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."



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

Could cows be the clue that leads to an HIV vaccine?

NHS Choices - Behind the Headlines -

"Cows have shown an 'insane' and 'mind-blowing' ability to tackle HIV which will help develop a vaccine, say US researchers," BBC News reports.

The report is based on new research in cows that were immunised against HIV before having their immune response to HIV assessed. There's currently no vaccine for HIV because the virus mutates so easily.

Scientists aim to develop a vaccine that is not only potent (produces a strong immune system response), but also causes the immune system to make "broadly neutralising antibodies" (able to protect against many different strains of virus).

The four cows in this study were immunised against HIV with a specially developed vaccine to test both strength and "breadth". Some cows developed a weak response with reasonable breadth (20% – or it helped protect against 1 in 5 strains tested in the lab) at 42 days. One cow in particular showed an impressive immune response to most of the lab strains of HIV ("96% breadth") 381 days after being vaccinated.

This research, done in a small number of cows, may help scientists work out if immune proteins made in cows could potentially be used to protect humans against a range of HIV strains.

While this is certainly welcome news, it doesn't mean an effective HIV vaccine is guaranteed to appear in the future. The most effective way to protect yourself from HIV is to always use a condom during sex, including oral and anal sex. Men who have sex with other men are particularly at risk if they don't practise safe sex.

Read more advice about HIV and gay health.


Where did the story come from?

The study was carried out by researchers from The Scripps Research Institute the International AIDS Vaccine Initiative, Texas A&M University, Kansas State University, and Ragon Institute of MGH, MIT and Harvard, all in the US.

The research was funded by various grants from the International AIDS Vaccine Initiative, the National Institutes of Health, the Centre for HIV/AIDS Vaccine Immunology and Immunogen Discovery and the US Department of Agriculture. The study was published in the peer-reviewed medical journal Nature.

The UK media reporting was generally accurate and made clear the research was carried out in cows and not humans. However, the Mail Online's claim that "An injection may soon be available that prevents the virus spreading and could rid sufferers of the infection" is incredibly optimistic.

This research is at a very early stage and will need to be repeated and refined before testing in humans is considered. There is no imminent vaccine for HIV.


What kind of research was this?

This was an investigational laboratory study carried out using cows. Researchers attempted to immunise cows against HIV and assessed their response to the vaccine.

HIV infects the body's immune system, causing progressive damage that eventually stops the body's ability to fight off infection. The virus attaches itself to immune cells that protect the body against bacteria, viruses and other germs. Once HIV has attached itself, it enters the cell and uses it to create thousands of copies of itself. The copies then leave the original immune cell and kill it in the process.

The process continues until the number of immune cells is so low, the immune system stops working. This process can take as long as 10 years, during which time the person may feel and appear to be well.

Thankfully, due to medical advances, antiretroviral drugs are now available that help protect the immune system from further damage and prevent secondary infections.


What did the research involve?

Researchers aimed to immunise cows with a substance called an immunogen, which are designed to provoke an immune response.

In this study the researchers used an immunogen called BG505 SOSIP. This mimics the outside of the HIV virus to produce an immune response. Researchers were able to see if the immunogens were "broad" (could neutralise many different viral strains) and potent by measuring how long it took for the immune response to occur; the quicker the response the more potent a vaccine tends to be.

Researchers chose to look at cows because, unlike most animals, they have longer amino acid chains.  Amino acids are the "building blocks" of proteins. Previous research has found that a small proportion of people with HIV who develop a level of natural immunity to the virus also have similarly long amino acid chains.

Four six-month-old calves were immunised with the BG505 SOSIP immunogen and the researchers looked at the subsequent immune response.

What were the basic results?

All cows developed immune cells to HIV 35 to 50 days following two injections. One cow showed an immune response that could neutralise 20% of HIV strains tested in the lab in 42 days and another neutralised 96% of HIV strains in 381 days.

When analysing the proteins created as part of the immune response, the researchers found that one in particular binds to a key HIV site that the virus uses to infect cells.


How did the researchers interpret the results?

The researchers conclude that they "have shown that immunization with a well-ordered immunogen in cows reliably and rapidly elicits broad and potent neutralizing serum responses in contrast to previous experiments in other animals."



This early stage research on cows indicates that they had a broad and quick immune response to HIV infection when given a specific vaccine. Because the immune proteins produced in cows are able to neutralise many different strains of HIV virus, the authors suggest this potentially gives them an edge over the human proteins that have been looked at so far.

As always with animal studies it is important to remember that what works in cows might not work in the same way in humans. Many drug studies that appear promising at first, fall at the first hurdle once humans are involved.

The study was also carried out on just four cows and the most promising finding – neutralisation of 96% of HIV strains in 381 days – was found in just one cow. It is therefore best seen as promising early research, rather than a proven cure.

While we all hope an HIV vaccine or cure may be on the horizon, until that time, using a condom during penetrative, oral and anal sex is the most effective method of preventing infection with HIV.

Links To The Headlines

'Mind-blowing' cows hold clue to beating HIV. BBC News, July 21 2017

Scientists may be one step closer to a cure for HIV: Injection prevents the virus spreading and could rid sufferers of the disease. Mail Online, July 21 2017

Links To Science

Sok D, Le KM. Vadnais M, et al. Rapid elicitation of broadly neutralizing antibodies to HIV by immunization in cows. Nature. Published online July 20 2017

Nine lifestyle changes may reduce risk of dementia

NHS Choices - Behind the Headlines -

"Nine lifestyle changes can reduce dementia risk," BBC News reports. A major review by The Lancet has identified nine potentially modifiable risk factors linked to dementia.

The risk factors were:

  • low levels of education
  • midlife hearing loss
  • physical inactivity
  • high blood pressure (hypertension)
  • type 2 diabetes
  • obesity
  • smoking
  • depression
  • social isolation

However, it's important to note that even if you add up the percentage risk of all of these factors, they only account for about 35% of the overall risk of getting dementia. This means about 65% of the risk is still due to factors you can't control, such as ageing and family history.

Although not guaranteed to prevent dementia, acting on the risk factors above should improve your physical and mental wellbeing.

What is dementia?

Dementia refers to a group of symptoms associated with the gradual decline of the brain and its abilities. Symptoms include problems with memory loss, language and thinking speed.

The most common cause of dementia is Alzheimer's disease. Vascular dementia is the next most common, followed by dementia with Lewy bodies.

For more information, visit the NHS Choices Dementia Guide.

Where did the review come from?

This review was written by the Lancet Commission on Dementia Prevention, Intervention and Care (LCDPIC). The commission is established by convening experts in the field to consolidate current and emerging evidence on preventing and managing dementia. It generates evidence-based recommendations on how to address risk factors and dementia symptoms. These are presented in this review.

The LCDPIC endeavoured to use the best possible evidence to make the recommendations. However, in cases where the evidence was incomplete, it summarised the balance of the evidence, drawing attention to the strengths and limitations.

The media in general has covered the review responsibly and accurately, with helpful comments from experts in the field.

What does the review say?

The review examines aspects of how better to manage the burden of dementia: the risk factors, interventions for prevention and interventions for treatment.

Risk factors

The LCDPIC discusses the effects of several different risk factors potentially linked to dementia.

The review reported population attributable fractions (PAFs). PAFs are an estimate of the proportion of cases of a certain outcome (in this case, dementia) that could be avoided if exposure to specific risk factors were eliminated – for example, how many lung cancer cases would be prevented if nobody smoked.

Using the available evidence, researchers calculated PAFs for the following risk factors.


Less time in education – specifically, no secondary school education – was responsible for 7.5% of the risk of developing dementia.

Hearing loss

The relationship between hearing loss and the onset of dementia is fairly new. It's thought that hearing loss may add stress to an already vulnerable brain with regard to the changes that occur. Hearing loss may also increase feelings of social isolation. However, it's also possible that old age could have a role to play in this association.

The LCDPIC analysis found that hearing loss could be responsible for 9.1% of the risk of developing dementia.

Exercise and physical activity

A lack of physical activity was shown to be responsible for 2.6% of the risk of dementia onset. Older adults who do not exercise are less likely to maintain higher levels of cognition than those who do engage in physical activity.

Hypertension, type 2 diabetes and obesity

These three risk factors are somewhat interlinked; however, all had PAFs lower than 5%, with hypertension contributing the greatest risk of the three:

  • hypertension – 2%
  • type 2 diabetes – 1.2%
  • obesity – 0.8%

Smoking was found to contribute to 5.5% of the risk of dementia onset. This is a combination of smoking being more widespread in older generations, and there being a link between smoking and cardiovascular conditions.


It's possible that depressive symptoms increase dementia risk due to their effect on stress hormones and hippocampal volume. However, it's not clear whether depression is a cause or a symptom of dementia. It was found to be responsible for 4% of the risk of developing dementia.

Lack of social contact

Social isolation is increasingly thought to be a risk factor for dementia as it also increases the risk of hypertension, heart conditions and depression. However, as with depression, it remains unclear whether social isolation is a result of the development of dementia.

It was found to contribute to 2.3% of the risk of developing dementia.

Prevention of dementia

The review highlights that although there are potentially modifiable risk factors for dementia, this does not mean dementia as a condition is preventable or easy to treat. It is evident that there are multiple risk factors contributing to the onset of the disease. However, some interventions that could prevent onset include:

  • Using antihypertensive drugs, such as ACE inhibitors, in people with hypertension.
  • Encouraging people to switch to a Mediterranean diet, which is largely based on vegetables, fruit, nuts, beans, cereal grains, olive oil and fish. This has been proven to improve cardiovascular health, and may help with the symptoms of type 2 diabetes, obesity and hypertension.
  • Encouraging people to meet the recommended physical activity levels for adults. Again, regular exercise may help with the symptoms of type 2 diabetes, obesity and hypertension.
  • Using cognitive interventions, such as cognitive training, which involves a series of tests and tasks to improve memory, attention and reasoning skills. The review points out, however, that the clinical effectiveness of most commercially available brain-training tools and apps is unproven.
  • Encouraging people to become more socially active. This could be by organising social activities – book clubs, for example – for older adults. 
  • Continuing to provide support to smokers who want to quit.

Read more about ways to reduce your dementia risk.

Links To The Headlines

Nine lifestyle changes can reduce dementia risk, study says. BBC News, July 20 2017

Lifestyle changes could prevent a third of dementia cases, report suggests. The Guardian, July 20 2017

Third of dementia cases are preventable through nine lifestyle changes, say researchers. The Independent, July 20 2017

The nine lifestyle changes that could save you from dementia. The Daily Telegraph, July 20 2017

A third of dementia cases are 'preventable' – with lifestyle choices a key factor, experts say. Daily Mirror, July 20 2017

These nine lifestyle changes could PREVENT dementia – 'stopping a third of Alzheimer's cases'. The Sun, July 20 2017

From hearing loss to loneliness, the NINE dementia risk factors: One in three cases could be prevented by changes to lifestyle. Mail Online, July 20 2017

Links To Science

Livingston G, Sommerlad A, Orgeta V, et al. Dementia prevention, intervention, and care. The Lancet. Published online July 19 2017

High-dose vitamin D 'doesn't prevent colds and flu in kids'

NHS Choices - Behind the Headlines -

"Vitamin D will not protect your child from a cold: myth-busting study says 'more isn't always better' to help toddlers stay healthy," says the Mail Online.

The story is based on a study that looked at whether giving healthy young children high doses of vitamin D in the winter protects them from colds and flu better than the standard recommended lower dose.

It found children taking the high dose were just as likely to get ill as children taking the standard dose – both groups got an average of about one case of cold or flu during the winter.

There was a reduction in flu cases with the high dose, but flu cases were uncommon and therefore the reduction was small (four fewer infections per 100 children over the winter season).

Current UK advice is that children aged one to four years old should be given a daily supplement containing 10 micrograms (mcg) of vitamin D – the same as the standard dose in this study.

Giving children the higher dose used in the study (50mcg) seems unlikely to offer much benefit for winter colds and flu if they're generally healthy.

Where did the story come from?

The study was carried out by a large group of researchers at various centres in Canada who were part of the TARGet Kids! Collaboration. This group is studying the health of Canadian children and the impact of early health in later life.

It was funded by the Canadian Institutes of Health Research Institutes of Human Development, Child and Youth Health and Nutrition, Metabolism and Diabetes, and the Thrasher Research Fund.

The vitamin D used in the study was provided for free by the manufacturer Ddrops.

The study was published in the peer-reviewed Journal of the American Medical Association (JAMA).

The Mail Online provides good coverage of this story, making it clear that the study isn't challenging the usefulness of the recommended vitamin D dosage, but saying more isn't better for colds.

What kind of research was this?

This randomised controlled trial (RCT) compared the effect of high- and standard-dose vitamin D on the risk of children catching a cold or flu in winter.

Observational studies have suggested that people with low vitamin D levels are at greater risk of getting viral infections affecting their upper airways – essentially colds or the flu.

Young children in the US and the UK are advised to take a daily dose of around 10mcg (400 international units, IU) of vitamin D.

The researchers wanted to see if taking five times as much (50mcg or 2,000 IU) during the winter might be even better for preventing colds and flu.

We get most of our vitamin D from sunlight and some food sources, such as eggs and oily fish like tuna.

Winter is when our vitamin D levels tend to be lower because there's less sunshine, and is also when we tend to get more upper airway infections. It's plausible that giving more vitamin D might be helpful at this time of year.

Assigning children to receive either the standard or high dose of vitamin D at random makes sure the groups are as similar as possible before the study starts.

This means that any difference between the groups in how many times they got ill would be directly caused by what vitamin D dose they were taking.

What did the research involve?

The researchers enrolled 703 healthy children aged between one and five years old.

They randomly assigned the children to receive either 10mcg or 50mcg of vitamin D by mouth each day during winter. They then compared how often the children got colds or flu over this time.

The children were all from Toronto in Canada and were recruited at "well-child visits" to paediatric or family medicine practices between September and November 2015.

Children with any chronic illnesses (other than asthma) and those born prematurely weren't eligible to take part. The vitamin D3 given to both groups was given as a drop a day of identical-looking and tasting liquid.

Parents and children didn't know what dose they were taking. The parents were told not to give their children any other supplements containing vitamin D during the study.

The children took the drops for between four and eight months.

Whenever the children got symptoms of a cold, their parents filled in a checklist to record what symptoms they had.

Parents were also trained to take a swab of the inside of their child's nose and send it to the lab. The researchers then tested the swab for viruses.

The main outcome the researchers were interested in was how often the children got colds or flu that could be confirmed as being viral infections by laboratory tests.

The researchers also compared how often the parents reported their child as having a cold or the flu.

Children went to the clinic to have blood samples taken to measure vitamin D levels at the four and eight-month mark.

Almost all (99.4%) of the children who started the study remained in it until the end and could be included in the analyses.

What were the basic results?

At the end of the study, children in the high-dose group had higher levels of vitamin D in their blood than those taking the low dose.

The parents didn't report noticing that their children had any side effects from taking the vitamin D drops.

But high-dose vitamin D didn't reduce the number of colds and flu the children got over the winter.

On average there were:

  • 1.97 cases in the high-dose group and 1.91 cases in the standard-dose group of parent-reported cases of cold and flu
  • 1.05 cases in the high-dose group and 1.03 in the standard-dose group of laboratory-confirmed cases of cold and flu

The differences between the groups were very small and not large enough to be statistically significant.

The higher dose of vitamin D did halve the risk of flu compared with the standard dose (incidence rate ratio [iRR] 0.50, 95% confidence interval [CI] 0.28 to 0.89).

But there were very few cases of flu – only 16 in the 349 children in the high-dose group and 31 in the 354 children in the low-dose group – so the difference of four fewer cases per 100 children (CI 1-8 fewer cases per 100 children) over the winter season wasn't considered to be an important reduction.

How did the researchers interpret the results?

The researchers concluded that giving 50mcg of vitamin D a day to healthy young children in the winter didn't reduce the number of upper airway infections overall compared with the standard dose of 10mcg a day.

They said: "These findings do not support the routine use of high-dose vitamin D supplementation in children for the prevention of viral upper respiratory tract infections." 


This study found giving a high dose of vitamin D to healthy children in the winter doesn't reduce their overall risk of upper airway infections compared with the standard recommended dose.

This well-designed study used several measures to ensure the results were robust. For example, researchers:

  • used randomisation to split the children into groups
  • blinded parents as to which treatment the child was receiving to make sure this knowledge couldn't affect their perception of their child's health
  • used laboratory tests to confirm that the child did have a viral infection

There was a reduction in flu with high-dose vitamin D, but the number of cases was very small, so this finding needs to be treated cautiously. The researchers have called for this to be looked at in further studies to see if this finding can be confirmed.

But there are some other important points to bear in mind. The study only included healthy children – it can't rule out possible benefits for children with chronic conditions or in specific subgroups, such as children who have asthma or particularly low vitamin D levels.

And researchers only looked at upper airway infections, so the study doesn't tell us about other outcomes that may be affected by vitamin D.

On balance, this study suggests that if your child is generally healthy, they aren't likely to get much extra cold and flu protection from taking more than the recommended dose of vitamin D in winter.

Flu is normally more serious than a cold – the NHS offers a free flu vaccine to children of certain ages and with certain conditions to reduce this risk. Check if your child is eligible for the children's flu vaccine.

Links To The Headlines

Vitamin D will not protect your child from a cold: myth-busting study says 'more isn't always better' to help toddlers stay healthy. Mail Online, July 18 2017

Links To Science

Aglipay M, Birken CS, Parkin PC. Effect of High-Dose vs Standard-Dose Wintertime Vitamin D Supplementation on Viral Upper Respiratory Tract Infections in Young Healthy Children. JAMA. Published online July 18 2017

Benefits of artificial sweeteners unclear

NHS Choices - Behind the Headlines -

"Artificial sweeteners linked to risk of weight gain," the Daily Mirror reports. Researchers looking at data gathered in previous studies reported a link between artificial sweeteners – ironically often associated with diet drinks – and weight gain. They also found a link with type 2 diabetes, high blood pressure and stroke.

However, the results of this review should be treated with caution. They are based on seven small, low-quality trials, and 30 cohort studies, which cannot show cause and effect. There was such a wide difference in the results and methods between the trials that pooling them increases the risk the results could have occurred by chance.

The best way to achieve and maintain a healthy weight and prevent type 2 diabetes is through a combination of a healthy diet, including at least five portions of fruit or vegetables a day, and regular exercise. And the ultimate diet drink? Water.

Where did the story come from?

The study was carried out by researchers from various hospitals and institutions in Canada, including the University of Manitoba. It did not receive any specific funding. The study was published in the peer-reviewed Canadian Medical Association Journal.

Neither The Independent nor the Daily Mirror explained any of the limitations in the underlying studies or recognised that pooling the results of such different types of studies increases the possibility that the results occur by chance.

The Mirror's claim that the study found artificial sweeteners could affect gut bacteria and appetite is inaccurate. Researchers speculated along these lines, but these factors were not included in the research.

What kind of research was this?

This was a systematic review of published research on the effect of artificial sweeteners on body mass index (BMI) and a range of medical conditions. The results of any relevant randomised controlled trials and cohort studies were pooled in a meta-analysis. This type of review is useful for collating a large amount of information, but the findings rely on the quality and strength of the underlying evidence.

What did the research involve?

The researchers searched three medical databases for relevant trials and cohort studies. After sifting through more than 11,000 article titles, they found seven randomised controlled trials and 30 cohort studies that looked at the consumption of artificial sweeteners and various outcome measures.

The trials included adults who were overweight, obese or had high blood pressure. They were randomised to consume either a non-nutritive sweetener, such as aspartame, taken as a capsule or in "diet drinks", or placebo or water daily for 6 to 24 months.

The cohort studies included between 347 and 97,991 adults whose weight ranged from healthy to obese. The researchers grouped adults into highest and lowest sweetener consumption, mostly from fizzy drinks. They then compared any change in weight or BMI, or development of type 2 diabetes or cardiovascular disease over a follow-up period ranging from 9 months to 38 years.

What were the basic results?

According to the randomised controlled trials:

  • Sweeteners did not have any effect on BMI (mean difference 0.37kg/m2, 95% confidence interval [CI] 1.10 to 0.36). This was based on three similar trials with 242 people.
  • Sweeteners did not have an effect on weight change (mean difference 0.17kg, 95% CI 0.54 to 0.21). Five studies of 791 adults were included, though there were major differences between the studies.

The cohort studies found that compared with those who consumed the least sweetener, those who consumed the most had a:

  • 14% increased risk of type 2 diabetes (relative risk [RR] 1.14, 95% CI 1.05 to 1.25; nine trials, 400,571 people)
  • 14% increased risk of stroke (RR 1.14, 95% CI 1.04 to 1.26; two trials, 128,176 people)
  • 12% increased risk of high blood pressure (RR 1.12, 95% CI 1.08 to 1.13; five trials, 232,630 people)
  • 31% increased risk of metabolic syndrome – a combination of high blood pressure, abdominal obesity and diabetes (RR 1.31, 95% CI 1.23 to 1.40; five trials, 27,914 people)

The cohort studies also found that compared with those who did not consume sweeteners at all, high consumers of sweeteners had a slight increase in BMI, obesity and waist circumference.

How did the researchers interpret the results?

The researchers concluded that evidence from the trials "does not clearly support the intended benefits of non-nutritive sweeteners for weight management", and the cohort studies suggest "routine consumption of non-nutritive sweeteners may be associated with a long-term increase in BMI and elevated risk of cardiometabolic disease". However, they say these results are tentative and need to be confirmed in higher-quality trials.


The study authors suggest artificial sweeteners may not aid weight loss, despite marketing claims to the contrary, and could actually increase the risk of type 2 diabetes. However, the results need to be treated with caution, as this review had numerous limitations:

  • The randomised controlled trials had great variability and few participants, increasing the possibility of the results occurring by chance. They were also judged to be at a high risk of bias – for example, the participants could not be blinded to the intervention, and adherence (drop-out) rates were not provided.
  • We do not know whether there were any other interventions, such as change in diet or exercise, in either group over the course of the trials. Some trials involved consuming an artificial sweetener capsule, but we do not know what other drinks – "diet", sugary or alcoholic – were also being consumed. It is unlikely that changing one dietary factor would result in major weight reduction.
  • The cohort studies relied on food-frequency questionnaires. Poor recall can make these inaccurate, and they may not adequately account for changes in people's diet over time.
  • Cohort studies can be useful for looking at trends in large groups, but they cannot account for all possible confounding factors. Most of the studies only controlled for age, sex, smoking and physical activity level.
  • The majority of cohort studies were from the US, with only one cohort study from the UK, so the results may not be generalisable to the UK population.
  • There was too much variability between the cohort studies – such as different outcome measures, type of sweetener and length of study – to pool the results.

In summary, although this was a reasonably thorough review, it does not provide firm conclusions as to the beneficial or potentially harmful effects of artificial sweeteners. This is not the fault of the researchers but is down to the lack and poor quality of available evidence.

If you are overweight or obese, the best way to lose weight is by combining dietary changes with more exercise.

There are plenty of tips on our Weight loss page.

Links To The Headlines

Diet coke could be making you FAT: Artificial sweeteners linked to risk of weight gain. Daily Mirror, July 17 2017

Artificial sweeteners linked to weight gain, finds new research. The Independent, July 17 2017

Links To Science

Azad MB, Abou-Setta AM, Chauhan BF, et al. Nonnutritive sweeteners and cardiometabolic health: a systematic review and meta-analysis of randomized controlled trials and prospective cohort studies. CMAJ. Published online July 17 2017

Some types of vegetarian diet can raise heart disease risk

NHS Choices - Behind the Headlines -

"Being vegetarian isn't always healthy: Plant-based diet may raise the risk of heart disease," the Daily Mail reports. A US study found a vegetarian diet based on less healthy food options, such as refined grains, could increase the risk of heart disease.

The researchers behind the latest study made the point that many previous diet and health studies "lumped together" all types of vegetarian diets as plant-based, without considering the actual content of specific diets. And not all plant-based diets are healthy and nutritious.

The researchers looked at data involving 200,000 health workers from the US and tried to analyse any link between diet and coronary heart disease.

Overall a high plant-based diet wasn't linked with a clear benefit for heart disease risk compared with a low plant-based/high meat-based diet.

When the plant-based diets were broken down and analysed further, the researchers found interesting differences.

Those eating a "healthy" plant-based diet high in wholegrains, fruits, vegetables and healthy fats were less likely to get heart disease than people eating "unhealthy" plant-based diets including foods like potatoes, refined grains and sweets.

While the study can't rule out the possibility that other health and lifestyle factors such as stress, job type and education could have influenced the links, the association between unhealthy plant-based diets and heart disease is plausible.

The diet advice for vegetarians is the same for everyone else: eat a balanced diet with at least five portions of fruit and vegetables every day, eat less sugar, salt, and saturated fat, and choose wholegrain carbohydrates where possible.


Where did the story come from?

The study was carried out by researchers from Harvard T.H. Chan School of Public Health, AbbVie (a pharmaceutical company), and Brigham and Women's Hospital, all in the US. It was funded by the US National Institutes of Health, US Department of Agriculture/Blueberry Highbush Council and the California Walnut Commission, and Metagenic. One author has served on the Scientific Advisory Committees of IKEA, Take C/O, and SPE, and another is also an employee of AbbVie.

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

The Daily Mail's reporting was generally accurate, but the statement claiming "refined grains and potatoes lead to a higher risk of cardio-metabolic disease" is not entirely representative. These were just two of a wide variety of foods included in the "unhealthy plant-based diet." Neither does this statement account for the fact that there may be many other health and lifestyle factors other than diet contributing to coronary heart disease risk.


What kind of research was this?

This was a study pooling data from three large cohort studies of health professionals. It aimed to see whether consuming a plant-based diet or a diet including meat was associated with risk of coronary heart disease.

Coronary heart disease is the general term used to describe when the arteries supplying the heart become clogged by a build-up of fatty substances. Complete blockage of the arteries causes heart attack, a major cause of death both in the UK and worldwide.

A prospective cohort study is a good way of looking at the link between an exposure (such as diet) and an outcome (like heart disease) as you can examine a large number of people over a long period of time.

However, you are unable to control the diets or all other lifestyle factors that could be having an influence, such as smoking and exercise. A randomised controlled trial would be needed for this, but it is not really possible to make sure people stick to a specific diet for a long period of time.


What did the research involve?

The research included:

  • 73,710 women (aged 30 to 55 years) involved in the Nurses' Health Study (1984 to 2012)
  • 92,329 women (aged 25 to 42 years) involved in the Nurses' Health Study 2 (1991 to 2013)
  • 43,259 men (aged 40 to 75 years) taking part in the Health Professionals Follow-up Study (1986-2012)

This study only included participants who, at the start of the study, did not have coronary heart disease, stroke and cancer.

Information on diet was collected every two to four years using a food frequency questionnaire. Participants recorded how often on average they consumed a specified portion of any of 130 food items in the past year. This ranged from "never or less than once a month" to "six or more times a day".

Three versions of a plant-based diet were created from these questionnaires based on intake of 18 main food groups:

  • An overall plant-based diet index (PDI) was created by assigning positive scores to plant foods and reverse scores to animal foods.
  • A "healthful plant-based diet index" (hPDI) was created by giving positive scores to healthy plant foods such as whole grains, fruit, vegetables, nuts, oils and tea. Both animal foods and less healthy plant foods such as juices, refined grains, fries and sweets received a negative score.
  • An "unhealthful plant-based diet" (uPDI) was created by giving positive scores to less-healthy plant foods, such as sweets, cakes, chips and crisps, and scores to animal and healthy plant-based foods.

The researchers looked at participant reports of coronary heart disease during follow-up assessments, and validated this through checking medical records. Deaths were identified through next of kin and a search of the US National Death Index.

Results were adjusted for the following confounding factors:

  • smoking
  • age
  • physical activity
  • alcohol
  • multivitamin use
  • family history of coronary heart disease
  • margarine intake
  • energy intake
  • high blood pressure
  • high cholesterol
  • diabetes
  • body mass index
  • post-menopausal hormone use and oral contraceptive use in women


What were the basic results?

During follow-up 8,631 people developed coronary heart disease.

High adherence to an overall plant-based diet (PDI) showed a trend for reduced risk compared to low adherence to a PDI and a mainly animal-based diet, but this fell just short of statistical significance (hazard ratio [HR] 0.92, 95% confidence interval [CI] 0.83 to 1.01).

However, when analysing "healthful" versus "unhealthful" plant-based diets separately:

  • Highest adherence to the healthy plant-based diet reduced risk of heart disease by 25% compared with a low adherence to this diet (i.e. consuming an unhealthy plant-based diet, including meat) (HR 0.75, 95% CI 0.68 to 0.83).
  • Highest adherence to an unhealthy plant-based diet increased risk of heart disease by 32% compared with lowest adherence to this diet (i.e. consuming a healthy plant-based diet, including meat) (HR 1.32, 95% CI 1.20 to 1.46).


How did the researchers interpret the results?

The researchers concluded that a "higher intake of a plant-based diet index rich in healthier plant foods is associated with substantially lower CHD risk, whereas a plant-based diet index that emphasizes less-healthy plant foods is associated with higher CHD risk."

They further add that "dietary guidelines and lifestyle interventions could recommend increasing intake of healthy plant foods, while reducing intake of less healthy plant foods and certain animal foods for improved cardiometabolic health."



This large pooled cohort study seems to demonstrate an association between a healthy plant-based diet and reduced risk of coronary heart disease, and an increased risk of heart disease with an unhealthy plant-based diet.

This adds to the evidence base supporting the possible benefits of healthy plant-based diets in protecting against certain illnesses. However there are some limitations to the research:

  • The cohort included only health professionals from the US so might not be representative of wider populations in the UK or elsewhere.
  • The study can't provide information on the benefits or otherwise of this diet in people with established coronary heart disease, stroke or cancer as these people were excluded.
  • The questionnaire was self-reported and asked for recall of food habits over the previous year so there might be some inaccuracies in reporting. Also, people might not want to admit to consuming less healthy foods – although if unhealthy foods were under-reported, this could have meant an even bigger difference in results.
  • Heart disease outcomes were mainly self-reported and then verified, so some cases may have been missed.
  • Although analyses adjusted for various health and lifestyle factors, there are likely to be many other confounding variables influencing likelihood of coronary heart disease, such as education, occupation or stress levels.

Nevertheless the study supports general understanding about the benefits of wholegrains, fruits and vegetables and healthy sources of fat.

Eating a purely plant-based, but unhealthy, diet may be good for your conscience but not so good for the heart.

Read more about healthy vegetarian diets.

Links To The Headlines

Being vegetarian isn't always healthy: Plant-based diet may raise the risk of heart disease. Daily Mail, July 18 2017

Vegetarian diets can lead to higher risk of heart disease, finds study. The Independent, July 17 2017

Links To Science

Satija A, Bhupathiraju SN, Spiegelman D, et al. Healthful and Unhealthful Plant-Based Diets and the Risk of Coronary Heart Disease in U.S. Adults. Journal of the American College of Cardiology. Published online June 17 2017

'Regular sex keeps you younger' claims are unsupported

NHS Choices - Behind the Headlines -

"Scientists have found you can hold back the hands of time with a regular romp," is The Sun's typically colourful headline.

While a healthy sex life may be a good thing, the research in question isn't exactly mind blowing.

The study included 129 mothers from San Francisco, half of whom had a child with an autism spectrum disorder (ASD) and were considered to have high stress levels.

The researchers wanted to assess the quality of these women's intimate relationships. Over a one-week period, they asked the women about their sex life and took blood samples to measure telomere length. Telomeres are the protective tips on the ends of our chromosomes that shorten as we age.

Overall they found that having sex in the past week was linked with increased telomere length that week.

The length of telomeres has been linked with being "genetically young" as longer telomeres may help protect against cell damage. But this association between telomere length and "youthfulness" has never been definitely proven.

Overall, this one-off assessment proves very little. It didn't look at how telomere length changed over time. And more importantly the longer term nature and quality of the relationship was not studied.

Even if there was a proven link between telomere length and a person's sex life, how this affects appearance and vitality is another matter.


Where did the story come from?

The study was carried out by researchers from the University of California and University of British Columbia, and was funded by the National Institute of Health and National Institute of Mental Health.

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

The Sun's question and answer – "How often do you need to be getting intimate to make a difference? Once a week apparently" – would seem to show the paper hasn't grasped the limitations of this research. The "once a week" bit is purely because the researchers carried out their assessment over a week. The study didn't even take into account how many times a week the person had sex.

What kind of research was this?

This was a cross sectional study of mothers taking part in a cohort study. It questioned their stress levels and relationship satisfaction and looked at whether this was linked with telomere length in blood cells.

Telomeres are repetitive sequences of DNA at the tips of our chromosomes. They have no effect on the body but are essentially there to protect the important chromosomal DNA from getting damaged each time the cell replicates.

As we age telomeres get shorter, and so they are taken as a marker of cellular ageing. Studies have also shown telomeres shorten in response to stress.

The researchers say social support and positive relationships can slow the rate of telomere shortening. As good quality intimate relationships are known to be good for health, and have been linked to better physical health and longevity, this study aimed to see whether relationship quality was linked with telomere length.


What did the research involve?

The study included women participating in the Stress, Aging, and Emotions (SAGE) study, set up to investigate the stress of mothers/caregivers raising children with or without autism spectrum disorders (ASD). The women were 20 to 50 years old and recruited from the San Francisco bay area.

This study takes data collected during one week at an 18 month assessment period into the SAGE study.

Stress was assessed using the Perceived Stress Scale (PSS), designed to assess feelings of being overwhelmed, anxious or stressed over the past month.

Women were classified as high-stress maternal caregivers if they had a child with ASD and scored 13 or more on the PSS. They were classified as low-stress if they had a child without ASD and scored 19 or less on the PSS.

Relationship quality was assessed by a 14-item Dyadic Adjustment Scale. Examples of questions were "To what extent were you satisfied with/experienced tension with your partner today?" A morning diary assessed sexual intimacy by asking participants "Did you have sexual relations last night?"

Blood samples were taken and telomere length assessed in whole blood (red cells, white cells and platelets) and specific white blood cells (peripheral blood mononuclear cells).

This study included 129 heterosexual women who were in a relationship and had the relevant information available. In analysing the link between sexual intimacy and telomere length they adjusted for potential confounders; specifically age, body mass index, caregiver stress and health behaviours, such as diet and exercise.


What were the basic results?

Mothers/caregivers were on average 42 years old, 78% of white ethnicity, 55% were classified as low stress and 45% as high stress caregivers.

Measures of relationship quality, such as satisfaction with their partner, were not linked with telomere length. Meanwhile sexual intimacy was linked with longer telomere length in the whole blood cells and the mononuclear cells, specifically.


How did the researchers interpret the results?

The researchers conclude: "These data provide preliminary data that sexual intimacy is associated with longer telomere length. Future studies investigating these associations are warranted."



Despite the media headlines that regular sex keeps you young, only limited implications can be drawn from this study.

This was a small sample of a specific group of women. All were mothers or caregivers, in heterosexual relationships from one region of the US. About half of them were caring for children with autism spectrum disorders and were perceived to have high stress levels as a result. Therefore they can't be assumed to represent all women.

Researchers only assessed relationship quality, intimacy and telomere length over the space of a single week. This can't prove that intimacy that week directly caused the telomere length at that point.

There are other important aspects this study couldn't account for:

  • how telomere length changed over time
  • the long-term nature and quality of the relationship
  • various factors that may influence the relationship quality and the health and wellbeing of the person

Simply asking a person how satisfied or not they've been with their partner in the past week and whether they had sex the night before tells you very little. And it doesn't tell you anything about the quality of that sexual relationship.

Even if it were proved that a regular sexual relationship was linked with telomere length it is unclear whether this would actually be a relevant finding. Telomere length my help protect against cell damage, but this is not the same thing as looking and feeling young.

Nevertheless, a healthy and fulfilling sexual life can boost both physical and mental wellbeing.

Read more about how to enjoy a good sex life.

Links To The Headlines

This is how often you should have sex if you want to stay young. The Sun, July 16 2017

Links To Science

de Baca TC, Epel ES, Robles TF, et al. Sexual intimacy in couples is associated with longer telomere length. Psychoneuroendocrinology . Published online March 24 2017

Long working week 'may increase risk of irregular heartbeat'

NHS Choices - Behind the Headlines -

"Long working days can cause heart problems, study says," The Guardian reports.

Researchers found people who work 55 or more hours a week had an increased risk of developing a type of irregular heartbeat known as atrial fibrillation, where the heart can beat very fast. 

Complications of atrial fibrillation include stroke and heart failure.

The researchers pooled data from eight studies across western Europe, including data from more than 85,000 adults.

Overall, they found people who worked the longest (55 hours or more) a week had about a 40% increased risk of developing atrial fibrillation over 10 years.

But only 1.2% of the whole group studied developed atrial fibrillation, so the actual baseline risk is very small. Even if your risk was increased by 40%, this is still only a 1.7% risk.

Many health and lifestyle factors could have contributed to the link – for example, people who worked longer hours may have been more likely to have unhealthier lifestyle habits. The studies may not have fully accounted for these.

The best way to reduce your risk of heart and vascular problems is to have a healthy, balanced diet, take regular exercise, and avoid smoking and drinking too much alcohol.

A healthy work-life balance is also important. Persistently working long hours can cause stress, which can in turn lead to problems with both your physical and mental health.

Read more about workplace health.

Where did the story come from?

The study was carried out by the Individual-Participant-Data Meta-analysis in Working Populations (IPD-Work) Consortium, comprised of researchers from extensive institutions worldwide.

Funding was provided by NordForsk, the Nordic Research Programme on Health and Welfare, the EU New OSH ERA research programme, the Finnish Work Environment Fund, the Swedish Research Council for Working Life and Social Research, the Danish National Research Centre for the Working Environment, and the UK Medical Research Council.

The study was published in the peer-reviewed European Heart Journal, and the article is free to read online.

The media coverage would have benefited from highlighting the very small overall risk of atrial fibrillation – estimated to be an increase from 1.2% to 1.7%.

The Sun's reporting was also inaccurate, stating that, "Working more than 50 hours a week 'increases your risk of heart failure and stroke by 40%'."

Working 55 hours, not 50, saw the increase in risk, and the research only looked at the development of atrial fibrillation, not subsequent health outcomes like heart failure and stroke.

What kind of research was this?

This collective analysis of data from several prospective cohort studies aimed to see whether working longer hours (over 55 hours a week) was linked to an increased risk of atrial fibrillation.

Atrial fibrillation (AF) is a completely irregular heart rhythm that's often also abnormally fast, and can cause strokes.

Some studies have suggested that stress and exhaustion can lead to AF, although the evidence isn't very strong.

The study aimed to look at this issue in a large population of people taking part in several cohort studies making up the IPD-Work project. This is a Europe-wide collaborative project looking at how working habits can impact on health.

What did the research involve?

The study analysed data from eight of the cohort studies in the IPD-Work Consortium that had data available on working hours and AF.

These were multi-purpose studies designed to examine health effects across a range of risk factors, including those related to the workplace.

The total sample for this study included 85,494 adults (65% women, 35% men) from the UK, Denmark, Sweden, and Finland who didn't have a diagnosis of AF at the start of the study between 1991 and 2004.

At the start of the study, researchers collected information on working hours.

People were grouped into:

  • part-time workers (less than 35 hours a week)
  • full-time workers with normal working hours (35-40 hours a week) – the control group
  • 41-48 hours a week – over standard working hours, but still in line with EU rules
  • 49-54 hours a week
  • 55 hours a week or more

AF was later identified through patient records, data on hospitalisations and deaths, and one of the cohorts had follow-up electrocardiograms (ECGs).

The researchers analysed and adjusted for extensive confounding factors. These included risk factors for AF assessed at the start of the study and during follow-up, such as respiratory infections, inflammatory conditions, diabetes, high blood pressure, stroke, and various forms of heart disease.

They also assessed various general confounders at baseline, including:

  • age
  • gender
  • socioeconomic status
  • body mass index
  • smoking history
  • alcohol use
  • physical activity levels
What were the basic results?

The average age of participants was 43.4 years at the start of the study. People were followed up for an average of 10 years. During this time, 1,061 were diagnosed with AF – a rate of 12.4 per 1,000, or around 1%.

The majority of study participants (62.5%; 53,468) worked standard working hours, with only 5.2% (4,484) working the longest hours of 55 hours or more each week.

When adjusting for age, sex and socioeconomic status, those who worked the longest hours had a 42% increased risk of developing AF compared with those who worked standard hours (hazard ratio [HR] 1.42, 95% confidence interval [CI] 1.13 to 1.80).

The general size of this association remained when adjusting for additional confounding factors like health, lifestyle and AF risk factors, including any previous history of heart disease or stroke (HR 1.36, 95% CI 1.05 to 1.76).

Other working hours patterns, such as working 41-48 hours a week, weren't associated with an increased risk compared with standard hours.

But although the eight pooled cohorts overall had an increased risk of AF, individually not a single one found a statistically significant increased risk of AF with long working hours.

How did the researchers interpret the results?

The researchers concluded: "Individuals who worked long hours were more likely to develop atrial fibrillation than those working standard." 


This study draws together data from a large group of people to investigate whether working hours could be linked to AF.

It found people who work 55 or more hours a week had an increased risk of developing an irregular heartbeat.

But before we jump to any conclusions, there are several important things to consider:

  • The number of people who developed AF during this study was small: only 1.24%. That's the absolute risk of AF. Even if working more than 55 hours a week does increase your risk of AF by around 40%, it would only be increasing it to something like 1.74% – which is still very small.
  • Only a small percentage of the cohort (5%) worked more than 55 hours a week. A further, much smaller, number of them will have developed AF. And analyses involving smaller samples are less accurate.
  • Although the eight pooled cohorts overall had an increased risk of AF, individually not a single one found a statistically significant increased risk of AF with long working hours.
  • Notable among these eight studies was the single Whitehall study, which took ECGs from the participants during follow-up and made the greatest adjustment for AF risk factors, so the results are likely to be more accurate. This study found no significant link with long working hours. Other studies were more variable in how they assessed AF, which may lead to an inaccurate representation of cases.
  • The number of working hours was only assessed at the start of the study and may have changed over time.
  • People who worked the longest hours were more likely to have unhealthier lifestyle habits, such as being obese, smoking, drinking too much alcohol, and getting less exercise. Even after adjusting for these factors, it's still difficult to prove that the working hours have directly and independently led to AF.

Although these findings on working hours are interesting, people shouldn't be overly alarmed. There are far more well-established lifestyle risk factors for heart disease, such as smoking, alcohol, diet, and activity.

Nevertheless, it's important to get a good work-life balance. Regularly working long hours could cause you physical and mental stress.

Read more about coping with stress at work.

Links To The Headlines

Long working days can cause heart problems, study says. The Guardian, June 14 2017

How working more than 55 hours a week raises your risk of developing serious heart problems by 40%. Mail Online, June 14 2017

Working 55 hours or more a week raises risk of irregular heartbeat, study shows. The Daily Telegraph, June 14 2017

Overtime is killing you! Working more than 50 hours a week 'increases your risk of heart failure and stroke by 40%'. The Sun, June 14 2017

Links To Science

Kivimäki M, Nyberg ST, Batty GD, et al. Long working hours as a risk factor for atrial fibrillation: a multi-cohort study. European Heart Journal. Published online July 13 2017

House dust linked to obesity – but only in mice

NHS Choices - Behind the Headlines -

"Bad news for those who hate cleaning: dusty homes could make you obese," reports the Mail Online.

Scientists in the US tested extracts of household dust on mouse "pre-fat" cells grown in a laboratory. These are cells known to develop into fat cells when exposed to fat-causing chemicals. 

The researchers found the cells were more likely to divide into fat cells and accumulate more fat after being exposed to most samples of dust.

They say the likely cause is commonly used chemicals, such as fire retardants, pesticides and plastics, which have been found in house dust before. They tested 40 different types of chemical on the mouse cells to see which had the most effect.

US environmental authorities estimate most children swallow or breathe in 50mg of household dust a day – well above the amounts tested. The researchers suggest that chemicals in household dust might be contributing to the increase in obesity seen in recent years.

But this study didn't look at whether those whose homes are dustier than others are exposed to more chemicals. And we don't know if the effects on the mouse cells would be seen in human cells.

Rather than suggesting we should keep our homes completely dust free, the best known way to prevent becoming overweight or obese is to eat a healthy, balanced diet and take regular exercise.

This research might also contribute to evidence on the potential harms of chemicals in consumer products.

Where did the story come from?

The study was carried out by researchers from Duke University and was funded by the National Institute of Environmental Health in the US. 

It was published in the peer-reviewed journal Environmental Science and Technology.

Both the Mail Online and The Daily Telegraph advised that people should, in the Mail Online's words, "reach for their feather dusters". The Daily Telegraph tells readers to "keep their homes spotless" to avoid putting on weight.

Both media outlets assume that people could reduce dust levels in their homes to a point where they wouldn't have adverse effects – but there's nothing in the study to suggest this is possible.

The researchers say the chemicals in dust are "near ubiquitous", meaning it would be very tough to remove them all.

The media outlets also assume that the results in mice cells will translate directly into obesity in humans, which may not be the case.

What kind of research was this?

This in-vitro laboratory study (a study involving cells) used cultured mouse pre-fat (pre-adipocyte) cells programmed to develop into fat cells when exposed to certain chemicals.

This type of cellular research is done to try to pinpoint harmful substances and get an idea of their biological effects, rather than testing chemicals on animals or people directly.

But in-vitro research using animal cells doesn't always translate into the same results in humans.

What did the research involve?

Researchers collected 11 samples of household dust from different homes in the US state of North Carolina.

The dust was then concentrated and introduced to mouse pre-fat cells being grown in tissue culture plates. The researchers also used a control sample of cells without household dust.

In a separate study, they tested 40 chemical substances previously shown to be associated with changing the way fat cells grow.

They looked for two outcomes:

  • whether the cells proliferated and divided into fat cells
  • whether the cells accumulated more triglyceride (fat)

They compared the results from house dust-exposed cells with control cells, and chemical exposed-cells compared with control cells.

What were the basic results?

Compared with control cells:

  • pre-fat cells exposed to 9 of the 11 samples increased in number and divided into fat cells
  • cells exposed to 7 of the 11 samples accumulated more triglycerides
  • cells exposed to 1 of the 11 samples showed no change in proliferation or triglycerides

Among the chemicals tested, 33 of the 41 compounds increased the triglyceride accumulation in the cells. The extent to which this happened varied widely.

The chemicals that had the strongest effect were:

  • tert-butyl-phenyl diphenyl phosphate (TBPDP), an organophosphate fire retardant
  • dibutyl phlalate (DBP), a plastics chemical
  • pyraclostrobin, an anti-fungal
How did the researchers interpret the results?

The researchers said: "Only one of the 11 dust samples appeared completely inactive, suggesting that the causative chemicals are nearly ubiquitous in the indoor environment."

They said there now needs to be research "to determine whether there are impacts" of the mixture of chemicals found in household dust "on the metabolic health of residents, particularly children, and to identify the causative chemicals". 


The main cause of obesity is an imbalance between calories taken into the body and the number of calories used up.

But other environmental causes may also play a part, and we're just starting to understand how certain chemicals affect fat storage in the body.

One area of interest is semi-volatile organic compounds, such as those tested in this study. These chemicals have been linked to hormonal changes, which may in turn affect the way the body processes glucose and stores it. This potentially could impact on the metabolism and increase weight gain.

This study suggests that chemicals already known to affect how cells store fat may be present in large enough quantities in household dust to affect our bodies.

But the study doesn't prove this is the case. It showed an effect of 11 small samples of dust on mouse fat cells cultured in a laboratory.

We don't know, for example, whether the people living in the homes where the samples were taken were overweight or not. And we can't tell at present how or if household dust – or the chemicals in it – affects human body fat or health.

Trying to remove every last mote of dust from your home is likely to be impossible, and may not have any effect on your weight – although vigorous housework may help burn off a few calories.

There's little point in obsessing about cleanliness if you're eating too much and moving to little. If you want to keep to a healthy weight, your best bet is to have a healthy diet and get plenty of exercise.

Links To The Headlines

Bad news for those who hate cleaning: Dusty homes could make you obese by spurring the growth of fat cells. Mail Online, July 12 2017

It's not food but dust making you fat as pollutants can cause fat cells to accumulate, new research claims. Daily Mirror, July 12 2017

House dust could spur the growth of human fat cells. The Independent, July 12 2017

Household dust makes people fat, groundbreaking research indicates. The Daily Telegraph, July 12 2017

Links To Science

Kassotis CD, Hoffman K, Stapleton HM. Characterization of Adipogenic Activity of House Dust Extracts and Semi-Volatile Indoor Contaminants in 3T3-L1 Cells. Environmental Science and Technology. Published online July 12 2017

Face-to-face bullying much more common than cyberbullying

NHS Choices - Behind the Headlines -

"Children suffer significantly more face-to-face bullying than online abuse," reports the Mail Online.

UK researchers questioned nearly 300,000 15-year-olds about their experiences of bullying in the biggest study of the subject to date.

They found 30% of the teenagers who replied experienced regular "traditional" physical, verbal or relationship bullying, while 3% experienced both traditional and "cyberbullying", such as being on the receiving end of unpleasant text messages or social media posts. Less than 1% experienced online bullying only.

Teenagers who reported being bullied twice a month or more were likely to have poorer mental wellbeing than those who weren't bullied that often.

But because the study was just a snapshot in time, we don't know whether poorer mental wellbeing was caused by the bullying.

Though the results suggest cyberbullying is less common, this finding is based on around 110,000 adolescents who took part in the survey. We don't know why 190,000 of the adolescents invited to take part in the study didn't respond to the bullying questionnaire.

This is very much a "good news, bad news" story. Cyberbullying may not be as big an issue as the media sometimes suggest. But traditional bullying remains a problem that hasn't been consigned to the past.

The researchers say any attempts to control the perceived rise in new forms of cyberbullying should also include efforts to crack down on traditional forms of victimisation.

Read more advice about bullying and what you can do to help your child.

Where did the story come from?

The study was carried out by researchers from the University of Oxford and had no specific funding. 

It was published in the peer-reviewed journal The Lancet Child and Adolescent Health.

The Times, Mail Online and BBC News all carried accurate and balanced reports of the study.

BBC News made the point that the study looked at those who'd experienced regular bullying in the past couple of months, so the 97% of teenagers who didn't report cyberbullying might have experienced it, but not regularly or recently.

The Times' photographs illustrating the piece showed very young children, and the headline suggested bullying took place in "the playground" – but the study only included teenagers.

The low response rate to the survey also wasn't pointed out by the media.

What kind of research was this?

The study had two parts. It was primarily a cross-sectional survey to gather data on how many teenagers had experienced different types of bullying.

It also measured mental wellbeing, and the researchers did an analysis to see how this was linked to experiences of bullying.

While cross-sectional studies are useful ways to spot links between issues, they can't tell us whether one causes the other.

What did the research involve?

Researchers contacted 298,080 15-year-olds in 150 local authorities across England using a database of pupils. Parents or guardians were sent letters allowing them to opt their child out of the survey.

Teenagers completed the survey on paper or online. They were asked to state how often they'd experienced eight types of bullying, including two types of cyberbullying. They were also asked to fill in a mental wellbeing scale.

Researchers used the results to assess the prevalence of different types of bullying and see whether regular bullying was linked to lower mental wellbeing.

The teenagers were asked how many times in the past two months they'd experienced the following:

  • I was called mean names, made fun of, or teased in a hurtful way.
  • Other people left me out of things on purpose, excluded me from their group of friends, or completely ignored me.
  • I was hit, kicked, punched, shoved around, or locked indoors.
  • Other people told lies or spread false rumours about me and tried to make others dislike me.
  • Other people made fun of me because of my body weight.
  • Other people made sexual jokes, comments or gestures to me.
  • Someone sent mean instant messages, wall postings, emails and text messages, or created a website that made fun of me.
  • Someone took unflattering or inappropriate pictures of me without permission and posted them online.

Teenagers also filled out the Warwick-Edinburgh Mental Wellbeing Scale, a 14-point questionnaire used to measure psychosocial health, wellbeing and functioning.

Researchers looked for correlations between reports of bullying and wellbeing.

They were able to adjust their figures to take account of gender, ethnic background and deprivation (based on postcode data), but not other potential confounding factors that might have played a role, such as mental ill health or abuse in the home.

What were the basic results?

Researchers got results from 120,115 teenagers, about 40% of those contacted. Girls were more likely to respond than boys.

  • Nearly one-third (33,363 or 30%) said they'd been bullied at least twice a month in the previous two months, either face to face or online.
  • Regular bullying was reported more often by girls (36%) than boys (24%).
  • Regular cyberbullying with no face-to-face bullying was reported by 406 teenagers, less than 1% of the total questioned.
  • Regular traditional and cyberbullying was experienced by 3,655 teenagers (3%).

The researchers said regular experience of any type of bullying was linked to lower mental wellbeing.

But they found no evidence that cyberbullying was more harmful than traditional bullying – in fact, traditional bullying seemed more strongly linked to lower mental wellbeing.

How did the researchers interpret the results?

The researchers concluded their results support the position that "cyberbullying is unlikely to provide a source for new victims, but can best be understood as a new avenue for victimisation for those already suffering traditional forms of bullying."

They say their findings "are in stark contrast to media reports that young people are now more likely to be victims of cyberbullying than traditional forms".

Those putting in place strategies to curb cyberbullying should be aware that measures are only likely to be effective if they also consider "the dynamics of traditional forms of bullying", the researchers say.


Being bullied is a relatively common and distressing experience for many children and adolescents.

Research in recent years has linked the experience of being bullied as a child to the development of mental health problems like anxiety and depression.

It's perhaps not a surprise that cyberbullying in this study almost always occurred when teenagers were also being bullied offline.

The internet is a tool, not a separate entity from the human world, and people who bully in one part of life may also use internet tools to bully in cyberspace.

If anything, it's surprising how few teenagers reported having experienced regular cyberbullying, given how common smartphone use is among this age group.

But this study has a few limitations:

  • Only 40% of the children contacted completed the questionnaire, and more than 9,000 didn't complete the bullying section. Though this is typical of survey response rates, we don't know whether adolescents are more or less likely to participate in such a survey if they're being bullied.
  • As a cross-sectional study, it can only look at what happened at one point in time, so those who experienced bullying more than two months before they filled in the questionnaire wouldn't have been picked up by this report.
  • Cross-sectional studies can't tell us which came first: bullying or low mental wellbeing. This means the study can't tell us whether bullying causes low mental wellbeing.
  • The researchers couldn't include possible relevant factors, such as teenagers' history of mental illness or difficult circumstances at home, in their calculations. The teens' varying levels of wellbeing might be caused by other factors that weren't measured.

The authors' conclusions – that good anti-bullying interventions are needed to tackle both traditional and cyber forms of bullying – seem sensible.

There are several organisations that can help if you or your child is experiencing bullying, such as Family LifeBullying UK and Kidscape.

Read more advice about bullying and ways you can help your child.

Links To The Headlines

Children suffer significantly more face-to-face bullying than online abuse, major study finds. Mail Online, July 12 2017

Cyber-bullying relatively rare, says study. BBC News, July 11 2017

Cyber bullying 'vanishingly rare' on its own – major new report. The Daily Telegraph, July 11 2017

Teenagers are still eight times as likely to be bullied face to face than online, study reveals. The Sun, July 11 2017

Children's worst bullying risk lurks in playground. The Times, July 12 2017 (subscription required)

Links To Science

Przybylski AK, Bowes L. Cyberbullying and adolescent well-being in England: a population-based cross-sectional study. The Lancet Child and Adolescent Health. Published online July 11 2017

Does coffee make you live longer?

NHS Choices - Behind the Headlines -

"Drinking three cups of coffee a day could add years to your life, suggest studies," reports the Metro.

It follows the results of European and US studies that looked at the relationship between how much coffee people drink and death.

The European study included more than 450,000 people. Researchers found men who drank the highest amounts of coffee had a 12% overall reduced risk of death at follow-up from causes including cancer and cardiovascular, digestive and respiratory conditions.

Women had a 7% reduced risk overall, but a greater risk of dying of cancer the more coffee they drank.

These findings need to be interpreted with caution – the research doesn't prove coffee reduces the risk of death. Many other factors that might have played a role weren't taken into account.

Drinking coffee can be part of a healthy, balanced diet. Current guidelines recommend drinking no more than around four cups a day. 

Pregnant women are advised to consume no more than 200mg of caffeine a day, the equivalent of two mugs of instant coffee.

There are no magic shortcuts (or magic coffee beans) for achieving good health and living a longer life.

Leading a healthy lifestyle by having a varied, healthy diet and getting regular exercise is the best way to achieve this. 

Where did the story come from?

The study was carried out by researchers from a range of more than 20 academic and health institutions across Europe, including Imperial College London and the International Agency for Research on Cancer in France.

The European research was funded by a number of institutions, including the European Commission Directorate General for Health and the Consumers and International Agency for Research on Cancer.

Two authors declared potential conflicts of interest, naming grants from the pharmaceutical companies Biogen, Merck and Pfizer, although the companies weren't involved in this study.

Another author declared receiving grants from Unilever and FrieslandCampina, two consumer goods companies also not involved in the research.

The study was published in the peer-reviewed journal Annals of Internal Medicine.

A second study from the US looking at the same topic was published in the journal at the same time, and reported similar positive results.

The UK media's coverage of this research was generally accurate, with The Guardian rightly highlighting the fact "scientists say that the link might just be down to coffee drinkers having healthier behaviours". 

What kind of research was this?

This cohort study looked at data from people enrolled in the European Prospective Investigation into Cancer and Nutrition (EPIC) to see if there were links between coffee consumption and overall deaths, as well as deaths from specific diseases.

This type of study is good for looking at this kind of issue, as it involves people already participating in other research and allows data on a large number of people to be examined.

But cohort studies can't show cause and effect, so aren't able to prove that drinking coffee decreases or increases likelihood of death.

randomised controlled trial where people are put into groups to either drink coffee or not drink coffee until they died would be needed to prove this, something that wouldn't be feasible.

What did the research involve?

The researchers took data from 451,743 participants, mostly over the age of 35, from the EPIC study and looked at their coffee consumption and death from all causes and specific causes.

Participants were recruited between 1992 and 2000, mostly from the general population of 10 European countries: Denmark, France, Germany, Greece, Italy, the Netherlands, Norway, Spain, Sweden, and the UK.

People who reported having cancer, heart disease, diabetes or a history of stroke at the start weren't included in the study.

Similarly, people who reported an extremely high or extremely low calorie consumption weren't included, as these people would not be representative of the population at large.

People were also excluded when follow-up information and information on coffee consumption was missing.

Participants recorded the number of cups of coffee they drank each month, week or day through self-reported questionnaires or interviews.

Coffee consumption (in ml a day) was calculated using the typical cup sizes for each institution involved per country.

The amount consumed was split into four quartiles:

  • non-consumers
  • quartile 1 (low consumption) – up to 83ml a day for UK data
  • quartile 2 (low to medium consumption) – up to 380ml for UK data
  • quartile 3 (medium to high consumption) – up to 488ml for UK data
  • quartile 4 (high consumption) – above 488ml

The quartiles were country specific, with the average daily amount ranging from 93ml a day in Italy to 900ml a day in Denmark.

Data on cause and date of death was collected from cancer registries, local health organisations and death records, as well as through active follow-up from other sources.

Specific causes of death included digestive, respiratory, circulatory and cerebrovascular causes, as well as ischaemic heart disease, cancer, suicide, and external causes.

Information on the following potential confounding factors was recorded and taken into account during the analysis:

  • education
  • smoking
  • alcohol consumption
  • physical activity
  • diet
  • body mass index
  • use of oral contraceptives and menopausal hormone therapy, as well as menopausal status
What were the basic results?

After an average follow-up of 16.4 years, there were 41,693 deaths. Among these, 18,003 were from cancer, 9,106 from circulatory diseases, 2,380 from cerebrovascular diseases, and 3,536 from ischaemic heart diseases.

For all causes of death:

  • Men who drank the highest amount of coffee had a 12% lower risk of death than non-consumers (adjusted hazard ratio [aHR] 0.88, 95% confidence interval [CI] 0.82 to 0.95).
  • Women who drank the highest amount of coffee also had a 7% lower risk of death than non-consumers (aHR 0.93, 95% CI 0.87 to 0.98).

For specific causes of death:

  • Men who drank the highest amount of coffee versus non-consumers and low consumers had a 59% lower risk of death from digestive disease (aHR 0.41, 95% CI 0.32 to 0.54).
  • Women who drank the highest amount of coffee versus non-consumers and low consumers had a 40% lower risk of death from digestive disease (aHR 0.60, 95% CI 0.46 to 0.78).
  • Women who drank the highest amount of coffee versus non-consumers had a 22% lower risk of death from circulatory disease (aHR 0.78, 95% CI 0.68 to 0.90).
  • Women who drank the highest amount of coffee versus non-consumers had a 30% lower risk of death from cerebrovascular disease (aHR 0.70, 95% CI 0.55 to 0.90).

One negative finding was that women who drank the highest amount of coffee had a 12% higher risk of death from cancer (aHR 1.12, 95% CI 1.02 to 1.23). No other associations were seen between coffee consumption and the other causes of death studied.

The US study showed similar findings in that higher coffee consumption was linked to a lower risk of death.

How did the researchers interpret the results?

The researchers concluded that, "Our results suggest that higher levels of coffee drinking are associated with lower risk for death from various causes, specifically digestive and circulatory diseases."

They added: "Because coffee consumption is so widespread and intakes are modifiable, its potentially beneficial clinical implications should be carefully considered." 


This study, conducted on a large number of people across Europe, was backed up by similar findings in the US. It appears to show some association between people who drink higher amounts of coffee and a reduced risk of death.

But the "potentially beneficial clinical implications" need to be considered carefully for a number of reasons:

  • Although the analyses were adjusted for some confounding variables, there may be a number of other factors that differ between the groups that account for the differences in death, such as socioeconomic status, family history, other medical conditions, and use of medication to name a few.
  • Participants with a range of illnesses, including cancer, heart disease, stroke or diabetes, were excluded from the study. These people may have different coffee habits from those included in the study, biasing the results.
  • Coffee consumption was self-reported and might have been over or underestimated, leading to inaccuracies in the results.
  • Coffee consumption was only assessed at one point in time – people's habits might vary greatly over days, months and years, so one snapshot might not give an accurate picture of lifelong coffee drinking habits.
  • Combining different cut-off levels of coffee per country may lead to inaccurate results.
  • Lots of analyses were carried out on a range of diseases, most of which weren't significant, and the likelihood of finding some significant results by chance would be fairly likely. Those significant results reported therefore need to be treated with caution.
  • Not all outcomes were positive: women had a greater risk of death from cancer if they drank higher amounts of coffee.

The media like to run stories on one single drink or "superfood" that will "guarantee" good health. This, of course, is nonsense: the only way to increase your chances of leading a longer, healthier life is to have a healthy, balanced diet and exercise regularly.

Links To The Headlines

Drinking three cups of coffee a day could add years to your life, suggest studies. Metro, July 11 2017

Coffee cuts risk of dying from stroke and heart disease, study suggests. The Guardian, July 10 2017

Coffee drinkers live longer – perhaps. BBC News, July 11 2017

Drinking coffee could reduce your chance of death, scientists say. The Independent, July 10 2017

Links To Science

Gunter MJ, Murphy N, Cross AJ, et al. Coffee Drinking and Mortality in 10 European Countries: A Multinational Cohort Study. Annals of Internal Medicine. Published online July 11 2017

Old meningitis B vaccine 'may also protect against gonorrhoea'

NHS Choices - Behind the Headlines -

"Meningitis vaccine may also cut risk of 'untreatable' gonorrhoea, study says," is the headline in The Guardian.

The news comes from the results of a study in New Zealand that found people who'd been given an old version of the meningitis B vaccine were less likely to be diagnosed with gonorrhoea.

But no protective effect was found for chlamydia, which is often diagnosed at the same time as gonorrhoea.

The publication of the study is timely – just last week the World Health Organization issued a warning about the rise in antibiotic-resistant strains of gonorrhoea.

The researchers claim this is the first vaccine to show any protective effect against gonorrhoea, but the vaccine in question is no longer in use.

variant of the vaccine is currently given to babies in the UK as part of the routine NHS vaccination schedule. As the New Scientist magazine speculates, if the biological mechanism is discovered, we may see a sudden drop in gonorrhoea cases in 20 years' time.

But it's unlikely that a dedicated vaccine against gonorrhoea will be available for at least a few years. And that prospect is not a certainty by any means.

For now, the most effective way to prevent gonorrhoea is to always use a condom during sex, including oral and anal sex.

Where did the story come from?

The study was carried out by researchers from Sexual Health Services, Waikato District Health Board, and the University of Auckland in New Zealand, and Cincinnati Children's Hospital in the US.

The research was funded by GSK Vaccines, a pharmaceutical company, and Auckland UniServices, a branch of the university that partners academics with industry. No conflicts of interest were declared.

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

The UK media's reporting was generally accurate – but the headlines weren't.

The Guardian's headline talks about "untreatable" gonorrhoea, but the study didn't look at whether any of the people had drug-resistant gonorrhoea or not. The research looked at data captured between 2004 and 2016, when drug-resistant gonorrhoea was less of a concern.

The Independent's headline – "World first as scientists develop vaccine that reduces chance of catching gonorrhoea" – is also inaccurate. The vaccine in question already existed, and it hasn't definitely been proven to reduce the chances of catching gonorrhoea.

What kind of research was this?

This case-control study looked at people with a gonorrhoea diagnosis and whether or not they'd had a meningitis vaccination in the past to see if there was an association. 

Gonorrhoea is a sexually transmitted infection caused by Neisseria gonorrhoeae bacteria, and is associated with multiple issues, including pelvic inflammatory disease, infertility and chronic pain.

Antimicrobial resistance has increased in recent years, and some strains of the infection are now resistant to drugs.

Researchers previously noted a decline in gonorrhoea diagnoses in New Zealand after a mass vaccination programme for meningococcal B, a serious cause of life-threatening infections such as meningitis and blood poisoning.

Meningitis B is caused by Neisseria meningitides, a bacteria similar to the one that causes gonorrhoea, so experts thought the MeNZB vaccine may be able to protect against both.

This type of research is useful for looking at a large population of people and examining trends and associations – but it can only show a link, not prove cause and effect.

randomised controlled trial would be needed to do this, where the vaccine is offered to some people and not others, but this would be unethical.

What did the research involve?

Researchers looked at 14,730 people aged between 15 and 30 who received a positive diagnosis of gonorrhoea or chlamydia at a sexual health clinic between 2004 and 2016.

They wanted to see if having the meningococcal B vaccine decreased the risk of getting gonorrhoea.

Of those involved, 1,241 people had a gonorrhoea-only diagnosis. Chlamydia-only diagnoses were used as the control group, which included 12,487 people.

Coinfection with both gonorrhoea and chlamydia is relatively common in sexually active adults who don't use condoms.

This means someone being diagnosed with chlamydia but not gonorrhoea could be the result of the meningococcal B vaccine.

Further analysis was done to include the 1,002 people who had both infections.

The researchers looked back over records from the New Zealand National Immunisation Register to identify which participants had received the MeNZB vaccine between 2004 and 2006.

They were able to link people diagnosed with gonorrhoea or chlamydia to their vaccine history through unique National Health Index numbers. They then adjusted the results for ethnicity, deprivation levels, geographical area and sex.

What were the basic results?

The researchers found 41% of the participants diagnosed with gonorrhoea only had been vaccinated against meningitis B, compared with 51% of the chlamydia-only group.

They also found:

  • People who had been vaccinated were 31% less likely to have a gonorrhoea diagnosis than a chlamydia diagnosis (adjusted odds ratio [aOR] 0.69, 95% confidence interval [CI] 0.61 to 0.79).
  • The effect of vaccination appeared to decrease over time. Subgroup analyses found the effectiveness of the vaccine was 20% in the period immediately after the vaccination programme from 2004-09 (95% CI 2% to 34%) compared with 9% from 2010-14 (95% CI 0% to 25%).
  • When people with coinfection were included in the gonorrhoea group, the effectiveness of the vaccine reduced to 23% (95% CI 15 to 30).
How did the researchers interpret the results?

The authors concluded that, "Exposure to [the] MeNZB [vaccine] was associated with reduced rates of gonorrhoea diagnosis – the first time a vaccine has shown any protection against gonorrhoea.

"These results provide a proof of principle that can inform prospective vaccine development not only for gonorrhoea but also for meningococcal vaccines." 


This large study found an association between having the MeNZB vaccine and a reduced likelihood of being diagnosed with gonorrhoea.

But it's difficult to form any firm conclusions because of the nature of the case and control groups.

For example, given that both groups were sexually active, we don't know why the majority of people with gonorrhoea didn't also have a chlamydia infection, and how this may have affected the results.

It could just be down to pure chance and have nothing to do with the vaccine.

So before we celebrate the alleged "cure of gonorrhoea", there are many things to consider:

  • The vaccine in question is no longer in use as a vaccine against meningococcal B. The Men4C jab is now used in the UK. Though it does have many similar components, we don't know if these are useful in protecting against gonorrhoea. Research now needs to focus on whether the association still exists with the new jab.
  • Although the authors adjusted for some variables, other factors might be at play that may have affected the results, such as people's education, diet, and immune system strength.
  • No new vaccine has actually been developed. The indication that something in the MeNZB vaccine might increase protection against gonorrhoea requires further research to pinpoint how it does so.
  • The research was only conducted on people who were diagnosed at a sexual health clinic, and didn't include data from GP surgeries. Many cases in the community could have been missed, and these people could have different immunisation trends.
  • We don't know how long the potential protective effect lasts for, as it seemed to decrease over time.

It's very much a case of "if" rather than "when" a gonorrhoea vaccine is developed. For now, the best way to protect yourself against gonorrhoea, chlamydia and other STIs is to always use a condom during vaginal, oral and anal sex.

Read more about how to have safe sex.

Links To The Headlines

Meningitis vaccine may also cut risk of 'untreatable' gonorrhoea, study says. The Guardian, July 10 2017

World first as scientists develop vaccine that reduces chance of catching gonorrhoea. The Independent, July 11 2017

First vaccine shows gonorrhoea protection. BBC News, July 11 2017

Links To Science

Petousis-Harris H, Paynter J. Morgan J, et al. Effectiveness of a group B outer membrane vesicle meningococcal vaccine against gonorrhoea in New Zealand: a retrospective case-control study. The Lancet. Published online July 10 2017

Does having a 'sense of purpose' in life help you sleep better?

NHS Choices - Behind the Headlines -

"Sense of purpose aids sleep, US scientists find," The Guardian reports on a new study that explored the relationship between having a sense of purpose in life and quality of sleep in older adults.

The study analysed data from 800 older adults with an average age of 80 in the US.

Researchers found that generally, having a greater sense of purpose in life was associated with better quality of sleep, as well as a decreased likelihood of sleep disorders such as sleep apnoea and restless leg syndrome

Although these are interesting findings, it's not possible to rule out the influence of other factors.

The fairly abstract concept of "sense of purpose" may be influenced by various health and lifestyle factors, such as levels of physical activity and mental health problems, and these may all in turn affect quality of sleep.

But this study wasn't able to pull out all of the intricacies of this complex relationship.

Problems with sleep are more common in the UK than most people realise, but there are proven ways to help combat insomnia.

As for having a "sense of purpose", research has shown that volunteering your time for a cause or charity you believe in can help improve your mental wellbeing.

Read more about how giving can improve your wellbeing

Where did the story come from?

The study was carried out by researchers from Northwestern University in the US, and was funded by the National Institute on Aging Grant Numbers and the Illinois Department of Health.

It was published in the peer-reviewed journal Sleep Science and Practice. It's available on an open access basis and is free to read online.

The UK media coverage around this research was generally balanced and well reported.

What kind of research was this?

This analysis of data from two cohort studies set out to explore the relationship between having a sense of purpose in life and quality of sleep.

Previous research has suggested that having a sense of purpose in life could protect against several negative health outcomes, one being sleep disturbances. Sleep disturbance is known to be more common among older adults.

Studies have also observed the prevalence of sleep disturbance to be higher among African Americans than white people. The researchers wanted to investigate this further.

Cohort studies are useful for looking at an association between an exposure and an outcome. But the study design means it isn't possible to fully rule out the influence of other confounding factors and prove that a purpose in life directly leads to better sleep.

What did the research involve?

The data sample for this analysis was taken from two ongoing Chicago-based cohort studies: the Minority Aging Research Study (MARS) and the Rush Memory and Aging Project (MAP).

MARS is a study of risk factors for cognitive decline that recruits older African Americans who haven't had a diagnosis of dementia.

MAP aims to look at the brain changes associated with ageing and cognitive decline. It recruited older adults of mostly white ethnicity (88%) without a diagnosis of dementia who agreed to annual clinical assessments, as well as brain autopsy after they died.

The analysis included 825 older adults with an average age of 79.

Purpose in life was measured at the start of the studies using a modified 10-item assessment derived from the Ryff and Keyes' Scales of Psychological Well-Being, a tool used to assess sense of purpose.

As part of the assessment, individuals were asked to respond to statements like "I feel good when I think of what I've done in the past and what I hope to do in the future", and "Some people wander aimlessly through life, but I am not one of them".

Participants used a five-point scale for their responses, ranging from 1 strongly disagree to 5 strongly agree. Higher scores were used to indicate higher levels of purpose in life.

Sleep quality and symptoms of potential sleep disorders were assessed using a 32-step questionnaire derived from the Pittsburgh Sleep Quality Index (PSQI), the Berlin Questionnaire, and the Mayo Sleep Questionnaire (MSQ). The questionnaire was given to participants at the end of each annual visit.

The PSQI assessed sleep quality, specifically looking at how long it takes to fall asleep, sleep duration, and how much you actually sleep during the night.

The Berlin questionnaire assessed risk of sleep apnoea, and the MSQ assessed the presence of restless leg syndrome and REM behaviour disorder, where dreams are acted out (for example, through sleepwalking or shouting out).

Sleep data was collected at baseline and follow-up points at the end of the first, second and third year.

The researchers analysed any links with purpose in life, adjusting for potential confounders like age, sex, race and years of education.

Changes in quality of sleep over the course of the two-year study were also taken into account.

What were the basic results?
  • Out of all the 825 respondents, at the beginning of the study 42% were at high risk of sleep apnoea, 23.6% were exhibiting symptoms of restless leg syndrome, and 7% had symptoms of REM behaviour disorder.
  • Higher levels of purpose in life were associated with better sleep quality. Over a one-year period, improved sleep quality was reported in people with a higher "purpose of life".
  • Increased levels of purpose in life were associated with a decreased risk of sleep apnoea (odds ratio [OR] 0.630, 95% confidence interval [CI] 0.454 to 0.875). This association continued during the first and second follow-up assessment.
  • Purpose in life wasn't significantly associated with symptoms of restless leg syndrome. But at year one of follow-up, it was associated with a decreased likelihood of having possible restless leg syndrome (OR 0.524, 95% CI 0.361 to 0.762).
  • Purpose in life wasn't significantly associated with REM behaviour disorder at baseline or years one, two and three of follow-up.
How did the researchers interpret the results?

The researchers concluded that, "In a biracial sample of over 800 older adults, the present findings provide support for the hypothesis that purpose in life is related to sleep quality, with indications that it could be a potentially useful clinical tool for assessing older adults."

They added: "We found that higher levels of purpose in life at baseline predicted better sleep quality at baseline, as well as increased change in sleep quality over a one-year period, a finding that is consistent with previous studies." 


This study explored the relationship between having a sense of purpose in life and sleep quality and sleep disorders.

Researchers found generally, having a greater sense of purpose in life was associated with better quality of sleep and a decreased likelihood of sleep disorders like sleep apnoea and restless leg syndrome.

The researchers suggest this may be down to people having better overall physical and mental health.

Although these are plausible hypotheses, there are a few points to note. As with the majority of cohort studies, it isn't possible to prove cause and effect and fully rule out the influence of other health, lifestyle and personal factors in the associations.

For example, having a healthy lifestyle can have an impact on quality of sleep. Drinking too much alcohol, smoking, not getting enough exercise, and mental health problems may reduce the chances of having a good night's sleep.

And it's difficult to know the exact impact of having less of a sense of purpose in life on sleep quality. This is a fairly abstract concept that may have various external influences this study wasn't able to fully explore.

The length of time a person has felt a particular way may also have an effect. For example, the effect on sleep may not be the same in someone who's felt they have no purpose in life for a long time compared with someone who's recently been under acute stress.

It would be interesting to conduct this study in young adults to see if the findings are similar. There may also be different possible influences on sleep, such as different dietary factors (like sugary drink consumption) or increased screen use, in other populations.

Learn about different ways to get a better night's sleep.

Links To The Headlines

Sense of purpose aids sleep, US scientists find. The Guardian, July 10 2017

How a sense of purpose helps you sleep well: Study finds those who feel their lives have meaning are less likely to suffer insomnia. Mail Online, July 9 2017

The secret of a good night's sleep has finally been found by scientists. The Daily Telegraph, July 10 2017

Links To Science

Turner AD, Smith CE, Ong JC. Is purpose in life associated with less sleep disturbance in older adults? Sleep Science and Practice. Published online July 10 2017

WHO issues warning about rise of drug-resistant gonorrhoea

NHS Choices - Behind the Headlines -

"Gonorrhoea fast becoming 'untreatable', WHO experts warn," reports Sky News.

Analysis of data from 77 countries by the World Health Organization (WHO) found antibiotic resistance exists against almost all antibiotics currently used to treat the sexually transmitted infection (STI) gonorrhoea.

In the past, gonorrhoea infections were treated effectively with a one-off dose of antibiotics.

Nowadays, gonorrhoea needs to be treated with both an antibiotic injection and a dose of antibiotic tablets.

And increased resistance to antibiotics, coupled with a lack of new treatments in the pipeline, raises concerns that the infection could be untreatable in the future.

This is concerning, as untreated gonorrhoea in women can cause complications that can lead to infertility and miscarriage. 

In this study, a WHO group outlined a new strategy to support the research and development of new treatments for gonorrhoea. Preventing the spread of the STI is also of paramount importance.

What is gonorrhoea?

Gonorrhoea is the second most common STI in the UK.

It's caused by the bacteria Neisseria gonorrhoeae, and can be transmitted easily through unprotected vaginal, oral or anal sex, infecting the genitals, back passage, and sometimes the eyes or throat.

Usual symptoms include an abnormal discharge from the vagina or penis, pain when passing urine, and bleeding in between periods in women.

Treatment involves an antibiotic injection and a single dose of antibiotic tablets.

But many people get no symptoms, so gonorrhoea can go unnoticed and untreated, which can lead to serious complications.

Around 10-20% of women can get pelvic inflammatory disease from gonorrhoea, which can then affect their fertility.

Gonorrhoea in pregnancy can also be transmitted to the infant, which can lead to newborn conjunctivitis and even threaten a baby's eyesight.

Where did the study come from?

The study was produced by the WHO Global Gonococcal Antimicrobial Surveillance Programme (WHO GASP), a group of researchers responsible for monitoring trends in drug-resistant gonorrhoea.

What is the new evidence?

The group analysed data from 77 countries, and found there is increasing resistance to all the drugs currently used to treat gonorrhoea – to both the first-choice antibiotic, and to the second-choice antibiotic used when the first one fails.

Bacteria have the ability to respond and adapt to antibiotics, with the potential to become effectively immune to the antibiotic's effects.

Even more worryingly, they can develop resistance to many different antibiotics, which now seems to be the case for the bacteria that causes gonorrhoea.

There also aren't many drugs currently being developed for the treatment of gonorrhoea. This raises the concern that the spread of drug-resistant gonorrhoea could outpace the development of new drugs, and may even result in doctors not being able to treat the STI.

In order to address this, the Global Antibiotic Research and Development Partnership (GARDP) initiative was launched in 2016 by the World Health Organization and Drugs for Neglected Disease (DNDi).

GARDP is a not-for-profit research organisation that sets up programmes around the world that aim to develop short- and long-term treatments for STIs, among other things.

As part of their initiative to improve research and development for new treatments for gonorrhoea, GARDP convened a panel of international experts from various institutions in different regions, including India, South Africa and China.

Together, they have outlined a research and development strategy that could help target the development of new treatments for gonorrhoea.


GARDP seeks to work with various experts to bring one new treatment for gonorrhoea to the market by 2023.

This is discussed in the research and development strategy, which outlines four components.

  • component 1: accelerate the development of a new chemical entity
  • component 2: evaluate the potential of existing antibiotics and their combinations
  • component 3: explore co-packaging and development of fixed dose combinations
  • component 4: support the development of simplified treatment guidelines and foster conservation

Explained simply, this means that GARDP hopes to:

  • Accelerate the development and registration of new molecules and drugs for the treatment of gonorrhoea, particularly those in the later stages of clinical trials that may be close to entering the market.
  • Conduct further research through randomised controlled trials to test whether the drugs currently used have the ability to treat gonorrhoea effectively. The drugs will be tested in populations with high numbers of sexually transmitted infections, as well as countries known to have various forms of antibiotic resistance.
  • Explore the use of combinations of antibiotics in fixed doses, which will help reduce costs and hopefully lead to more people taking the drugs as prescribed.
  • Support the development of evidence-based guidelines to ensure any new treatments are globally accessible, but mainly to make sure they're used and prescribed in an appropriate manner to reduce the emergence of more antimicrobial resistance to the drugs – it would be counterproductive to produce a new antibiotic to which gonorrhoea then becomes resistant.

The increase in antimicrobial resistance towards drugs used to treat gonorrhoea is reaching a critical stage, especially given how common the infection is worldwide, with an estimated 78 million new cases in 2012.

This study raises concerns around an important topic while also proposing strategies to help address the slow pace of research and development of new drugs.

The prevention of gonorrhoea is equally, if not more, important. The most effective way to prevent gonorrhoea is to always use a condom during sex, including anal and oral sex.

Read more advice about sexually transmitted infections and how to prevent them.

Links To The Headlines

Gonorrhoea fast becoming 'untreatable', WHO experts warn. Sky News, July 7 2017

Oral sex spreading unstoppable bacteria. BBC News, July 7 2017

Gonorrhoea becoming 'untreatable', experts warn. ITV News, July 7 2017

Untreatable gonorrhoea 'superbug' spreading around world, WHO warns. The Guardian, July 7 2017

Links To Science

Global Antibiotics Research and Development Partnership. Multi-drug-resistant gonorrhoea: a research and development roadmap to discover new medicines. July 2017 (PDF, 230kb)

Frequent ejaculation may decrease prostate cancer risk

NHS Choices - Behind the Headlines -

"Ejaculating at least 21 times a month significantly reduces a man's risk of prostate cancer," is the headline on the Mail Online. This is based on research from the US that asked men how often they ejaculated per month and subsequent reporting of prostate cancer.

They found that men who ejaculated 21 times or more a month were less likely to report prostate cancer at follow-up than those ejaculating four to seven times per month.

However, it does not prove that ejaculating more frequently prevents cancer, only that it is associated with a reduction in risk. It might be that a range of other factors such as genetics, lifestyle, number of children, diet, nature of sexual activity and education contribute to this risk, but we cannot say for sure what factors might increase the risk.

The researchers offer a number of hypotheses why ejaculation may help reduce prostate cancer risk, such as reducing stress or keeping cell metabolism well regulated. But these suggestions remain in the realm of speculation.

Despite any lurid tales you may have heard growing up, masturbation is entirely safe. So if you want to do it as a preventative method then it wouldn't pose any health risks.

Initial signs of prostate cancer usually involve problems with urination, such as needing to urinate more frequently, due to the prostate getting larger. While prostate enlargement can occur as men grow older, it is important to check symptoms like these with your GP.


Where did the story come from?

The study was carried out by researchers from Boston University School of Public Health, Harvard T.H. Chan School of Public Health, and Harvard Medical School, all in the US. It was funded by the National Cancer Institute and grants from the Prostate Cancer Foundation Young Investigator Award.

The study was published in the peer-reviewed medical journal European Urology on an open-access basis, making it freely accessible online.

The UK media reporting was generally accurate and, as you would imagine, some of the coverage, and the associated photos, were a little tongue in cheek.

The Sun's claim that "having 21 orgasms a month could be the key to preventing CANCER in men because it helps the prostate 'flush out toxins'" is unsupported. The claim that it flushes out toxins was not studied in this research and it is not proven that ejaculation is a "key to preventing cancer". 


What kind of research was this?

This was a cohort study following up male health professionals from 1992 for 18 years. It was designed to look at multiple health outcomes. In this particular analysis, the researchers aimed to determine their ejaculation frequency at different ages and whether it was associated with likelihood of getting prostate cancer.

A cohort study is best for this type of research as it allows reporting of people's habits and lifestyles without interfering and means a lot of people can be followed over a long period of time to see long-term health outcomes. However, a cohort study cannot control for other factors that may affect outcomes, a randomised controlled trial would be needed for that – but they are very time consuming, expensive, and intrusive on people's lives.


What did the research involve?

Researchers took data from the Health Professionals Follow-up Study, a study that began in 1986 aiming to look at links between men's lifestyles and health outcomes. They took 31,925 men's answers to a questionnaire about ejaculation frequency and looked to see if there was an association with developing prostate cancer.

The men were aged between 40 and 75 at baseline in 1986 and were all health professionals. They were asked questions about medical history and lifestyle every two years. Ejaculation frequency was assessed in the 1992 questionnaire.

The specific question asked was: "On average, how many ejaculations did you have per month during these ages?: age 20-29; age 40-49; past year."

The frequency of ejaculation per month was recorded in the following categories:

  • none
  • 1-3
  • 4-7
  • 8-12
  • 13-20
  • over 20

Follow-up was complete for 96% of the men still alive.

For men reporting they had prostate cancer, medical records were obtained to determine age at diagnosis; prostate specific antigen (PSA) level – PSA is a hormone associated with prostate enlargement; and tumour stage and grade.

To see if the link between ejaculation frequency and prostate cancer differed according to the specific characteristics of the cancer, clinical information was used to group prostate cancer into four risk categories:

  • Low risk = T1/T2 tumour, PSA<10 nanograms (ng) per millilitre (ml), Gleason score 6 (the Gleason score is a measurement of how likely the cancer is to spread out of the prostate into surrounding tissue)
  • Intermediate risk = T1/T2 tumour, PSA 10-20 ng/ml, Gleason score 7
  • High risk = T3 tumour, PSA 20-50 ng/ml, Gleason score 8
    Regional or distant metastases =
  • T4/N1/M1 tumour, PSA ≥50 ng/ml

Analyses were adjusted for a range of potentially confounding factors, including:

  • race
  • family history of prostate cancer
  • vigorous physical activity
  • body mass index
  • diabetes
  • marital status
  • diet
  • smoking
  • history of vasectomy
  • history of PSA testing


What were the basic results?

Over follow-up, a total of 3,839 cases of prostate cancer were diagnosed. Frequency of ejaculation per month decreased with age. The proportion of men reporting average frequency of 13 or more ejaculations per month was 57% aged 20-29 but dropped to 32% at age 40-49.

Excluding men with erectile dysfunction, compared with men who ejaculated four to seven times per month:

  • There was a 20% decreased risk of prostate cancer for those who ejaculated 21 times or more per month aged 20-29, (adjusted hazard ratio (aHR) 0.80, 95% confidence interval (CI) 0.69 to 0.92).
  • There was an 18% decreased risk of prostate cancer in ages 40-49 for those who ejaculated 21 times or more per month, (aHR 0.82, 95% CI 0.70 to 0.96).
  • There was a 26% reduction in risk of prostate cancer for men aged over 50 who had ejaculated 21 times or more per month in the previous year, (aHR 0.74, 95% CI 0.58 to 0.94).
  • There was also a decreased risk of prostate cancer in ages 40-49 for those who ejaculated 13-20 times per month (aHR 0.81, 95% CI 0.72 to 0.90).
  • There were similar yet smaller reductions in risk at all ages for men ejaculating 13 or more times per month.

For men ejaculating over 13 times per month compared with four to seven times per month:

  • For ejaculation while aged 20-29, there was a 25% lower risk of getting "low risk" prostate cancer, (aHR 0.75, 95% CI 0.63 to 0.89).
  • For ejaculation while aged 40-49, there was a 28% lower risk of getting "low risk" prostate cancer, (aHR 0.72, 95% CI 0.61 to 0.83).
  • For ejaculation in the year before the questionnaire, while aged over 50, there was a 25% lower risk of getting "low risk" prostate cancer, (aHR 0.75, 95% CI 0.62 to 0.92).
  • For ejaculation aged 20-29, there was a 27% lower risk of getting "intermediate risk" prostate cancer (aHR 0.73, 95% CI 0.61 to 0.88).
  • No significant differences were found for ejaculation frequency at older ages and "intermediate risk" cancer, or for any age and "high risk" prostate cancer.


How did the researchers interpret the results?

The researchers concluded that "this large prospective study provides the strongest evidence to date of a beneficial role of ejaculation in prevention of prostate cancer".

They add that "more frequent ejaculation in the absence of risky sexual behaviours could represent an important means of reducing the profound medical costs and physical and psychological side effects of unnecessary diagnosis and treatment of low-risk tumours, even though it appears to be less strongly associated with aggressive disease".



This research showed an association between ejaculating more frequently and a lower chance of getting prostate cancer in three different age groups.

Before too much is read into these findings, there are some limitations of the research to consider:

  • Three age groups were looked at; ages 20-29, 40-49 and 50 and over. It is not known what the differences are within these groups and it is not known what the outcomes would be if ejaculation was measured in different age categories.
  • Although the authors adjusted for some variables, there are still some factors that might have influenced the results, such as sociodemographic background, education level and whether the men had children.
  • The circumstances of ejaculation were not considered – in other words whether the occurrences were mostly through masturbation or with a sexual partner. This might have had an influence on the results.
  • The questionnaire relied on self-reporting and considering past history, which may have led to recall bias where participants inaccurately reported their ejaculation history.
  • Prostate cancer was self-reported through medical history and not specifically screened for. It might be that men who are more sexually active are less likely to seek cancer screening and therefore may be unaware of the presence of prostate cancer.
  • The study was conducted on mostly white health professionals in the US and might not be generalisable to the entire UK male population – especially as prostate cancer tends to be more common in men of African-Caribbean or African descent.

Aside from ejaculating frequently, other methods that may help reduce your risk of prostate cancer include achieving or maintaining a healthy weight, and regular exercise. 

Links To The Headlines

Ejaculating at least 21 times a month significantly reduces a man's risk of prostate cancer. Mail Online, July 5 2017

Having 21 orgasms a month could be the key to preventing CANCER in men because it helps the prostate ‘flush out toxins’. The Sun, July 5 2017

Links To Science

Rider JR, Wilson KM, Sinnott JA, et al. Ejaculation Frequency and Risk of Prostate Cancer: Updated Results with an Additional Decade of Follow-up. European Urology. Published online March 28 2016

Researchers try to unknot Alzheimer's protein tangles

NHS Choices - Behind the Headlines -

"Abnormal deposits that build up in the brain during Alzheimer's have been pictured in unprecedented detail by UK scientists," reports BBC News.

Alzheimer's disease is characterised by two proteins that take abnormal forms and build up in the brain: beta amyloid plaques and tangles of tau protein, both of which are thought to contribute to the symptoms of Alzheimer's.

Recent drug research has focused on amyloid plaques, but without much success. Interest is now shifting to tau tangles.

Researchers used a new ultra-magnifying technique called cryo-electron microscopy to picture tangles of tau protein in detail.

Cryo-electron microscopy involves freezing a tissue sample (which helps preserve it) and then using powerful microscopes to study the sample at a molecular level.

From this, researchers produced models of the molecules in the protein fibres. Eventually, this work may lead to therapies that can prevent the fibres spreading.

But that's not going to be easy. Brain cells need tau protein to function. The key will be to prevent overgrowth of tau protein fibres without stopping tau carrying out its vital work.

Any drug that targets tau would need to get inside brain cells. One expert estimates it may take 10-15 years before new drugs could be developed from this starting point.

So, this is just the start – but it's a good start. As well as Alzheimer's disease, tau is implicated in several neurological diseases, including Parkinson's disease, so other patients may also benefit from this advance.

Where did the story come from?

The study was carried out by researchers from the Medical Research Council Laboratory of Molecular Biology in Cambridge in the UK, and Indiana University School of Medicine in the US.

It was funded by the UK Medical Research Council, the European Union, the US National Institutes of Health, and Indiana University School of Medicine.

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

BBC News carried a balanced and accurate report of the study findings, but failed to spell out how much work now needs to be done before any new treatments can be developed.

What kind of research was this?

This pathology study used donated brain tissue, which was processed and underwent imaging to examine its protein structure.

This type of study is important for advancing our understanding of disease. It doesn't automatically lead to a cure.

What did the research involve?

Researchers used brain tissue donated by the family of a woman who died of Alzheimer's disease 10 years after diagnosis, aged 74. The tissue was processed to extract fibres of purified tau protein.

These were spread across a carbon grid, frozen, and hundreds of images taken using an electron microscope.

The researchers used the images to describe the molecular structure of the protein fibres and create 3-D molecular models of them.

They also carried out other analysis of the tau fibres, such as checking whether they could "seed" growth of the protein fibres in cultured cells, and compared them with other Alzheimer's disease brain cell samples.

What were the basic results?

Researchers found two types of tau fibres: a straight filament and a paired helical (spiral-shaped) filament.

The detailed molecular maps of the filaments show an ordered c-shaped core, common to both types of fibre. This core seemed to be necessary to seed the fibres through cultured brain cells.

The core is attached to what researchers describe as a "fuzzy coat", which doesn't have any clear molecular order and may grow randomly from the core.

The results were corroborated by other tests, which they said were "in good agreement" with proteins found in earlier research and mass spectrometry imaging of 10 other cases of Alzheimer's disease.

How did the researchers interpret the results?

The researchers said the structures they identified "establish a basis for understanding the differences between molecular conformers of tau aggregates [build-ups]".

They say the research "opens up new possibilities for studying the molecular mechanisms underlying a wide range of neurodegenerative disease". 


There's a tendency when scientists announce a breakthrough in our understanding of a disease to immediately start thinking about whether this could lead to a cure.

While the ultimate aim of research into Alzheimer's disease is of course to be able to prevent or treat it, early research like this is more about understanding the disease mechanisms.

This piece of research demonstrates how a new technique can be used to identify the molecular structure of abnormal protein deposits in the brain. That's a big step forward for use of this technology, which may be useful for other diseases, too.

The causes of Alzheimer's disease still aren't well understood. The brain is complex. Tangles of tau protein may be an important part of the development of Alzheimer's disease – but we don't know whether stopping the spread of tau tangles would halt the memory problems and mental decline characteristic of the disease.

While we can celebrate this advance as a scientific breakthrough in our understanding of Alzheimer's disease, we need to be patient about the chances of a cure.

Until then, while there's no guaranteed way of preventing Alzheimer's, the following may help lower your risk of developing the condition:

  • stopping smoking
  • not drinking large amounts of alcohol
  • eating a healthy, balanced diet, including at least five portions of fruit and vegetables every day
  • exercising for at least 150 minutes (2.5 hours) every week
  • staying mentally active

Read more about how to prevent Alzheimer's.

Links To The Headlines

Sharp focus on Alzheimer's may help target drugs. BBC News, July 5 2017

Links To Science

Fitzpatrick AWP, Falcon N, He S, et al. Cryo-EM structures of tau filaments from Alzheimer's disease. Nature. Published online July 5 2017

Toothpaste ingredient linked to antibiotic resistance

NHS Choices - Behind the Headlines -

"A common ingredient of soap and toothpaste could be causing antibiotic resistance and fuelling the spread of superbugs," the Mail Online reports.

This news follows the results of a study that looked at whether there could be a common reason why some gut bacteria have resistance to both the quinolone class of antibiotics and the chemical triclosan.

Triclosan has antibacterial properties and is found in a wide range of products, ranging from soap to cleaning products to children's toys. It's also found in some brands of toothpaste as it protects against gum disease. Quinolones are antibiotics often used to treat digestive infections such as E. coli and salmonella.

This study found E. coli and salmonella bacteria with mutations to a particular gene (gyrA) had some degree of resistance to both triclosan and quinolones. The mechanism of resistance was slightly different for the two substances.

The researchers also found that when certain mutant E. coli strains were exposed to low levels of triclosan, they became more dominant (grew more) than other bacteria, but only if they were already present.

Reassuringly, triclosan exposure didn't lead to new mutations developing in previously normal E. coli bacteria. But this doesn't rule out the possibility that triclosan could contribute to bacterial resistance in other ways.

In an accompanying press release, the researchers point out that traditional cleaning methods, such as soap, water and bleach, can be just as effective as antimicrobial branded products – and they don't contribute to the increasing threat of antibiotic resistance

Where did the story come from?

The study was carried out by researchers from the Institute of Microbiology and Infection at the University of Birmingham, and the Quadram Institute and John Innes Centre at Norwich Research Park.

It was supported by training grants received by individual researchers, and published in the peer-reviewed Journal of Antimicrobial Chemotherapy.

The Mail Online's coverage was accurate, and included some useful background information on how the US Food and Drug Agency has recently banned triclosan from personal cleaning products such as soap and body gel because of concerns about safety and antibiotic resistance.

The chemical is still used in some brands of toothpaste, both in the US and the UK, and has not been banned in the UK.

What kind of research was this?

This laboratory study aimed to see whether there could be a common link between bacterial resistance to quinolone antibiotics and resistance to triclosan.

Antimicrobial resistance is a global public health problem. As bacteria develop resistance to increasingly stronger antibiotics, we're reaching a point where this is overtaking the rate at which new antibiotics can be developed.

A world without effective antibiotics would see a return to a situation where routine surgeries become far riskier, and some conditions become untreatable.

Triclosan is a biocide – a chemical that can destroy micro-organisms. It's found in many household and cosmetic products like antiseptic soaps, body washes and toothpastes.

Quinolones are a group of commonly used antibiotics, including drugs like ciprofloxacin. Drugs in this group are used to treat a wide range of digestive tract infections, such as salmonella, as well as various respiratory, skin and urinary tract infections.

Quinolones mainly destroy bacteria by targeting a particular bacterial enzyme called DNA gyrase. The gyrA gene codes for this enzyme, and bacteria with mutations to this gene are resistant to quinolones because the antibiotics can no longer bind to this site.

A recent study has shown that salmonella bacteria with gyrA mutations were also less susceptible to triclosan.

The researchers aimed to investigate what mechanism could be causing the bacteria to become more tolerant to quinolone after being exposed to triclosan (a process known as "cross resistance"). 

What did the research involve?

This study involved normal (wild type) strains of E. coli and salmonella bacteria, as well as those with gyrA gene mutations.

Researchers looked at how well the bacteria were able to grow in the presence of quinolones and triclosan, and the minimum concentration of each drug or chemical needed to prevent bacterial growth.

They used laboratory methods to introduce new gyrA mutations and see how drug resistance differed by specific mutation.

As triclosan isn't known to directly target DNA gyrase in the same way as quinolones, they investigated the mechanism by which gyrA mutations could influence triclosan resistance.

The researchers finally tested the possibility that a suboptimal concentration of triclosan – below the level normally needed to stop bacterial growth – might support the growth of bacteria with gyrA mutations.

What were the basic results?

The research showed that both E. coli and salmonella bacteria with gyrA mutations were resistant to some degree to both the quinolone ciprofloxacin and to triclosan.

Eight times the ciprofloxacin concentration was needed to prevent bacterial growth, and four times the concentration of triclosan.

The researchers showed that there was some difference in the susceptibility of E. coli and salmonella to ciprofloxacin depending on the specific mutation the bacteria carried.

They confirmed that, as expected, triclosan doesn't directly target DNA gyrase. They found gyrA mutations in E. coli bacteria increased activity of the bacteria's main "stress response pathways", and this was how they were resistant to triclosan.

Stress response pathways is a term used to describe molecular "defences" that protect against environmental stresses or "threats".

The mechanism was slightly different for salmonella. In the "competitive fitness" tests, researchers found that exposure to low concentrations of triclosan led to E. coli bacteria with a specific gyrA mutation (Asp87Gly) becoming more dominant than other bacteria. The same effect wasn't seen with salmonella.

However, a promising finding was that previous exposure to low-concentration triclosan didn't lead to new quinolone-resistant mutations developing among the wild type bacteria. 

How did the researchers interpret the results?

The researchers concluded that, "Our data suggest gyrA mutants are less susceptible to triclosan due to up-regulation of stress responses. The impact of the gyrA mutation differs between E. coli and Salmonella."

They went on to say that, "The impacts of the gyrA mutation beyond quinolone resistance have implications for the fitness and selection of gyrA mutants in the presence of non-quinolone antimicrobials." 


This study mainly explored why bacterial resistance could be common for both quinolone antibiotics like ciprofloxacin and the antibacterial triclosan.

It confirmed previous findings that one cause seems to be bacteria developing mutations in the gyrA gene.

In the case of quinolones, the mutation alters the enzyme that they normally bind to. Triclosan resistance is largely because the already-mutant bacteria have boosted stress response pathways, or molecular defences.

The main finding of this research was that small triclosan concentrations led to resistant E. coli bacteria becoming the more dominant strains more likely to survive and reproduce.

This may cause concern that low concentrations in everyday products like toothpastes and body washes could lead to the development of antibiotic-resistant bacteria.

But this study didn't find direct evidence for this. Certain mutant E. coli strains did become more dominant, but only if they were already present.

Importantly, triclosan exposure didn't lead to new mutations developing in previously normal E. coli bacteria. This means that this research didn't demonstrate that triclosan causes the development of drug-resistant bacteria.

Nevertheless, there could be other mechanisms that cause resistance, aside from gyrA gene mutations. And triclosan exposure could also have an effect on the effectiveness of other antimicrobials.

This study will undoubtedly be an important contribution to the body of evidence on triclosan.

In 2016, the US Food and Drug Administration (FDA) banned the sale of antiseptic washes containing triclosan (and other ingredients) because of concerns that exposure could carry risks to human health, including being a possible cause of cancer, as well as potentially contributing to antimicrobial resistance.

The EU is also phasing out its use in domestic products, and European agencies are monitoring evidence on its safety and effectiveness.

Triclosan is still used in some brands of toothpaste, as it's thought to prevent gum disease.

Links To The Headlines

Common disinfectant found in soap and toothpaste could be causing antibiotic resistance. Mail Online, June 4 2017

Links To Science

Webber MA, Buckner MMC, Redgrave LS, et al. Quinolone-resistant gyrase mutants demonstrate decreased susceptibility to triclosan. Journal of Antimicrobial Chemotherapy. Published online July 3 2017

Heartburn drugs linked to premature death

NHS Choices - Behind the Headlines -

"Millions of people taking common heartburn and indigestion medications could be at an increased risk of death," The Guardian reports after a US study found people taking proton pump inhibitors (PPIs) had a slightly higher risk of death than the control group.

PPIs reduce the amount of acid in the stomach. As well as being used to treat heartburn, they're often given to people as a protective measure if they're thought to be at risk of a stomach ulcer – for example, people who take daily low-dose aspirin, which is known to irritate the lining of the stomach.

This headline is based on research in 350,000 predominantly male US veterans who were prescribed PPIs or H2 blocker drugs to either treat heartburn or protect the stomach. PPIs and H2 blockers both work by reducing stomach acid.

The researchers found people who took PPIs had a greater risk of death from any cause compared with those who took H2 blockers or nothing at all.

But there was no proof that the increased risk of death was directly caused by the PPI drugs. The researchers tried to adjust for underlying health factors, such as cardiovascular disease, which is often treated with daily aspirin, but it's possible the effects of these or other factors could still have influenced the results.

If you've been prescribed PPIs, you shouldn't stop taking them without first consulting your GP. The risk of not taking them (such as a stomach bleed) may be greater than any risk associated with taking them.

Where did the story come from?

The study was carried out by researchers from VA Saint Louis Health Care System, Washington University School of Medicine, and Saint Louis University in the US.

No information on funding was provided, but the data the researchers analysed came from the US Department of Veterans Affairs.

The study was published in the peer-reviewed journal BMJ Open and is open access, so it's free to read on the BMJ website.

The UK media's coverage of the story was generally accurate, but the headlines failed to reflect the inherent limitations of the study – including the fact that the conditions people were taking PPIs for in the first place may also have been one of the main causes of death.

What kind of research was this?

This large cohort study of US veterans aimed to look at whether PPIs or H2 blockers were associated with risk of death.

H2 blockers are drugs like ranitidine (Zantac) that reduce stomach acid, and are commonly used to treat acid reflux or heartburn.

PPIs such as omeprazole work in a slightly different way, but are also used to protect the stomach, often in people who have ulcers or those at risk because they take anti-inflammatories or aspirin long term.

Both types of drugs are available on prescription, and some can be purchased over the counter in pharmacies.

As this was a cohort study, it can't prove that taking one drug directly causes death – it can only show there's an association. It might be the case that other health, sociodemographic or lifestyle factors, such as high body mass index (BMI), contributed to the higher risk of death.

randomised controlled trial (RCT) would give more reliable evidence on the direct effect of either taking the different drugs or doing nothing (control group) while controlling for other factors.

But RCTs can be expensive and time consuming to carry out. Cohort studies can be useful to assess potential adverse effects, as they're able to follow an extensive number of people (in this case 349,312) over a long period of time.

What did the research involve?

Researchers used the US Department of Veterans Affairs national databases to identify 349,312 people (average age 61, 94% male) who'd been prescribed acid suppression therapy (PPIs or H2 blockers) between 2006 and 2008. They looked at their likelihood of death by any cause over 5.71 years on average.

Information on deaths is routinely gathered by the Veterans Benefit Administration for all US veterans.

The 275,977 participants whose first acid reflux drug was a PPI were placed in the PPI group, while the 73,335 participants who received H2 blockers first were the reference group.

In the H2 blocker group, 33,136 participants were later prescribed a PPI and were placed in the PPI group from the point they started taking PPI drugs.

The main outcome of interest was drug use in relation to death.  The researchers also looked at how long the drugs were prescribed for.

They adjusted their data to take into account a number of things that could have influenced the results, including:

  • age
  • race
  • gender
  • kidney function
  • number of hospitalisations

They also took into account a range of chronic illnesses, including:

  • diabetes
  • hypertension
  • cardiovascular disease
  • peripheral artery disease
  • stroke
  • chronic lung disease
  • hepatitis C
  • HIV
  • dementia
  • cancer
  • a range of gastrointestinal illnesses
What were the basic results?

Overall, 23.3% of the entire cohort died over the 5.71-year follow-up. The rate was 12.3% in those using H2 blockers at the start of the study, 24.4% in those using PPIs at the start of the study, and 23.4% in those who'd ever used PPIs.

The researchers found:

  • PPI use was associated with increased risk of death compared with H2 blocker use (hazard ratio [HR] 1.25, 95% confidence interval [CI] 1.23 to 1.28)
  • PPI use versus no known exposure to acid suppression therapy (PPIs or H2 blockers) was also linked with a similar increased risk of death (HR 1.23, 95% CI 1.22 to 1.24)

Risks were similar when only looking at participants with no known gastrointestinal problems:

  • PPI versus H2 blocker use (HR 1.24, 95% CI 1.21 to 1.27)
  • PPI versus no known acid suppression therapy (HR 1.22, 95% CI 1.21 to 1.23)

Compared with participants taking PPIs for 30 days or less, risk of death gradually increased with the length of time they were taking them:

  • 31-90 days (HR 1.05, 95% CI 1.02 to 1.08)
  • 91-180 days (HR 1.17, 95% CI 1.13 to 1.20)
  • 181-360 days (HR 1.31, 95% CI 1.29 to 1.34)
  • 361-720 days (HR 1.51, 95% CI 1.47 to 1.56)
How did the researchers interpret the results?

The researchers concluded that, "The results suggest excess risk of death among PPI users; risk is also increased among those without gastrointestinal conditions and with prolonged duration of use. Limiting PPI use and duration to instances where it is medically indicated may be warranted." 


This larger set of observational data finds that PPI drugs are associated with an increase in the risk of early death compared with either H2 blockers or no acid suppression drugs. This was the case for participants both with and without gastrointestinal problems.

It also appears as though the longer the PPIs drugs are taken, the greater the risk of death.

Considering that these drugs are widely used in the UK, these findings may cause concern. But the research has a number of important limitations:

  • The study was conducted in a population of mostly white, older US male veterans, which might limit the ability to generalise the results to the whole UK population.
  • Deaths can't be linked directly to the use of PPIs. The researchers have tried to adjust for many health and other characteristics that could be linked with both PPI use and higher risk of death, such as cardiovascular diseases, but we still can't be certain the influence of the disease has been fully taken into account.
  • Many of the deaths occurred in the first year, so could well be linked to underlying causes. There was also no information on cause of death.
  • The follow-up period only lasted around five years. Longer term death outcomes weren't examined – it may be that PPIs are associated with better outcomes for participants in the long term, but we can't say for sure either way.
  • The length of follow-up in the PPI group was more than two years longer than in the H2 blocker group, so it's unsurprising there was a greater risk of death given the extra two years of data collection.
  • The drugs were all prescribed in outpatient settings. Some brands of these drugs are available over the counter in the UK. There might be a difference between the groups of people who have their drugs prescribed and those who buy them over the counter, both in terms of risk and in the dose of the drugs.
  • This study can't attribute risk to any individual PPI drug. If there is a direct mortality risk from PPIs, it may differ according to which drug it is – but this study isn't able to tell us this.

Overall, this large study of good-quality data raises a clear link that needs further examination.

But people who have been prescribed PPIs shouldn't stop taking them – the risk of not doing so may be much greater than any risk the drugs pose. For example, a bleeding stomach ulcer can be very serious and potentially life threatening.

If you're concerned about your medication, you should discuss your treatment options with your GP or the doctor in charge of your care.

Links To The Headlines

People taking heartburn drugs could have higher risk of death, study claims. The Guardian, July 4 2017

Heartburn drugs taken by millions may increase risk of early death, study suggests. The Daily Telegraph, July 3 2017

Indigestion pills 'may increase the risk of an early death': People who use one type of treatment for heartburn are 25% more likely to die within six years. Daily Mail, July 4 2017

Acid reflux drugs linked to heightened risk of premature death in new study. The Independent, July 4 2017

Links To Science

Xie Y, Bowe B, Li T, et al. Risk of death among users of Proton Pump Inhibitors: a longitudinal observational cohort study of United States veterans. BMJ Open. Published online July 4 2017

Brain training app used to treat memory condition

NHS Choices - Behind the Headlines -

"Brain training games boost the memory and may reduce the risk of dementia, new research suggests," The Daily Telegraph reports.

Researchers used an app called Game Show to treat people with amnestic mild cognitive impairment.

Amnestic mild cognitive impairment, which is characterised by problems with short-term memory worse than expected for a person of that age, can be the first sign of dementia. But not everyone with this condition will go on to develop full-blown dementia.

The app game involved associating different geometric patterns with different locations. The small study, involving 42 adults, found playing games on the app for eight hours over four weeks improved the participants' performance in memory tests.

The participants also reported that they enjoyed playing the games and were motivated to continue using the app after the study ended. This would be important if the game was prescribed to help people with amnestic mild cognitive impairment in real life.

This research is in its very early stages. It's not yet clear whether the game would be able to improve the symptoms of people with this condition in everyday life, or slow the development of dementia.

As one expert commentator has pointed out, this type of training is unlikely to prevent or cure dementia, but may help with symptoms.

Get more advice on activities that may be useful for people with early-stage dementia.

Where did the story come from?

The study was carried out by researchers from the University of Cambridge and the University of East Anglia.

It was funded by a grant from Janssen Pharmaceutica/Johnson & Johnson, and the study's authors received funding from the Wellcome Trust, Eton College, and the Wallitt Foundation.

The authors note that they have consulted for or received grants from various medical companies.

The study was published in the peer-reviewed International Journal of Neuropsychopharmacology. It's open access, so it's free to read online.

Most UK news sources reported on the study using an appropriate degree of caution, given the early stage of the research.

The Times and The Daily Telegraph say that the app "may" reduce the risk of dementia or slow its progression in their headlines, and the Mail Online included a prominent section describing some of the study's limitations.

The Independent refers to the participants as having "early-stage dementia" in its headline, and the Mail Online also refers to them as having "early onset dementia". But this isn't quite correct.

The participants were older adults with mild cognitive impairment, a condition where people have problems with their memory that aren't severe enough to be classed as dementia. 

While people with mild cognitive impairment are at increased risk of developing dementia, not all will go on to develop the condition.

What kind of research was this?

This randomised controlled trial (RCT) assessed whether a new "brain training" app called Game Show might help people with a form of memory impairment with their memory difficulties. This study design is the best way to test treatments to see if they have an impact.

Participants in this study had amnestic mild cognitive impairment (aMCI). People with this condition have problems with memory that are worse than would be expected for a healthy person of that age, but not severe enough to be classed as dementia and don't affect their ability to perform everyday tasks independently.

The condition is more common in older people, and people with the condition are at increased risk of developing dementia.

The Alzheimer's Society reports that different studies have found between about 5 and 15% of people with aMCI develop dementia each year. The charity has published a factsheet on aMCI (PDF, 1.05Mb).

Amnestic mild cognitive impairment may also reduce motivation, which could have an impact on whether or not people with the condition take part in programmes that might help them, or stick with them.

There are no effective drug treatments for aMCI, but cognitive training – essentially a form of "brain training" – has been reported to show benefits.

The study's authors say that existing cognitive training programmes are reported to be boring and repetitive. They developed a cognitive training game and tested it to see if it would help with memory as well as be enjoyable to play.

What did the research involve?

The researchers enrolled 42 adults with aMCI and assigned them at random to either play Game Show for eight hours over four weeks, or just carry on with their usual clinic visits (the control group). They then tested their memory at the end of the four weeks.

The participants, who were about 75 years old on average, took a range of standard memory tests and had their symptoms assessed at the start of the study.

The two groups – game playing and control – were similar at the start of the study.

The participants took the memory tests again at the end of the four-week study.

The main assessment was the Cambridge Neuropsychological Test Automated Battery Paired Associates Learning (PAL), which assessed episodic memory, or the ability to remember locations and events.

This test involves being shown boxes at various positions on a touch-sensitive screen, and opening in a random order.

One or more boxes contain a pattern. The patterns are then shown again in the middle of the screen, and participants are asked to touch the box in which that pattern originally appeared.

The task increases in difficulty, starting with a single pattern, and ending with a series of eight patterns. If the participant makes an error, the patterns are shown again in their original positions, and the participant can try to locate them again.

The Game Show app employed a similar task of pattern and location mapping, but involved appealing and engaging visual displays, music, and a virtual "quiz show" host.

Participants in the group playing the game did so for an hour at a time on an iPad, and were supervised by the researchers while they did it.

After each hour of play, participants rated how much they had enjoyed the game and how much they wanted to continue playing, as well as their self-confidence and memory.

What were the basic results?

Playing the Game Show app improved various aspects of the participants' performance on the PAL test of episodic memory.

Compared with the control group, at the end of the four-week study Game Show players:

  • made significantly fewer errors remembering where patterns were located in the two and three-pattern stages, but not at later, more difficult, stages
  • took fewer goes to get the two-pattern stage correct, but not in the more difficult stages
  • correctly located many patterns in their first go at each stage of the game

The people who played Game Show reported high levels of enjoyment and motivation to continue playing that lasted up to the end of the four-week study.

How did the researchers interpret the results?

The researchers concluded that episodic memory improved in people with aMCI by playing the Game Show cognitive training app.

Turning the training into a game improved motivation, and therefore engagement with the training.

The researchers suggest that the game "could complement [drug] treatments for aMCI and mild Alzheimer's disease", but more controlled trials are needed to confirm these findings and extend them to other groups.


This small trial suggests that an iPad game aimed at training episodic memory – memory of locations and events – can lead to improvements in this aspect of memory in older adults with aMCI.

The fact the study used a control group and an RCT design increases confidence in these findings.

But there are some important things to bear in mind at this very early stage:

  • The study was very small – the authors acknowledge that it needs to be repeated in a larger sample of people to confirm the findings.
  • The game hasn't been tried in people with dementia, so we don't know if it would help them.
  • The study only followed participants for four weeks. More studies are needed to see how long the improvements last, especially if participants stop playing the game, and whether motivation to play the game is maintained in the longer term.
  • The researchers largely focused on performance in specific tests of episodic memory. It isn't clear whether the benefits seen in these tests would mean that the participants' memories were better in everyday situations. The participants playing the game did rate their memory as better, but it's unclear if they just meant their memory performance in the game or their memory in general.
  • The group that played the game did so under the supervision of research staff. This level of attention may have contributed to their feelings of motivation and confidence. The opposite is true of the control group, who knew they weren't getting to play the game. This could potentially contribute to the memory results seen. Ideally, in future studies the control group would have the same level of interaction with the research staff (an attention control) to make sure this doesn't have an effect.

As one expert commentator pointed out, this type of training is unlikely to prevent or cure dementia – but it may help with the symptoms.

With an ageing population, research like this is increasingly important. The use of technology like computerised touch screen games to deliver this training is very appealing, and could potentially be used in the home without the need for supervision.

Links To The Headlines

Brain training games boost memory and may reduce the risk of dementia, research suggests. The Daily Telegraph, July 3 2017

Could an app reverse the early signs of dementia? Brain training game improves memory in people with mild cognitive impairment. Mail Online, July 3 2017

New brain training app improves memories of people with early-stage dementia. The Independent, July 3 2017

Links To Science

Savulich G, Piercy T, Fox C, et al. Cognitive Training Using a Novel Memory Game on an iPad in Patients with Amnestic Mild Cognitive Impairment (aMCI). International Journal of Neuropsychopharmacology. Published online July 2 2017

Some women in the UK still unaware of cervical screening

NHS Choices - Behind the Headlines -

"Nearly a quarter of women who don't make cervical screening appointments are unaware that the process even exists, according to a UK survey," BBC News reports.

Cervical cancer is a type of cancer that starts in the cervix, the entrance to the womb. It's responsible for around 900 deaths a year in the UK.

Regular screening appointments to check for abnormal cell growth are offered to all women aged between 25 and 64.

This study found about a quarter of eligible women didn't go for a cervical screening test. Most women who didn't attend either said they were unaware of screening or that they intended to go, but were overdue for their appointment.

Cervical cancer became a high-profile media topic after the untimely death of reality TV star Jade Goody from the disease in 2009. It now seems that almost a decade later, the issue has dropped off the radar for many women.

The researchers suggest that interventions to increase the uptake of cervical screening should focus on three main types of non-participants:

  • those who intend to go to screening but don't actually confirm an appointment
  • those unaware of screening
  • those who actively decide not to be screened

Read more about cervical cancer screening, including why it's offered and who's invited for a screening test.

Where did the story come from?

The study was carried out by researchers from University College London (UCL) in the UK and the National Cancer Institute in the US.

It was funded by a grant from Cancer Research UK.

The study was published in the peer-reviewed European Journal of Cancer. It's available on an open access basis and is free to read online.

BBC News' coverage was balanced and accurate.

What kind of research was this?

This cross-sectional study wanted to assess the prevalence of women who didn't participate in the UK cervical cancer screening programme, and better understand the reasons why they didn't attend.

Cervical screening is used to detect any abnormal changes in cells in the cervix that could potentially develop into cervical cancer.

All women between the ages of 25 and 64 who are registered with a GP are invited for cervical screening.

But the uptake of cervical screening has been decreasing in the UK. The researchers wanted to investigate the reasons behind the fall in attendance.

Cross-sectional studies are useful for analysing data from a population at a specific point in time. But a drawback is that they can't confirm the cause for any observations or explore which factors could be having an influence.

What did the research involve?

Researchers surveyed 3,113 women eligible for screening in the UK using face-to-face computer-assisted personal interviews (CAPIs).

Four questions were asked around past screening behaviour and whether the women intended to attend screening in the future.

The questions were:

  • Have you ever heard of cervical screening, also known as the smear test or Pap test?
  • Have you ever had a cervical screening test?
  • When was the last time you had a cervical screening test?
  • Do you intend to go when next invited?

From their responses, the women were categorised as either participants or non-participants.

Non-participants were classified as:

  • unaware
  • unengaged
  • undecided
  • decided not to be screened
  • intending to be screened

Data was also collected on sociodemographic characteristics, such as:

  • age
  • marital status
  • number and age of children
  • occupational status
  • ethnicity
  • first language spoken
What were the basic results?

Of the 3,113 women, 793 (27%) were classed as non-participants:

  • 219 women (28%) were unaware of screening
  • 406 women (51%) were overdue for screening but intended to be screened
  • 118 women (15%) had decided not to be screened

Women between the ages of 25 and 34 were more likely to be classed as non-participants. They were also the most likely age group to be unaware of screening. Women aged 55-64 were most likely to have decided against screening.

Women from lower socioeconomic groups and who didn't work were more likely to be unaware of screening, overdue for screening, or to have decided against screening.

Single women were more likely to be unaware or to have decided not to be screened compared with married women.

Women from ethnic minority groups were more likely to be unaware of screening. But South Asian and black women were more likely to intend to go to screening than white British women.

When language was adjusted for, there was no difference between white British women and those from different ethnic backgrounds.

How did the researchers interpret the results?

The researchers concluded that, "This work suggests that the vast majority of women in Britain who are not participating in cervical screening as recommended are not making an active decision not to attend.

"Most non-participants are either unaware or would like to be screened but are unable to translate their positive intentions to be screened into action." 


This study presents interesting findings on the proportion of women who don't go for cervical screening tests, and the possible reasons for their non-attendance.

Researchers found most non-participants were either unaware of screening or intended to go to screening but still failed to go. This was most common in single women aged 25-34.

One point to note is that the data was collected through self-reported questionnaires, which carry the risk of inaccurate reporting because of the perceived social stigma around screening and the desire to give the "right" response.

In the case of cervical cancer screening, it's possible women know they should attend screening but for whatever reasons don't want to attend, but feel more comfortable saying that they do in fact plan to attend screening, even when they might not in reality.

Another point is that women who agree to participate in market research screening interviews may be from different socio-demographic groups to those who don't.

This means we can't be completely sure that this sample – despite being large – represents the views and screening participation of the population as a whole. 

The researchers suggest that this study will help focus interventions on three main types of non-participants to increase the uptake of cervical screening:

  • those who intend to go to screening but are overdue for the test
  • those unaware of screening
  • those who actively decide not to be screened

This incredibly useful study highlights the need for further exploration into the reasons why some women don't go for cervical screening – what is the exact reason women are unaware of screening, and why do they choose not to attend?

These questions are important, as cervical cancer is often preventable if abnormal cell changes are detected early.

In England, screening is offered to all women aged 25-64. Teenage girls aged 12-13 are offered the HPV vaccine, which helps protect against cervical cancer, as part of the routine NHS childhood vaccination schedule.

Links To The Headlines

No-show women at cervical screening 'unaware of test'. BBC News, June 30 2017

Links To Science

Marlow LAV, Chorley AJ, Haddrell J, et al. Understanding the heterogeneity of cervical cancer screening non-participants: Data from a national sample of British women. European Journal of Cancer. Published online May 20 2017


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