkinson's disease, is unknown. As with many conditions, it's thought both genetic and environmental factors could play a role.

Research like this helps us gain a better understanding of the disease and how it might be treated or prevented.

But Parkinson's is a complex disease, and this new study has only looked at one small piece of a much bigger puzzle. For redheads, it may be comforting to know this link has not yet been proven beyond a doubt.

And not all studies in humans have found a link between variants in the MC1R gene and Parkinson's. In fact, a recent systematic review by some of the authors of this study looked into this.

The review gathered studies published to date that have investigated the link between red hair variants of the MC1R gene and Parkinson's disease.

Six studies assessing links with two variants of this gene were identified, but the studies couldn't quite exclude the possibility of no effect when pooled.

The review also identified two studies looking at hair colour. These studies found people with red hair were more likely to develop Parkinson's than people without red hair.

But these observational studies have several limitations – notably, they can't prove clear cause and effect because many other genetic, environmental and lifestyle factors could also be influencing any links seen.

And even if there is some increase in risk caused by this pigment gene, it's likely to be relatively small.

Links To The Headlines

Redheads are more likely to develop Parkinson's: Gene that makes gingers susceptible to skin cancer also drives up risk of brain disease, study reveals. Mail Online, March 3 2017

Ginger Gene: Ed Sheeran, Nicole Kidman and Prince Harry are at greater risk of these diseases – and their red hair is to blame. The Sun, March 3 2017

Links To Science

Xiqun Chen, Hongxiang Chen, Waijiao Cai, et al. The Melanoma-Linked "Redhead" MC1R Influences Dopaminergic Neuron Survival. Annals of Neurology. Published online January 23 2017

Artificial mouse embryos created

NHS Choices - Behind the Headlines -

"Artificial human life could soon be grown from scratch in the lab, after scientists successfully created a mammal embryo using only stem cells," reports The Daily Telegraph. This is an extremely premature claim as it is based on a laboratory study using mouse stem cells. Stem cells are cells that have the potential to be transformed into specific and specialised cells, such as bone marrow or fat cells.

Rather than using a fertilised egg, researchers from Cambridge University artificially grew an embryo in a three-dimensional structure by combining two types of stem cells – those that would develop into an embryo and those that would normally develop into the placenta. They found that the arrangement of cell development was very similar to the development of a usual mouse embryo.

While the media described the possibility of artificially formed human life soon becoming a reality, this is very early-stage research. Aside from the strict regulations about embryo research, the technical challenges of developing artificially formed human life are immense.

Reports about artificially created "designer babies" remain the stuff of science fiction.

A more down-to-earth implication of this research is that it may help provide more information about the early stages of pregnancy, which could eventually lead to new fertility treatments.

 

Where did the story come from?

The study was carried out by researchers from the University of Cambridge and Akdeniz University, Turkey.

The study was funded by the Wellcome Trust and the European Research Council and was published in the peer-reviewed journal Science.

The UK media reporting of the story was generally accurate, describing the methods used by the researchers in this exploratory lab study.

The Guardian reported: "Artificial mouse cells grown from outside the body in a blob of gel shown to morph into primitive embryos, roughly equivalent to one third of way through pregnancy", making clear that this was a study carried out in mice and not humans.

 

What kind of research was this?

This was an experimental laboratory study in mice that aimed to mimic interactions in the development of an embryo by combining the early embryonic stem cells with the cells that form the placenta within a 3D scaffold to try to develop an artificial embryo. This scaffold is a gel that allowed the structure to grow in three dimensions

While these laboratory studies are good at discovering new biological processes and ways of mimicking them, it must be remembered that they are often – as in this case – very early-stage research that cannot yet be applied to humans. Laboratory research involving human embryos is strictly controlled and regulated.

 

What did the research involve?

The study looked at the development of mouse embryos combining embryonic stem cells and cells that form the placental tissue, rather than starting from a fertilised egg.

The researchers took mouse embryonic stem cells (ES cells) and trophoblast stem (TS) cells, which are cells that are used to develop the placenta in normal pregnancy, and put them in a scaffold in a gel culture that allowed them to develop together.

 

What were the basic results?

They found that as the cells multiplied, structures made from the ES and TS cells developed in the 3D scaffold.

Following the seven days, the TS cells, which will go on to become the placenta, grew in a separate section to the ES cells – which will form the embryo.

Of all the structures they created, 22% were made from both ES and TS cells, 61% from ES cells only and 17% from TS cells only.

The ES and TS cells developing together in a 3D scaffold arranged themselves into a structure very similar to a natural embryo.

The ES cells further split into two groups, one cluster called the mesoderm would normally go on to develop into the heart, bones and muscles. The other section would normally go on to develop into the brain, eyes and skin.

They found that the timing and spatial arrangement of the cell development was very similar to the development of a usual mouse embryo.

 

How did the researchers interpret the results?

The authors conclude that "our study demonstrates the ability of distinct stem cell types to self-assemble in vitro (in laboratory settings) to generate embryos whose morphogenesis, architecture and constituent cell types resemble natural embryos".

 

Conclusion

This early-stage research offers a good insight into the development of mouse embryos and the sequence of biological steps that take place up to the point of implantation in the womb and immediately afterwards. They could provide an insight into the early stages of human life.

However, this does not mean that the creation of artificial human life is now possible:

  • The study was carried out on mice stem cells, which have a very different biological make-up to humans so the processes may not be identical with human cells.
  • While the artificial mouse embryo seemed to behave like a natural one, it is unlikely it could develop to a healthy foetus, as other components – such as the yolk sac that provides nutrition – were missing.
  • Not all embryonic and trophoblast structures developed and the biological reason for this is not known.

Most importantly, experiments involving human embryos or embryonic tissues are strictly regulated in the UK. Current legislation prohibits the development of embryos beyond a limit of 14 days.

As Professor James Adjaye, Chair of Stem Cell Research and Regenerative Medicine at Heinrich Heine University says: "As always, these types of experiments using human stem cells are regulated but there is no 'universal regulatory body'. Each country has its own regulatory body, which will ultimately decide on whether human [embryonic and trophoblast stem cell] embryos can be generated and for how long they can be left in the petri dish to develop further. Of course, there should be an international dialogue on the regulation of such experiments."

It is reported that the research team behind this work now plans to carry out similar work using human cells – a move that is sure to attract more media controversy.  

Links To The Headlines

Artificial human life could soon be grown in lab after embryo breakthrough. The Daily Telegraph, March 2 2017

Artificial 'embryos' created in the lab. BBC News, March 3 2017

Cambridge scientists create first self-developing embryo from stem cells. The Guardian, March 3 2017

Babies created ‘WITHOUT sperm or eggs’ could be reality as scientists grow artificial mouse embryos. The Sun, March 3 2017

Links To Science

Harrison SE, Sozen B, Christodoulou N, et al. Assembly of embryonic and extra-embryonic stem cells to mimic embryogenesis in vitro. Science. Published online March 2 2017

Regular activity may help some people stay 'fat and fit'

NHS Choices - Behind the Headlines -

"You can be fat and healthy," is the misleading headline from the Daily Mail. While a Dutch study did find that activity could help avoid the increased risk of cardiovascular disease associated with obesity, it didn't look at the risks of other obesity-related conditions such as type 2 diabetes and some types of cancer.

The study of 5,344 people aged 55 or over concluded that:

  • people who are a healthy weight and do plenty of physical activity had the lowest risk of heart attack or stroke
  • people who were overweight or obese, but physically active, had the same risk as people of a healthy weight who exercised regularly
  • people at highest risk were those who were obese and did less exercise

It is worth noting that the category researchers used to define "low activity" – an average of two hours of moderate activity a day – was actually more than many people manage in the UK. So the risks of heart disease may actually be higher for people in the UK who are not regularly physically active, whatever their weight.

Another important point is that the study only looked at the risk of cardiovascular disease. Other obesity-related conditions were not considered. And as we have covered previously, 11 types of cancer are now linked to being overweight.

In conclusion, exercise is always beneficial, but if you can make the extra effort to achieve a healthy weight, then the benefits may be enhanced. If you want to lose weight you can try the NHS Weight Loss Plan.

 

Where did the story come from?

The study was carried out by researchers from Erasmus University Medical Centre in the Netherlands and was funded by Erasmus University, the Netherlands Organisation for Scientific Research, the Netherlands Organisation for Health Research and Development, the Research Institute for Diseases in the Elderly, the Ministry of Education, Culture and Science, the Ministry for Health, Welfare and Sports, the European Commission and the municipality of Rotterdam.

Although several of the researchers work for a research centre funded by Nestlé, there does not seem to be a conflict of interest. The study was published in the peer-reviewed European Journal of Preventative Cardiology.

The Daily Mail's headline that "You can be fat and healthy" is misleading as the study looked only at cardiovascular disease. Being overweight or obese also affects the chances of other conditions, including cancer and diabetes.

And this came only a day after the same newspaper reported "How being obese can increase the risk of developing 11 types of cancer including breast, stomach and bowel", so you could forgive their readers for being more than a little confused.

Also, the study's authors specifically say their results do not refute the cardiovascular risk associated with overweight and obesity. 

 

What kind of research was this?

This was a prospective cohort study which followed up groups of adults aged 55 and over for an average of 10 years.

This type of study is useful for spotting patterns and links between factors such as body weight, activity levels, and the development of disease over time. But it cannot prove that one factor causes another.

 

What did the research involve?

Researchers interviewed and measured 6,510 people aged 55 or above in Rotterdam, in two phases (1990 to 1993 and 2000 to 2001). They were asked about their activity levels and diet, using a questionnaire. Researchers recorded their body mass index (BMI).

They then followed up what happened to people over the following years.

They analysed the figures to see whether people who were overweight or obese were more likely to have a heart attack or stroke during follow up, and how their reported levels of physical activity affected this risk.

Researchers excluded people who already had cardiovascular disease, had important missing data, or who were underweight. They were left with 5,344 people to include in the analysis.

Physical activity was defined as high or low, based on whether they did more or less than the average amount of moderate physical activity reported by people in the study.

Average amounts of activity in the high group were four hours a day, while average amounts in the low group were two hours a day.

Moderate physical activity is activity that raises your heart rate and makes you a little out of breath, such as brisk walking.

The researchers took account of the following potentially confounding factors:

  • alcohol use
  • education level
  • smoking
  • dietary information (although this was missing for almost a quarter of participants)
  • family history of early heart attack

 

What were the basic results?

People who were obese or overweight did not have an overall increased risk of heart attack or stroke compared to people of a healthy weight, above that which might have been caused by chance. However, when the researchers took account of physical activity levels, patterns emerged.

Compared to people of normal weight with high activity levels:

  • People who were overweight with low physical activity levels had a 33% higher risk of a heart attack or stroke (hazard ratio [HR] 1.33, 95% confidence interval [CI] 1.07 to 1.66).
  • People who were obese with low physical activity levels had a 35% higher risk of heart attack or stroke (HR 1.35, 95% CI 1.04 to 1.75).
  • People with low physical activity levels were at higher risk of heart attack or stroke, compared to people with high activity levels, regardless of how much they weighed (HR 1.22, 95% CI 1.06 to 1.41).

 

How did the researchers interpret the results?

The researchers said: "Our findings suggest that the beneficial impact of physical activity on CVD [cardiovascular disease, including heart attack or stroke] might outweigh the negative impact of body mass index among middle-aged and elderly people." They say this "emphasises the importance" of physical activity for everyone, at all ages.

However, they don't say that being overweight has no health consequences. They say that being very physically active might offset the known cardiovascular risk associated with being overweight.

 

Conclusion

As people often say, if exercise was a medicine, it would be hailed as a miracle cure. This study suggests that what we already know about the benefits of exercise may extend to reducing risk of cardiovascular disease for middle aged and older people, even if they are overweight or obese.

But the study has some limitations. This type of study can't prove that one factor – exercise – is responsible for the lower risk of heart attack and stroke among overweight or obese people who exercise more. It's possible that other factors are important – for example people's income may be linked to their opportunities for exercise.

In addition, people are more likely to be physically active when they are in good health, so lower levels of physical activity might suggest people are already unhealthy, and therefore more at risk of heart attack or stroke.

The amounts of exercise people reported are strikingly high. The study didn't measure activity through monitoring devices, so we can't be sure that people didn't overstate how much activity they were doing.

The study included physical activity for transport as well as leisure, so one possibility is that people in Rotterdam get around on foot or bicycle a lot (a factor that may be more significant in the Netherlands than the UK).

So the differences in activity levels from the usual levels reported in the UK mean that the results may not translate to a UK population. Latest figures show only 67% of men and 55% of women in England meet guidelines to do half an hour, five days a week, of moderate physical activity.

While physical exercise is certainly a good thing, we can't be sure that it completely negates the importance of keeping to a healthy weight. Obesity increases the chances of diabetes, cancer and other diseases, as well as cardiovascular disease.

Read more about the benefits of exercise.

Links To The Headlines

You can be fat AND healthy: Obese middle aged are at no greater risk of a heart attack...if they exercise. Daily Mail, March 3 2017

Links To Science

Koolhaas CM, Dhana K, Schoufour JD, et al. Impact of physical activity on the association of overweight and obesity with cardiovascular disease: The Rotterdam Study. European Journal of Preventive Cardiology. Published online February 28 2017

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