NHS Choices

Probiotics 'aid memory in people with Alzheimer's disease'

NHS Choices - Behind the Headlines -

"Probiotics found in yoghurt and supplements could help improve thinking and memory for people with Alzheimer's disease," The Daily Telegraph reports after a small study found people given the bacterial supplement had improved scores on brain function tests.

Probiotics are live bacteria and yeasts promoted as having various health benefits, and are often added to yoghurt.

An Iranian research team gave people with severe Alzheimer's disease a probiotic drink every day for 12 weeks, and then measured the changes in brain function test scores before and after the treatment.

They found small improvements after the probiotics were given compared with the placebo group, but it is unclear if these improvements were enough to be clinically useful or noticeable.

While the results are far from conclusive, they do add to a previous body of research that suggests there may be an association between gut health and brain function.

Exploring this association could lead to new insights and possible treatments for Alzheimer's and other forms of dementia.

There are no known safety concerns about probiotics. But based on the small size and short-term nature of this study, more rigorous research would be required before probiotics could be recommended as an evidence-based treatment for people with Alzheimer's disease.

Where did the story come from?

This Iranian study was carried out by researchers from Kashan University of Medical Sciences in Iran and was funded by a grant from the same university.

It was published in the peer-reviewed journal, Frontiers in Aging Neuroscience. This journal is open access, so the study is free to read online.

The UK media's coverage of this study was generally accurate, although this is early research and its limitations were not fully discussed.

What kind of research was this?

This randomised controlled trial (RCT) looked at whether probiotic supplements help improve cognitive function in patients with Alzheimer's disease.

It also investigated the effect of probiotics on biomarkers for inflammation and metabolism in the body.

Probiotics are often referred to as "good" or "friendly" bacteria, and are found in yoghurts and other dairy products.

Although probiotics have traditionally been recommended for people with gut conditions such as irritable bowel syndrome (IBS), recent research has shown they may benefit the brain, too.

This is because there may be a link between the gut and the brain along what's known as the micro biota-gut-brain axis.

This axis is a biochemical signalling pathway that runs between the brain and the digestive system. But its full role in terms of health outcomes is thought by many to not be fully understood. 

Double-blind randomised controlled trials like this one are thought to be the gold standard when it comes to investigating a potential association between an exposure and an outcome – in this case, between probiotic supplements and changes in cognitive function.

What did the research involve?

This 12-week trial recruited 60 patients with Alzheimer's disease with a mean age of 80. The participants were all matched for disease severity based on gender, age and body mass index (BMI).

They were then randomly assigned to two treatment groups (30 participants in each): the control group received plain milk, while the intervention group received probiotic milk (200ml a day).

The probiotic drink contained the bacterial strains Lactobacillus acidophilus, Lactobacillus casei, Bifidobacterium bifidum and Lactobacillus fermentum. 

The patients' cognitive function was measured before and after the 12-week trial using a Mini-Mental State Examination (MMSE). This scale is a 30-point questionnaire used extensively to measure cognitive impairment.

The test takes about 10 minutes to complete and assesses cognitive – or thinking – abilities such as attention, calculation, recall, language, and the ability to follow simple commands.

One example question is to ask people to count backwards from 100 in sevens. Any score greater than or equal to 24 points out of 30 indicates normal cognition.

Blood samples were also collected to assess levels of biomarkers for oxidative stress, which is an indicator of cell damage, as well as inflammation and metabolic profiles.

During the study, four patients from each treatment group died from old age. A total of 52 patients went on to complete the study. The data from these 52 patients was analysed and the findings were compared between the two treatment groups.

What were the basic results?

Overall, the 12-week treatment with probiotic supplements resulted in an improvement in the MMSE score of +27.9%, compared with a decrease of -5.03% in the control group.

In absolute terms this means that the control group deteriorated from 8.47 to 8.00, remaining severely impaired on the 30-point scale. Those taking probiotics improved from 8.67 to 10.57.

Although the difference was statistically significant, it is still a small change and suggests that even after taking probiotics everyone remained severely cognitively impaired.

The probiotic treatment also had a positive influence on a range of other blood markers that were of interest to the researchers.

However, changes in biomarker levels for oxidative stress, fasting plasma glucose (a marker of insulin sensitivity) and other lipid (fat) profiles remained insignificant.

It is not clear if these have a bearing on the development of Alzheimer's and how any link between them and drinking probiotics might be acting.

How did the researchers interpret the results?

The researchers concluded that, "The current study demonstrated that the probiotic administration for 12 weeks has favourable effects on MMSE score, MDA, hs-CRP, markers of insulin metabolism and triglycerides levels of the AD patients; however, the changes in other biomarkers of oxidative stress and inflammation, FPG and other lipid profiles are negligible." 


This randomised controlled trial looked at whether probiotic supplements help improve cognitive function in patients with Alzheimer's disease over 12 weeks.

It also investigated the effect of probiotics on biomarkers for inflammation and metabolism in the body.

It found treatment with probiotic supplements resulted in a small improvement in cognitive function compared with the control group.

But everyone remained severely cognitively impaired, and it's not clear if the change in score was clinically important in terms of function.

Although these are interesting findings, there are a few things to bear in mind:

  • This was a small trial involving 60 people. This intervention would need to be tested on a larger sample size to confirm the findings, as it's still possible that the change observed is a chance finding.
  • The participants were mainly female – only 12 male patients were involved – and everyone had severe dementia at the start of the study, so it's unclear whether probiotics are able to prevent dementia in the general population.
  • The trial was conducted for 12 weeks. As Alzheimer's is a progressive disease, it would be beneficial to monitor the long-term effects of probiotics in patients with Alzheimer's disease to know whether the improvement in cognitive function would last longer than three months.
  • The participants in the trial were an average age of 80. It would be interesting to see if the same effect was observed in patients at an earlier stage of Alzheimer's disease.

Dietary advice for people with Alzheimer's disease is the same for most other people – to eat a healthy, balanced diet.

Read more advice about caring for someone with Alzheimer's or other forms of dementia.

Links To The Headlines

Probiotics can help thinking and memory for people with Alzheimer's disease. The Daily Telegraph, November 10 2016

Eating probiotics 'boosts' brain power in Alzheimer's patients. The Sun, November 10 2016

Yoghurt 'can help treat Alzheimer's'. The Times, November 11 2016 (subscription required)

Links To Science

Akbari E, Asemi Z, Kakhaki RD, et al. Effect of Probiotic Supplementation on Cognitive Function and Metabolic Status in Alzheimer's Disease: A Randomized, Double-Blind and Controlled Trial. Frontiers in Aging Neuroscience. Published online November 10 2016

Scouts and Guides 'grow up to have better mental health'

NHS Choices - Behind the Headlines -

"Scouts and guides provide 'mental health boost for life'," BBC News reports. A study of adults with a scouting or guiding background found they were less likely to be anxious or depressed in later life.

But the difference in average mental health scores was quite small (2.2 points on a 1 to 100 scale). About 21% of people who'd been Scouts or Guides had scores that suggested a mood or anxiety disorder, compared to 25% of those with no history of involvement in Scouts or Guides.

The researchers also found the expected poorer mental health associated with coming from a lower social class did not seem to apply to children who'd been Scouts or Guides.

This may suggest that the inclusivity of both charity organisations, which welcome children from all backgrounds, may play a positive role in adulthood.

This type of research may be complicated by other factors. The researchers tried to take account of other factors, such as whether people took part in other clubs, but it is hard to be sure that other factors don't partly explain the findings.

While the overall results may appear modest, when it comes to mental health, every little helps.

Interestingly, the "Scouting principles" described by founder Robert Baden-Powell in the first decade of the 20th Century seem to chime with many of the steps that experts now think can lead to improved mental wellbeing.

These include connecting with others, lifelong learning, being mindful of the world around you and helping others.


Where did the story come from?

The study was carried out by researchers from the University of Edinburgh and the University of Glasgow and was funded by the Economic and Social Research Council.

The study was published in the peer-reviewed Journal of Epidemiology and Community Health on an open access basis, so the study is free to download (PDF, 351kb).

The UK media was enthusiastic about the possibility that Scouts and Guides were protected against poor mental health in middle age, and reporting was broadly accurate.

Many papers included quotes from individuals involved with the Scouting and Guiding movements, such as 18 year old Girlguiding member Emma Brodey, who said "Girlguiding is … for the girl. It offers a safe space where they can be themselves, build their confidence and escape from the ever-increasing pressures in their lives. Women tell us every week that their accomplishments and memories through guiding have lasted throughout their lives".


What kind of research was this?

This was a cohort study, intended to find out whether Scout or Guide participation in childhood was linked to adult mental health, and how this interacted with social class. Cohort studies are good ways to show links between factors, but it's much harder to show that one factor causes another.


What did the research involve?

Researchers used information from the UK's National Child Development Study, set up to study people born in one week in 1958.

A group of 9,790 people from this study were interviewed about their mental health in 2008, at age 50.

Researchers used information about the people from childhood onwards to adjust their figures for confounding factors, then looked to see whether they had better mental health if they'd been Scouts or Guides, and how this was affected by social class.

Only 4,020 people had complete records, so the researchers used statistical techniques to fill in the gaps. Some people were then excluded from the study if there was too little information about them. The researchers included 9,603 people in total.

Social class was assessed by their father's status, and educational aspiration by whether their parents wanted them to stay at school past the minimum leaving age of the time.

The research also looked at family history of mental health problems, and how often they played indoor or outdoor games or sports.

To try to take account of possible confounding factors, researchers looked at whether people took part in other clubs, voluntary groups or religious groups, and whether that was linked to their mental health.

They also looked at whether geographical areas with higher or lower Scout and Guide participation had differing mental health status.

They also considered if the amount of time people attended Scouts and Guides was linked to mental health (a so-called "dose response" where the effect size is in line with the amount of attendance – "the more the better").


What were the basic results?

The average mental health score (from a scale 0 to 100, where higher is better) was 74.8.

Researchers found 28% of the group had been Scouts or Guides, and for them:

  • average mental health score was 2.28 points higher
  • the chance of having a score of 65 or less, which the researchers used as a mark of having anxiety or mood disorder, was 18% lower, at 21 in 100 compared to 25 in 100 for people who weren't scouts or guides (odds ratio 0.82, 95% confidence interval 0.74 to 0.92)
  • the effect of social class, in which people with lower social class had poorer mental health aged 50, was less pronounced. People from lower social classes who'd been Scouts or Guides had as good or better mental health than those from higher social classes who hadn't been Scouts or Guides

Current membership of churches or voluntary organisations did not have any effect on mental health. However, surprisingly the researchers found that previous membership of a voluntary organisation was linked to a 27% increased chance of anxiety or mood disorder. Possible reasons for this were not explored.


How did the researchers interpret the results?

The researchers say their research "suggests that scout-guide attendance may be protective, instituting a resilience to stressful life events that may lead to mental ill health." They say that the relationship "does not appear to be explained by potential confounding factors".

They conclude: "encouraging interventions in youth that are low cost and available worldwide through existing institutional structures may be an important and cost-effective policy response" to poor mental health in later life.



The theory that being in the Scouts or Guides could set you up for good mental health for life is very attractive.

Scout and Guide membership is designed to help young people learn life skills, take part in communal activities and enjoy the outdoors, all of which are likely to help with better mental health.

However, there are a few issues to be aware of:

  • Observational studies can't prove beyond doubt that one factor causes another, even when the researchers try to account for alternative explanations for their findings.
  • The results threw up one odd finding – that past participation in voluntary groups greatly raised the risk of poor mental health, by much more than participation in Scouts or Guides reduced it. This surprising result casts doubt on the reliability of the other findings.
  • More than half of the participants in the study had missing data that had to be added in by researchers, making assumptions about the participants. This could introduce errors.
  • The researchers didn't find any evidence of a dose response – that the more people attended Scouts or Guides, the better their mental health.

However, whether or not these results are completely reliable, Scouts and Guides are low-cost, volunteer-run charity organisations which may offer young people support and life skills that could help them through life. To paraphrase the Scouting motto, it's always better to be prepared.

Links To The Headlines

Scouts and guides provide 'mental health boost for life'. BBC News, November 10 2016

Scouts and Guides are more likely to be happy adults: Getting members outdoors helps the chance of anxiety in middle age by a fifth. Daily Mail, November 10 2016

Being a scout or guide ‘can help improve mental health in later life’. The Independent, November 10 2016

Scouts and guides grow up to have better mental health. The Daily Telegraph, November 10 2016

Scout skills lower risk of anxiety. The Times, November 10 2016 (subscription required)

Links To Science

Didden C, Playford C, Mitchell R. Be(ing) prepared: Guide and Scout participation, childhood social position and mental health at age 50—a prospective birth cohort study. Journal of Epidemiology and Community Health. Published online November 10 2016

Teen vapers 'more likely to take up smoking'

NHS Choices - Behind the Headlines -

"Vaping raises likelihood of teenagers starting to smoke, study suggests," The Guardian reports.

A study of US teens found those who regularly vaped were more likely to progress to tobacco smoking than their non-vaping peers.

The study used questionnaires to assess e-cigarette and cigarette use in 3,000 adolescents aged 15.

The teenagers completed questionnaires twice: at the start of the study and six months later.

Researchers found there was an association between frequent use of e-cigarettes at the start of the study and smoking tobacco at follow-up.

Despite the association, it's difficult to say that the cigarette smoking was caused directly and independently by the use of e-cigarettes.

While the researchers took into account other risk factors for smoking, such as family smoking history, they did not look at all possible contributing factors.

For example, it could be the case that if e-cigarettes didn't exist, some teenagers may have started smoking tobacco anyway.

And these results are based on a small number of people.

The overall prevalence of smoking three or more cigarettes in the past month, or vaping three or more times, was below 5%.

Daily use of either, which may indicate a more serious habit, was also not examined.

E-cigarettes are best used as a quitting aid for people addicted to tobacco. Recreational use may be unwise.

While they are much safer than tobacco, e-cigarettes may still pose both short- and long-term health risks.

Where did the story come from?

The study was carried out by researchers from the University of Southern California Keck School of Medicine, the University of California, and the University of Pennsylvania Perelman School of Medicine, all in the US.

The research was funded by grants from the US National Institutes of Health. The authors report no conflict of interest.

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

The UK media generally reported the story accurately, suggesting the link between e-cigarette use and smoking uptake was "tentative", and acknowledging that the number of adolescents who used e-cigarettes or cigarettes at all in the study was very small.

The media also acknowledged that other factors could have contributed to the uptake of smoking, such as the home environment.

The one exception to this measured reporting was on the Mail Online, which ran the headline: "E-cigarettes are a gateway to smoking". This implies that the research proved a direct causal relationship – but this is not the case.  

What kind of research was this?

This prospective cohort study followed adolescents over time to see whether e-cigarettes were associated with progression to cigarette smoking. It could be that using e-cigarettes is associated with the beginnings of a smoking habit.

But as some adolescents who smoke cigarettes use e-cigarettes as an aid to help them quit, it could be that those who use e-cigarettes are more likely to cut back on how much they smoke over time.

The researchers therefore wanted to see what the associations were between e-cigarettes and subsequent smoking frequency and heaviness.

A prospective cohort study is the best way of examining whether a particular factor is linked with a particular outcome.

But it can be difficult to account for all other variables that may be involved – for example, previous smoking, the frequency of other risk behaviours, or other environmental influences.

For this reason, cohort studies cannot prove cause and effect.

A randomised controlled trial, which could prove cause and effect, would not be ethical because we know smoking has harmful effects.

What did the research involve?

The researchers included students from 10 public high schools in Los Angeles County, California who were already enrolled in a longitudinal study.

The analysis used data from 3,084 students who completed surveys twice: once at the start of the study and again six months later. Their average age was 15.5 at baseline.

The surveys categorised e-cigarette use at baseline into "never", "prior" (ever used, but not in the previous 30 days), "infrequent" (1 to 2 days during the past 30 days), or "frequent" (3 or more days in the past 30 days).

Smoking use was also recorded at baseline and follow-up. Smoking frequency was categorised into "non-smoker", "infrequent smoker" (1 to 2 days in the previous 30 days) or "frequent smoker" (3 or more days in the past 30 days).

The amount smoked was categorised into none, less than one, one, or two or more cigarettes a day on smoking days.

The researchers assessed the association between e-cigarette use at baseline and how often and how heavily teenagers smoked at the follow-up stage.

The results were adjusted for confounders, including:

  • age
  • sex
  • ethnicity
  • highest parental education
  • whether the student lived with both parents
  • ever used alcohol or drugs
  • ever used any combustible tobacco product
  • family history of smoking
  • depressive symptoms
  • impulsive behaviour
  • sensation seeking
  • peer smoking
  • smoking susceptibility
  • smoking expectancies
What were the basic results?

At follow-up, those who had used e-cigarettes more frequently at baseline were more likely to have become smokers.

Frequent e-cigarettes use was associated with a subsequent increased possibility of frequent tobacco smoking (odds ratio [OR] 1.37, 95% confidence interval [CI] 1.16 to 1.61) and heaviness (OR 1.26, 95% CI 1.07 to 1.48).

Of those who had:

  • never used e-cigarettes – 0.9% were infrequent smokers and 0.7% were frequent smokers
  • used e-cigarettes at some point prior to the study – 4.1% were infrequent smokers and 3.3% were frequent smokers
  • used e-cigarettes infrequently at baseline – 9% were infrequent smokers and 5.3% were frequent smokers
  • used e-cigarettes frequently at baseline – 11.6% were infrequent smokers and 19.9% were frequent smokers

These trends were found to be stronger for those who had not been smokers at baseline (OR 2.51, 95% CI= 2.30 to 2.75).

How did the researchers interpret the results?

The researchers concluded "vaping more frequently was associated with a higher risk of more frequent and heavy smoking six months later".

They added: "Although some youths use e-cigarettes for cessation purposes, vaping was not associated with smoking reductions in baseline smokers.

"However, because the reason for vaping was not assessed, further investigation is required."


This research shows an association between using e-cigarettes at baseline and smoking frequency six months later among adolescents in US high schools.

The study has several strengths, including:

  • data was collected prospectively, meaning the researchers did not know the outcomes at the start of the study
  • adolescents were followed up over six months, which is a reasonable time period

However, the use of e-cigarettes and cigarette smoking was measured by self-reporting, and may be inaccurate.

While some factors were accounted for, it is difficult to account for all factors that may make smoking more likely.

These could include engaging in other risky behaviour or living in a home environment where teens are exposed to e-cigarettes or cigarette smoking.

Although it was a reasonably large sample size, with data from more than 3,000 adolescents, the number of teens who actually reported using e-cigarettes or cigarettes was low and therefore a small sample to base any conclusions on.

The categories used were fairly broad – "prior" use included people who had used e-cigarettes just once. "Frequent" users included those who used e-cigarettes three times in the previous month, which could be considered fairly low.

This study looked at students from US high schools, and the findings may not have as much relevance in the UK.

Find out more about quitting smoking if you're a teenager.

Free stop smoking treatments are available for both adults and children aged 12 to 18. Get more advice about quitting smoking.

Links To The Headlines

Vaping raises likelihood of teenagers starting to smoke, study suggests. The Guardian, November 8 2016

E-cigarettes ARE a gateway to smoking: Experts say high usage leads teenagers 'to take up the real thing'. Mail Online, November 8 2016

Links To Science

Leventhal AM, Stone MD, Andrabi N, et al. Association of e-Cigarette Vaping and Progression to Heavier Patterns of Cigarette Smoking. JAMA. Published online November 8 2016

Hopes raised that Zika virus could be treated in the womb

NHS Choices - Behind the Headlines -

"Scientists say they may have found a way to protect babies in the womb from the harmful effects of Zika," BBC News reports.

Researchers have had success using antibody therapy to treat mice when they were still in their mothers' womb.

There is evidence that Zika virus, which has become widespread in South America recently, can damage the development of babies in the womb. One of the most striking birth defects associated with Zika is babies being born with abnormally small heads and brains (microcephaly).

The hope is that by treating babies in the womb it may be possible to prevent, or at least reduce the extent of, birth defects.

The study involved isolating strains of antibodies (infection-fighting proteins) from the blood of people who'd recovered from Zika. Scientists picked the antibodies that were most active against several strains of the virus. They then tested their effect on pregnant mice infected with Zika.

The mouse foetuses were much more likely to survive if their mothers had been given antibodies, and there was less evidence of damage to the foetus or placenta.

Results in mice cannot tell us whether the treatment will be safe or effective in humans. So the researchers say the treatment should next be tested on monkeys, as their pregnancies and reactions to Zika virus are more similar to humans.

The need for effective Zika treatments is pressing as a study from earlier this summer estimated the current epidemic would last for at least three more years.  

Where did the story come from?

The study was carried out by researchers from Vanderbilt University Medical Center in Nashville and Washington University School of Medicine in the US.

It was funded by the US National Institutes of Health and grants from the charitable institutions Burroughs Wellcome Fund and the March of Dimes.

The study was published in the peer-reviewed journal Nature on an open-access basis so it's free to read online (PDF, 8.5Mb).

BBC News covered the main findings of the study accurately and made it clear that the treatment is not yet ready to be used in humans.


What kind of research was this?

This was experimental research carried out on mice in a laboratory.

Research in mice is a common early step when scientists are developing a treatment, but it doesn't tell us whether the treatment will be safe or effective in humans.

What did the research involve?

Researchers analysed blood from three people who'd had Zika, and isolated antibodies that seemed to bind to the Zika virus and inhibit its spread. They tested the most promising antibody as a treatment for mice infected with Zika virus, and also on pregnant mice infected with the virus.

They compared results for those given the antibody treatment and those given an inactive treatment.

Because mice have natural resistance to Zika virus, the researchers had to give them a treatment that suppressed their immune system and made them more vulnerable to the infection.

After treatment, researchers checked to see how long the mice survived, how many of the mouse pregnancies survived, and how much virus was found in the placenta or the mice brains.

They also tested giving the treatment before the mice were infected with Zika, on the same day, or five days after infection.


What were the basic results?

Mice treated with antibodies on the day after infection all survived for at least 20 days, while only 40% of untreated mice survived Zika infection for 20 days.

Later treatment was less successful, but mice treated five days after infection were still much more likely to survive.

Almost all mouse pregnancies survived up to 13 days where the mother had been treated with antibodies a day before being infected with Zika virus, while most pregnancies of untreated mice did not survive Zika virus infection.

When the researchers looked at tissues from the mice at the end of the study, they found much higher concentrations of Zika virus in the head of the mouse foetus and the foetal placenta, in untreated mice, compared to those treated with antibodies.

Levels of the virus were also higher in the brains and blood of the mice mothers who didn't have antibody treatment.


How did the researchers interpret the results?

The researchers say they've shown that antibody therapy, either before or after exposure to Zika virus, "reduced infection in mothers, and in placental and fetal tissues." Importantly, they say that "the extent to which these observations in mice translate to humans remains unclear", and recommend further animal studies in monkeys.

They say that if these results were positive, antibody treatment could be developed as a way of treating Zika infection during pregnancy.



For most people, Zika virus infection causes a mild flu-like illness. But it can cause serious damage to unborn children, if their mothers catch the virus while they are pregnant.

At present, there's no treatment that can help protect these babies against the effect of the virus, so news that a treatment may be on the way is welcome.

However, this research is in the very early stages. Mice and humans react very differently to Zika virus, and there are important differences in the structures of mouse and human bodies during pregnancy.

This means we don't know whether this treatment would work in the same way, or if it would even be safe for humans. Much more work is needed before this is a viable human treatment.

For now, the best thing you can do is to try to avoid becoming infected in the first place – especially if you're pregnant.

Pregnant women are being advised to postpone non-essential travel to areas with active Zika virus transmission. If you travel to an affected area, you can reduce your risk of catching the virus by using insect repellent and wearing loose clothing that covers your arms and legs.

Public Health England (PHE) provides regular updates about the current spread of the disease.

Links To The Headlines

Zika therapy 'works in the womb'. BBC News, November 8 2016

Links To Science

Sapparapu G, Fernanadez E, Kose N, et al. Neutralizing human antibodies prevent Zika virus replication and fetal disease in mice. Nature. Published online November 7 2016

Common food additives 'linked' to bowel cancer

NHS Choices - Behind the Headlines -

"Why processed food may cause bowel cancer: Common additives change gut bacteria which allow tumours to grow," reports the Mail Online.

This follows a study in mice investigating whether common food additives (E numbers) called emulsifiers cause inflammation in the gut that in turn triggers bowel cancer.

The researchers divided the mice into three groups: two received emulsifiers, either sodium carboxymethycellulose (CMC) or polysorbate 80 (P80), and the third group received water. They also gave the mice toxins to trigger inflammation and cancer.

Overall, they found more and bigger cancerous tumours in mice given the emulsifiers, in addition to some inflammatory changes. It was suggested the reason could be that emulsifiers altered the balance of gut bacteria, creating an environment more favourable to the development of cancer.

But while these findings may be alarming, it's too early to say if they apply to humans. Findings of animal studies aren't directly transferable to humans. The mice were also given far greater doses of emulsifiers than a human would consume, in addition to toxins that cause inflammation and cancer.

It is well known that bowel cancer is linked to high levels of body fat and eating lots of processed meat, but the link with emulsifiers needs further research.

All food additives undergo a safety assessment before they can be used and it's not yet possible to say for certain whether any of these pose a risk of cancer in humans at the levels permitted.

The Food Standards Agency (FSA) has more information about additives and E numbers.

Where did the story come from?

The study was carried out by researchers from Georgia State University in Atlanta and was funded by a National Institutes of Health (NIH) grant.

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

It has largely been reported accurately in the media, which for the most part did mention the limitations of the research.

The Sun provided a quote from Professor Sanders from Kings College London who said the mice were fed the E numbers at a level of 1%, described as: "a very high intake of the food additives compared to what might be found in human diets".

He added: "We can't assume this study is applicable to humans, so it shouldn't be cause for concern."

But some headlines oversimplified the research and implied that a definite link between additives and bowel cancer in humans had been found. Moreover, some of the coverage didn't mention the study's important limitations.

What kind of research was this?

This was an animal study in mice that aimed to see whether food additives (E numbers) called emulsifiers found in processed food could be responsible for bowel cancer.

Emulsifiers prevent foods from separating and give food body and texture. They're commonly found in food such as ice cream.

The researchers suggested that emulsifiers may cause low grade inflammation in the gut and increase levels of bad gut microbes, resulting in increased levels of cancer.

This kind of research is a valuable first step in understanding the processes by which emulsifiers may lead to inflammation in the gut, and then seeing whether this could be linked with cancer risk.

But this is early, animal based research and we can't be sure whether the findings would be the same in humans. 

What did the research involve?

The researchers split mice into three groups, with each group being given one of the following:

  • sodium carboxymethycellulose (CMC) – a soft and lubricating "gum" found in products like ice cream and toothpaste
  • polysorbate 80 (P80) – a thickening liquid, also found in things like ice creams and sauces to stop them separating
  • water (control group)

The mice received these solutions for 13 weeks during which time they had their bodyweight measured and faeces collected on a weekly basis.

Following the 13 week period, the mice were given an injection of azoxymethane (AOM), a strong cancer-causing substance in rodents, to induce colon cancer. Five days later a dose of dextran sulfate sodium (DSS) used to induce colitis (inflammation of the lining of the colon).

Five days later they were given a dose of dextran sulfate sodium (DSS) used to induce colitis (inflammation of the lining of the colon).

At the end of the experiment, the mice were killed, and colon length, colon weight, spleen weight and body fatness were measured. Any cancerous tumours found were counted and measured.

What were the basic results?

The mice receiving CMC and P80 showed a small but significant increase in their body mass. The emulsifier treatment also impaired blood glucose regulation. This was evident from increased food consumption and poor fasting blood glucose levels.

All mice receiving AOM and DSS lost weight during DSS treatment. When examined after death they had features of inflammation, including increased colon and spleen weights.

The mice in the two groups given emulsifiers were found to have more inflammatory changes compared to mice in the control group. There was also increased tumour development in the mice that consumed emulsifiers in comparison to the control group.

Further exploration suggested that the greater inflammatory changes and cancer development in the emulsifier groups were caused by these substances altering the balance of gut bacteria.

How did the researchers interpret the results?

The researchers conclude: "We found that emulsifier induced alterations in the microbiome were necessary and sufficient to drive alterations in major proliferation and apotosis [cell death] signalling pathways thought to govern tumour development."

"Overall, our findings support the concept that perturbations in host-microbiota interactions that cause low-grade gut inflammation can promote colon carcinogenesis [tumour formation]."


This animal study aimed to investigate whether additives called emulsifiers promote inflammation that in turn triggers cancer.

The findings suggest emulsifiers could lead to greater inflammation and bowel cancer in mice, and this may be caused by them altering the balance of gut bacteria. But there are important limitations to note:

  • The mice were fed large doses of the substances not comparable to the levels found in food humans would eat.
  • The mice were also given strong drugs both to cause cancer and trigger bowel inflammation. Without these substances, the emulsifiers alone may have had minimal effect.
  • Findings of animal studies aren't directly transferable to the effect that may be seen in humans consuming food products containing emulsifiers. Human studies would be needed to confirm these findings. For example, researchers could analyse the effect of directly adding emulsifiers to bowel tissue samples in the laboratory.
  • It's difficult to understand the biological processes that may be behind the increased cancer development in mice exposed to emulsifiers. For example, they may be due to increased weight gain or poor glucose control, rather than the substances being the direct cause.

It's too early to apply these findings to humans. While it's well known that bowel cancer is linked to high levels of body fat and higher consumption of processed meats, the link with emulsifiers is one that needs to be researched further.

Links To The Headlines

E-numbers in ice cream 'could increase your risk of bowel cancer'. The Sun, November 7 2016

Why processed food may cause bowel cancer: Common additives change gut bacteria which allow tumours to grow. Mail Online, November 7 2016

'Junk' food linked to soaring cases of bowel cancer. Daily Express, November 7 2016

Links To Science

Viennois E, Merlin D, Gewirtz AT, et al. Dietary emulsifier-induced low-grade inflammation promotes colon carcinogenesis. Cancer Research. Published online November 7 2016

Smoking causes hundreds of genetic mutations

NHS Choices - Behind the Headlines -

"Research quantifies genetic damage caused by smoking," the Mail reports, saying a pack a day causes 150 mutations in lung cells.

This study analysed the DNA sequence of cells from more than 5,000 cancers. About half came from smokers and the rest from non-smokers, which allowed researchers to compare mutations between the two.

Overall, the study found cancer cells from smokers tended to contain a higher number of mutations and abnormal substitutions in the DNA sequence.

The researchers were able to estimate the number of mutations that would be caused in different types of cells – not just in the lung – from smoking one pack a day for one year.

For example, one year's smoking would cause 150 mutations in lung cells, 97 mutations in cells of the voice box (larynx), and 39 in the throat (pharynx).

As the researchers say, their genetic analysis isn't able to tell for certain the mechanism by which these changes occur, or know whether other behaviours associated with smoking, such as drinking alcohol, may be involved in the changes.

Nevertheless, the study highlights the known harms of tobacco smoking and the mix of cancer-causing chemicals cigarettes contain. Any amount of smoking may be harmful, but it's never too late to stop.

Where did the story come from?

The study was carried out by researchers from Los Alamos National Laboratory and the University of New Mexico Comprehensive Cancer Center, both in the US, and various other international institutions.

It was funded by the Wellcome Trust, among other sources, and was published in the peer-reviewed journal Science. The article is openly available to access online.

The media gave reliable coverage of this study overall.

What kind of research was this?

This genetic study aimed to analyse the DNA mutations found in thousands of different types of cancer cells that are linked with smoking.

Smoking is well known to be harmful to health. It's said to be associated with 17 different types of cancer and behind the cause of death for six million people worldwide every year.

Of the chemicals in tobacco, 60 of them are reported to be known cancer-causing substances (carcinogens).

Many of them cause DNA damage and gene mutations in body cells that then replicate to result in large numbers of abnormal cells. 

This study aimed to analyse the different genetic mutations caused by tobacco smoke.

What did the research involve?

The study examined the DNA sequences in 5,243 cell samples from cancers linked to smoking. The samples included lung, mouth, throat, liver, kidney, bladder, pancreatic and cervical cancers.

The researchers focused on analysing the particular positions within the DNA sequence of these cells where mutations were occurring, called mutational signatures.

Of the samples, 2,490 were reported to come from smokers and 1,062 from never-smokers, so they were able to compare the number and type of mutations found in smokers with non-smokers.

What were the basic results?

The researchers found that in smokers there were a greater number of instances where points in the DNA sequence had been substituted, in particular for lung, throat, liver and kidney cancers. 

Smokers had a greater number of mutations within certain mutational signatures than non-smokers. For example, most lung and throat cancers from smokers had many mutations in signature 4. 

However, 13.8% of non-smokers also showed many signature 4 mutations, which the researchers speculate could be down to passive smoking or past non-reported smoking habits.

The researchers went on to describe the other individual mutational signatures where they found differences for smokers versus non-smokers, including signatures 2, 5, 13 and 16. 

They then used this information on mutational signatures by cancer type to calculate the age-adjusted risk of a person who smokes 30 or more cigarettes a day developing specific cancers. 

For example, a male smoker was 22 times more likely to develop the most common type of lung cancer (adenocarcinoma) and 13 times more likely to develop cancer of the larynx. A woman had almost double the risk of cervical and ovarian cancers.

The researchers calculated that the number of abnormal substitutions in the DNA sequence increased with the number of pack years smoked – one pack year meaning smoking one pack of cigarettes a day for one year.

They estimated one pack year smoked would cause 150 mutations in lung cells, 97 mutations in cells of the larynx, 39 in the pharynx, 23 in the mouth, 18 in the bladder, and 6 mutations in liver cells. 

How did the researchers interpret the results?

The researchers concluded that their results are consistent with the theory that smoking causes cancer by increasing the number of mutations found in the cellular DNA, though the exact mechanism by which this happens isn't completely clear.

They said: "Although we cannot exclude roles for covariate behaviours of smokers or differences in the biology of cancers arising in smokers compared with non-smokers, smoking itself is most plausibly the cause of these differences."


This study serves to highlight the known harms of cigarette smoking. The research benefits from analysing thousands of different cancer cell lines, and carefully comparing the mutations found in smokers with those of non-smokers.

It shows that there are differences between the two – even in cancers of the same type – with those from smokers generally tending to have a higher number of mutations and abnormal substitutions in the DNA sequence. 

However, it can't tell us much more than that. For example, it can't tell us whether the same cell type and stage of lung cancer in a smoker is likely to have a poorer prognosis than the same cancer in a non-smoker because it contains more mutations.

As the researchers acknowledge, they can't tell from this study the exact biological mechanisms that may be causing the mutations in smokers and non-smokers, or know whether other smoking-related behaviours, such as alcohol consumption, may have an influence.

It's also important to emphasise that the number of mutations caused per pack year smoked are very general estimates based on only this single dataset.

For example, we can't know for definite that a man who has smoked one pack a day for 20 years now has 3,000 mutations in his lung cells.

The amount of DNA damage caused by smoking in any individual may be greatly influenced by their underlying genetic profile, lifestyle, environment, and the type of tobacco smoked.

Nevertheless, this study highlights the known harms of tobacco smoking and the mix of cancer-causing chemicals that cigarettes contain. Any amount of smoking may be harmful, but it's never too late to stop.   

Links To The Headlines

Research quantifies genetic damage caused by smoking. Mail Online, November 3 2016

DNA study lays bare devastating damage caused by smoking. The Guardian. November 3 2016

Smoking 'causes hundreds of DNA changes'. BBC News, November 3 2016

Links To Science

Alexandrov LB, Seok Ju Y, Haase K et al. Mutational signatures associated with tobacco smoking in human cancer. Science. Published November 4 2016


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