NHS Choices - Behind the Headlines

Can exercise offset some of the harms of regular drinking?

"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

'Chocolate good for the heart' claims sadly too good to be true

"Regularly tucking into a bar of chocolate may actually be good for us," reports the Mail Online.

Researchers in Denmark say people who eat chocolate one to six times a week are less likely to get a heart condition called atrial fibrillation than those who eat it hardly at all (less than once a month).

Atrial fibrillation (AF) – an irregular heartbeat – can increase the risk of blood clots forming, and so raises the risk of a stroke.

However, as is often the case with health news that sounds too good to be true, the research is not particularly persuasive. People who ate chocolate less than once a month were also more likely to have diabetes, high blood pressure and cardiovascular disease; all of which are risk factors for atrial fibrillation. So they may have been avoiding chocolate for health reasons.

There is also no evidence from this study that eating chocolate will help with symptoms of atrial fibrillation if you already have it.

If anything, the opposite may be true: regularly overindulging in chocolate could increase your blood pressure and diabetes risk, which could eventually trigger the symptoms of atrial fibrillation.


Where did the story come from?

The study was carried out by researchers from Beth Israel Deaconess Medical Center in Boston, US, Aalborg University Hospital and the Institute of Cancer Epidemiology in Denmark, and Western University in Canada.

It was funded by grants from institutions including the US National Heart, Lung and Blood Institute, the European Research Council, the EU, the Harvard Clinical and Translational Science Centre, the Danish Cancer Society and the Danish Council for Strategic Research.

The study was published in the peer-reviewed journal Heart on an open-access basis, making it free to read online.

The study was covered widely in the UK media. The headlines, as you would expect, provided a simplistic "chocolate can be good for us" slant. But the actual "meat" of the reporting in most papers described the limitations and made it clear the study did not prove cause and effect.


What kind of research was this?

This was a prospective cohort study. Cohort studies are useful for spotting patterns but cannot prove that one thing (in this case chocolate consumption) directly causes another (chance of getting AF).


What did the research involve?

Researchers recruited 55,502 people in Denmark aged 50 to 64. Everyone completed a food questionnaire, had health checks and gave other information about their health and lifestyle.

Participants were followed up for an average 13.5 years. Researchers checked them against a Danish health registry to see if they were treated in hospital for AF. After adjusting for potential confounding factors they looked to see whether chocolate consumption was linked to their chances of getting AF.

The research takes advantage of the Danish National Patient Register, which makes it possible to track large numbers of people over time. Researchers included the following potential confounding factors:

  • sex
  • body mass index (BMI)
  • blood pressure
  • total cholesterol
  • total calorie intake
  • coffee consumption
  • smoking
  • years of education
  • hypertension, diabetes and cardiovascular disease

The researchers analysed figures for men and women both separately and together.


What were the basic results?

Over 13.5 years, there were 3,346 cases of AF among the 55,502 people taking part in the study. People were less likely to have AF if they ate chocolate at least once a month:

  • 10% less if they ate chocolate one to three times a month (hazard ratio [HR] 0.9, 95% confidence interval [CI] 0.82 to 0.98)
  • 17% less if they ate chocolate once a week (HR 0.83, 95% CI 0.74 to 0.92)
  • 20% less if they ate chocolate two to six times a week (HR 0.80, 95% CI 0.71 to 0.91)
  • 16% less if they ate chocolate every day – but the numbers of people who ate chocolate daily and had AF were so low that we can't be sure these results were not just down to chance (HR 0.84, 95% CI 0.65 to 1.09)

The separate figures for men and women show men seemed to have the lowest risk if they ate chocolate two to six times a week, and women if they ate it once a week. However, these differences were small and may be down to chance and the fact that fewer women had AF.


How did the researchers interpret the results?

The researchers say higher levels of chocolate consumption "were associated with an 11-20% lower rate of clinically apparent AF among men and women." They say they adjusted the figures using "extensive data" on diet, lifestyle and other illnesses, but that "we cannot preclude the possibility of residual or unmeasured confounding."

They suggest that "antioxidant, anti-inflammatory and antiplatelet properties of cocoa" may be the reason for lower rates of AF among chocolate eaters.



Health stories that suggest eating or drinking something we like, whether it's chocolate or wine, are always popular. But they don't really tell us anything we don't know already. Certain foods may have a small impact on certain types of diseases, but it's the overall diet that counts.

Previous studies have already suggested that the antioxidant properties of cocoa could reduce the risk of cardiovascular disease, so it's surprising that this study focused on one particular cardiovascular disease, atrial fibrillation.

AF is a common condition that affects heart rate, often causing a faster than normal, irregular rhythm. It isn't usually life-threatening, although you may need treatment to reduce risk of linked conditions such as stroke.

While the study had some strengths, such as being very large, using a reliable database and taking account of a number of confounding factors, this type of study cannot show that chocolate actually prevents AF. It's quite possible that other factors could be more important than diet.

A plausible interpretation of this study is not that eating chocolate prevents AF, but that people with AF (or associated risk factors) avoid eating chocolate, possibly on the advice of their doctor.

It's worth remembering that – as well as cocoa – chocolate contains a lot of fat and sugar. In the study, one portion of chocolate was 30g. There's nothing wrong with eating a small amount of chocolate as part of a healthy, balanced diet – but hoping that a single "superfood" such as chocolate will make a big difference to your health is misguided.

Read more about so-called superfood claims and the evidence behind them.   

Links To The Headlines

Chocolate six days a week will save your heart, chaps... but sorry, ladies, it's only once for you. Mail Online, May 24 2017

Six bars of chocolate a week could cut risk of common heart condition. The Daily Telegraph, May 24 2017

Eating just one chocolate bar a day ‘can reduce risk of stroke by 23 per cent,’ says study. The Sun, May 24 2017

Chocolate may help reduce risk of irregular heart rate, finds research. The Independent, May 24 2017

Links To Science

Mosotofsky E, Johansen MB, Tjønneland A, et al. Chocolate intake and risk of clinically apparent atrial fibrillation: the Danish Diet, Cancer, and Health Study. Heart. Published online May 23 2017

Just half a glass of wine a day may increase breast cancer risk

"Just half a glass of wine a day ups the risk of breast cancer by nine per cent, experts warn," The Sun reports. A major report looking at global evidence found that drinking just 10g of alcohol a day – 1.25 units – was linked to an increased risk of breast cancer.

The report was produced by the World Cancer Research Fund which reviews the global evidence on the link between diet, weight, physical activity and breast cancer. Overall, this report supports what is already known, that alcohol consumption is a risk factor for breast cancer.

The report found that for each 10g of pure alcohol consumed each day, the risk of premenopausal breast cancer increases by 5%, and the risk of postmenopausal breast cancer increases by 9%. Experts have suggested that this would equate to about one extra case of cancer per 100 women, based on current rates of breast cancer in the UK.

After a recent review by expert groups of the evidence on all of the health effects of alcohol, the UK Chief Medical Officer's advice is that men and women should not regularly drink more than 14 units in a week to try and keep overall risks at a low level.


What is the basis for these current reports?

These news stories are based on a report from the not-for-profit World Cancer Research Fund (WCRF). The WCRF has an ongoing project to regularly assess the evidence on links between diet, nutrition, physical activity and different types of cancer, and provide recommendations based on this. Its current report is an update on the links between these factors and breast cancer in women.

To prepare the report, the WCRF systematically searched for relevant studies published since its last update in 2010. It looked at randomised controlled trialscohort studies and nested case control studies.

These new studies were assessed by a panel of independent international scientists to see if they should be included in this latest report.

Those that were relevant were then interpreted along with the older evidence in the previous WCRF reports. They carried out statistical pooling of the study results where possible. All together the panel considered 119 studies looking at more than 12 million women, and over 260,000 cases of breast cancer.


What impact did the report find for alcohol on breast cancer risk? Premenopausal breast cancer

The report identified eight new or updated studies on the link between alcohol and premenopausal breast cancer. Premenopausal breast cancer cases account for around one in five cases of breast cancer in the UK.

It was possible to pool the results of 10 studies on premenopausal breast cancer, and this showed that an additional 10g of ethanol (pure drinking alcohol) a day increased risk of premenopausal breast cancer by 5% (relative risk [RR] 1.05, 95% confidence interval [CI] 1.02 to 1.08).

Postmenopausal breast cancer

The report identified 21 new or updated studies on the link between alcohol and postmenopausal breast cancer. Of these studies, 22 could be pooled, showing that an additional 10g of ethanol (pure drinking alcohol) a day increased risk of postmenopausal breast cancer by 9% (RR 1.09, 95% CI 1.07 to 1.12).

One unit of alcohol is 8g and is equivalent to about:

  • half a small glass (76ml) of standard 13% ABV (alcohol by volume) wine
  • 218ml of standard 4.5% cider
  • 250ml of standard 4% beer or standard 4% alcopop
  • 25ml of standard 40% whiskey

Drinking 10g of ethanol every day for a week would be equivalent to 8.75 units of alcohol, which is less than the UK's current maximum upper limit for women. The UK Chief Medical Officer's advice is that, to keep overall risks from alcohol at a low level, it is safest that men and women do not regularly drink more than 14 units in a week.

The report concluded there is strong evidence that consuming alcoholic drinks probably increases the risk of premenopausal breast cancer, and convincing evidence that it increases the risk of postmenopausal breast cancer.


What does this actually mean in terms of numbers of women with breast cancer in the UK?

The report itself did not estimate how many extra cases of cancer this was equivalent to. One expert from the UK, Professor Kevin McConway, Emeritus Professor of Applied Statistics from The Open University said:

"...according to Cancer Research UK, of 100 UK women, about 12 or 13 will develop a breast cancer at some point in their lives. Imagine that these 100 women all drank an extra small glass of wine or half a pint of beer every day, compared to what they drink now. On WCRF's figures, that would lead to 1 more of them developing a breast cancer during their lifetime."

To put this into context, Professor McConway added: "Any increase is a bad thing, but it's only one more out of the 100 women, and that has to be set against whatever pleasure the women might obtain from their drinking. Drinking alcohol has a greater effect on the risks of several other cancers (such as cancers of the mouth, oesophagus and bowel) than it does on the risk of breast cancer, so there are other reasons to give up or cut down, but that just shows the importance [of] looking at the whole picture and not just at breast cancer."


What about other factors?

The report also reported on other factors that could influence risk of breast cancer.


The report found strong evidence that vigorous physical activity (enough to get you out of breath) probably decreased risk of premenopausal breast cancer. There was also strong evidence that physical activity as a whole, including vigorous and less strenuous exercise, probably decreased risk of postmenopausal breast cancer.


The report found strong evidence that breastfeeding probably decreased risk of breast cancer overall.


There was limited evidence that including the following in your diet may reduce your risk of breast cancer:

  • non-starchy vegetables
  • dairy products (for premenopausal breast cancer only)
  • foods containing carotenoids, such as carrots, spinach and kale
  • foods high in calcium, such as sardines and broccoli
Body weight

The relationship between body weight and breast cancer risk seemed to be complex.

For premenopausal breast cancer, greater body fatness during adulthood actually had a protective effect. More body fatness between the ages of 18-30, also had a protective effect against postmenopausal breast cancer risk.

However, greater body fatness during adulthood as a whole, and greater weight gain during adulthood increased postmenopausal breast cancer risk.

So, the WCRF continues to maintain its advice that we should keep our weight in the healthy range for as long as possible for overall cancer prevention.

Read more about breast cancer prevention.

Links To The Headlines

'Half a glass of wine every day' increases breast cancer risk. BBC News, May 23 2017

Just one small glass of wine a day raises the breast cancer risk: Study means even following safe drinking guidelines could endanger health. Daily Mail, May 23 2017

Just half a glass of wine a day raises breast cancer risk by nine per cent, experts warn. The Sun, May 23 2017

Ditch alcohol and take up gardening to prevent breast cancer, experts say. The Daily Telegraph, May 23 2017

One alcoholic drink a day 'can increase the risk of breast cancer'. ITV News, May 23 2017

One small drink a day raises risk of breast cancer. The Times, May 23 2017 (subscription required)

Links To Science

World Cancer Research Fund. Diet, nutrition, physical activity and breast cancer (PDF, 4.09Mb). Published online May 2017

Dementia saliva testing 'shows early promise'

"Simple saliva test for dementia 'shows promise' in bid to diagnose the disease early," the Daily Mirror reports.

This news is based on a laboratory study that took saliva samples from 12 healthy adults, nine adults with Alzheimer’s disease, and eight with mild cognitive impairment (MCI), which is often seen as the stage just before dementia.

Researchers looked at 22 chemical substances (biomarkers) in the saliva, to see if there was a distinct pattern that could indicate whether a person was healthy, had MCI, or had Alzheimer's. They found that a specific chemical make-up of saliva could predict, with a relatively good degree of accuracy, which of these three groups a person fell into.

The findings show promise but this is only preliminary work, as the sample is too small to be conclusive. The next stage is to see if the results can be verified in a much larger sample of people. The researchers calculated that they need ideally at least 100 people in each group.


Where did the story come from?

The study was carried out by researchers from the Beaumont Research Institute and Oakland University William Beaumont School of Medicine in the US, and the University of Alberta in Canada. Funding was provided by the Fred A. and Barbara M. Erb Family Foundation.

The study was published in the peer-reviewed Journal of Alzheimer's Disease.

The Mirror and The Sun's reporting of the study was accurate and appropriately cautious, saying that the test shows promise, without suggesting a test is currently available.


What kind of research was this?

This was a proof-of-concept study. It aimed to see whether it was possible to look at levels of certain substances in saliva to determine whether a person is likely to have mild cognitive impairment (MCI) or Alzheimer's disease.

Alzheimer's is the most common form of dementia, where there is a build-up of characteristic clumps of protein called plaques and tangles in the brain. However, there is no conclusive diagnostic test for Alzheimer's as it can only be diagnosed with certainty by looking at brain tissue after death. A likely diagnosis of Alzheimer's is made on the presence of these characteristic features and by ruling out other causes.

Mild cognitive impairment (MCI), where people start to experience memory problems but fall below the threshold for dementia, can be a preliminary stage to dementia (any type). About 1 in 10 people with MCI progress to dementia each year.

A simple early biological test for Alzheimer's could allow it to be recognised at an early stage, helping people to access the right treatment and to make decisions about their future. Previous studies have already shown it may be possible to distinguish between different types of degenerative brain diseases based on the presence of certain chemical substances, or biomarkers, in body fluids or tissues.


What did the research involve?

The researchers looked at whether there were characteristic chemical differences in saliva samples from healthy people, people with MCI, and people with Alzheimer's.

Saliva samples were collected from 12 healthy adults (controls), eight people with MCI and nine people with Alzheimer's.

All participants were recruited from a centre specialising in care of the elderly. Their diagnoses were made using a variety of tried and tested assessments of brain function (cognitive function), such as the Clinical Dementia Rating Scale, Mini-Mental State Examination and Geriatric Depression Scale.

Saliva samples were analysed using a technique called nuclear magnetic resonance spectroscopy, which allowed the researchers to measure levels of the different biomarkers.


What were the basic results?

The researchers found that the different groups of people could be distinguished with good accuracy based on specific patterns of biomarkers in their saliva.

In particular:

  • high levels of acetone and imidazole and low levels of galactose could distinguish people with MCI from healthy controls
  • high levels of propionate and acetone could distinguish people with Alzheimer's from healthy controls
  • high levels of creatinine and 5-aminopentanoate could distinguish people with Alzheimer's from those with MCI
How did the researchers interpret the results?

The researchers conclude that they have provided "preliminary evidence that salivary metabolites may be useful for [Alzheimer's disease] biomarker development."

They say: "Given the convenience and the frequency with which saliva can be obtained, larger studies are justified."



The researchers are appropriately cautious in their conclusions. These findings have potential, but this is an early stage pilot – a starting point for further study.

The tests were carried out in small samples of healthy people and those with cognitive impairment. They would have to be validated in much larger groups, in which it's possible the test would give different findings. The researchers calculate that they would need at least 100 people per group to develop models that could reliably detect significant differences in biomarkers between the groups.

Even among this small sample, we don't know from the information provided that the people definitely had Alzheimer's disease. They were assessed using a range of cognitive assessments, but we don't know other aspects such as their medical history and results of brain imaging. It's possible, for example, that some of these people could have had vascular dementia.

Even if further research finds a profile of biomarkers that is reliable enough at identifying people with MCI or Alzheimer's, there would still be many more considerations before introducing this as a screening test. For example, who should be screened and would testing offer any benefit over current diagnostic methods based on clinic assessment?

Currently, though there are drugs that can be prescribed for people with mild to moderate dementia, there is no treatment that can prevent or cure dementia. Therefore earlier recognition at this stage would help people get the support they need, but is unlikely to change the course of the disease. This may change if there are future drug developments.

Current advice stands, that if you or a family member or friend are having problems with memory and understanding, it's important to contact a health professional to get the support needed. Memory and cognitive problems can have a wide range of causes so it would be unwise to assume that they are a sign of dementia.

For more information visit the NHS Choices dementia guide.

Links To The Headlines

Simple saliva test for dementia 'shows promise' in bid to diagnose the disease early. Daily Mirror, May 22 2017

Simple saliva test could be used to identify early signs of Alzheimer's Disease, researchers say. The Sun, May 22 2017

Links To Science

Yilmaz A, Tim G, Han B, et al. Diagnostic Biomarkers of Alzheimer's Disease as Identified in Saliva using 1H NMR-Based Metabolomics. Journal of Alzheimer's Disease. Published online  May 11 2017

Instagram 'ranked worst for mental health' in teen survey

"Instagram is rated as the worst social media platform when it comes to its impact on young people's mental health, a UK survey suggests," BBC News reports.

The survey asked 1,479 young people aged 14-24 to score popular social media apps on issues such as anxiety, depression, loneliness, bullying, body image and "fear of missing out" – where your social media peers seem to be enjoying a better quality of life.

The survey fed into a larger report looking more generally at the impact of social media on people in this age group – so-called "digital natives", who have never lived in a world without the internet.

Despite many headlines flagging the negative effects, the report – published by the Royal Society for Public Health (RSPH) – also explored the potential positive benefits for teenagers, such as improved sense of community and self-identity.

YouTube was found to have the most positive impact on young people, and photo-sharing platform Instagram the most negative.

Acting on this information, the report calls for measures to help protect individuals when using social media platforms.

Their recommendations revolve around increased education on cyber safety and providing more help to protect the mental wellbeing of young people.

Who produced the report?

The report was produced by the Royal Society for Public Health (RSPH) and the Young Health Movement. 

The RSPH is an independent charity that works to improve the health and wellbeing of the public.

The Young Health Movement, run by RSPH, is a collective of individuals striving to raise public health awareness in young people.

How accurate were the media reports ?

The study was covered broadly accurately by the UK media, although some of the headline writers were a little unfair on some social media giants.

The Guardian led with, "Facebook and Twitter 'harm young people's mental health'," even though Twitter ranked second best and Facebook third overall.

Why is this survey so timely?

Social media use is booming: 91% of 16-24-year-olds in the UK use the internet and other social networking sites regularly.

Although social media can connect people from all over the world to provide a strong sense of community, rates of anxiety and depression in young people have increased by 70% over the last 25 years.

Recent studies have already suggested associations between social media use and a rise in teen mental health problems.

A Danish study we discussed in 2016 found regular users of Facebook encouraged to quit for a week reported greater satisfaction with their life at the end of the week.

What evidence did they look at?

Evidence was pulled from several sources, including the Office for National Statistics, looking at the effect social media has on different things like sleep, body image, self-expression (their feelings, thoughts or ideas), and self-identity (their qualities as an individual).

As part of their research, the RSPH surveyed 1,479 young people in the UK aged 14-24 to find out more about their use of five of the most popular social media platforms: Facebook, Instagram, Snapchat, Twitter, and YouTube.

The survey aimed to better understand how social media affects the health and wellbeing of young people, making comparisons between the different platforms.

Young people were asked about:

  • their awareness and understanding of other people's health experiences
  • access to trustworthy expert health information
  • emotional support
  • anxiety
  • depression
  • loneliness
  • sleep
  • body image
  • real-world relationships
  • self-expression
  • self-identity
  • community building
  • bullying
  • "fear of missing out" (FOMO)

The results from the survey were used to rank the social media platforms in terms of positive and negative impact on mental wellbeing.

What are the main findings?

Based on the health and wellbeing questions, the researchers ranked the social media platforms as follows, from having the most positive impact to the most negative:

1. YouTube
2. Twitter
3. Facebook
4. Snapchat
5. Instagram

Across all five social media platforms, the greatest negative impact was around sleep, bullying and FOMO.

The greatest positive impact was felt around self-expression, self-identity and community building.

What recommendations did the report make?

The report rounded off with several calls to action, summarised below. It's hoped these will be adopted to help safeguard young people when online.

A pop-up heavy usage warning on social media

Social media sites can track a person's usage and provide a pop-up warning when they've been online for a length of time deemed potentially harmful. The user can decide whether or not to act on the warning.

An icon to highlight when photos of people have been digitally manipulated

The use of a small watermark or icon to be added to the bottom of a person's photo when an airbrush or filter has been added that may significantly alter their appearance.

Health information on social media to be certified as trustworthy

The Information Standard certification scheme, as used by NHS Choices, should be applied to social media so individuals can know when health information available on social media is trustworthy.

Safe social media use to be taught during lessons in schools

Education should feature information around the safe use of social media, covering topics on cyber bullying, social media addiction and other potentially harmful effects on mental wellbeing. The curriculum should also include information on where young people can seek help.

Social media platforms to identify vulnerable users and signpost to support

Technology can be used to identify posts that suggest the user is affected by mental health problems. The user can then be provided with discreet information on how and where they could seek help, such as The Samaritans.

Youth workers to have social media training

Training should be available for all adults working with young people so they can better understand the potential risks and benefits of social media.

More research to be carried out into the effects of social media on young people's mental health

RSPH calls for more research into the effects of social media on younger people's mental wellbeing, as this research is currently lacking.


This timely report should be welcomed, given that almost all young people use social media, and it undoubtedly can affect their wellbeing. It also offers well-considered recommendations.

However, the study does have some limitations. Researchers gauged the potential positive and negative effects of different social media platforms by asking young people to answer whether they felt better or worse by using them. This can't prove that social media is directly responsible for increasing rates of depression and anxiety.

It's difficult to explore all the various ways the social media sites may make people feel better or worse. It could be that it's dependent on the content and subject matter people are viewing or participating in.

For example, sites like YouTube and Twitter may have been generally rated more positively because individuals were mostly viewing things more removed from their immediate lives, such as celebrity figures, or amusing or interesting video clips, whereas Facebook, Snapchat or Instagram tend to involve friends and family, and be more directly related to their users' lives. 

And there will be various forms of "negative" content available on YouTube, so it shouldn't be concluded too strongly that this is necessarily "better" or "safer" than all other platforms.

It would be valuable to further explore why certain platforms could have different effects on wellbeing. The report raises important questions, and we have yet to see the response to the society's recommendations.

If you or a friend or relative are experiencing low self-esteem or symptoms of low mood or anxiety, it's very important to seek help from your GP or speak to someone from school or college so you can get the support you need.   

Links To The Headlines

Instagram 'worst for young mental health'. BBC News, May 19 2017

Instagram rated worst media for mental health. Sky News, May 19 2017

Facebook and Twitter 'harm young people's mental health'. The Guardian, May 19 2017

Instagram ranked worst social network for young people's mental health. Sky News, May 19 2017

Links To Science

Royal Society for Public Health. #StatusOfMind – Social media and young people's mental health and wellbeing (PDF, 13.70Mb). May 2017

Swallowable gastric balloon could help with weight loss

"Swallowable gastric balloon could help the obese lose weight without surgery," The Guardian reports. The news, which was widely reported, is based on a study presented at the European Congress of Obesity in Portugal.

Researchers in Italy found obese patients who used a swallowable gastric balloon lost on average about 15kg over a four-month period.

Gastric balloon treatment for obesity involves inserting a balloon in the stomach and filling it with air or liquid. This means you can't or won't need to eat as much to feel full.

Currently, deflated gastric balloons usually have to be inserted – and later removed – in a hospital setting. This involves being sedated or having a general anaesthetic and having an endoscopy, where a thin tube with a camera and light is passed down your throat.

The swallowable gastric balloon used in this study can be inserted without any invasive procedures such as endoscopy. The balloon is swallowed by the patient and then filled with liquid once it's in the stomach. The balloon stays in the stomach for four months, until it automatically deflates and is excreted.

Overall, the study found the swallowable gastric balloon was a safe procedure that led to weight loss in obese patients, when used alongside a low calorie diet. However, the rate of weight loss slowed down after 12 weeks of treatment, until the introduction of a very low calorie diet.

This is early stage research involving a small number of patients who were followed up for just 16 weeks. Long-term studies are needed to see if the swallowable gastric balloon can help people not only lose weight but also keep the weight off.

Where did the story come from?

This research was carried out by researchers from Sapienza University in Italy. No external sources of funding were mentioned.

The research was presented as a conference poster at the 24th European Congress on Obesity taking place in Portugal from May 17-20 2017. The poster is also available online (PDF, 530kb).

The media coverage around this research was generally accurate, though several reports made no mention of the fact that any weight loss achieved may not last beyond the period when the gastric balloon is in place, unless patients make long-term changes to their diet.

What kind of research was this?

This prospective non-randomised study investigated whether treatment with a swallowable gastric balloon is a safe and effective option to help obese people lose weight.

Used alongside a low calorie diet, the balloon can make it easier to adhere to the strict intake of the diet because it makes you feel fuller.

Non-randomised prospective studies like this one are useful to follow up on medical interventions, and assess their safety and effectiveness by looking at the number of adverse events. However, the best way to validate these findings would be by using a randomised controlled trial (RCT).

What did the research involve?

Researchers studied 38 obese patients (28 men and 10 women) for 16 weeks after insertion of the gastric balloon.

The mean age of the participants was 46, their mean initial weight was 110kg, and they had a mean BMI of 39.

The people recruited for the study had struggled to lose weight through dieting alone, and had refused other treatments involving gastric balloons because of the need for sedation and endoscopy.

The participants were asked to swallow the gastric balloon, which is packaged inside a capsule the size of a pill and attached to a thin tube. The capsule disintegrates when it's in the stomach, and the balloon is then filled with 550ml of liquid.

The thin tube is then detached and the gastric balloon remains in the stomach. After four months, the release valve in the balloon opens automatically, which empties the fluid, and the balloon is then excreted.

For the first 12 weeks of treatment, the patients were given a low calorie diet, which was then switched to a very low calorie ketogenic diet (~700 kcal/day) for the last four weeks.

Follow-up took place every two weeks. At the end of the 16 weeks, the balloon was excreted and participants were asked to follow a Mediterranean diet to maintain their weight loss.

What were the basic results?

Overall, treatment with the gastric balloon was well received by all the patients involved in the study. In all cases, the balloons were swallowed, filled and excreted successfully.

There were no reports of serious adverse events. Side effects such as nausea, vomiting and abdominal pain resolved on their own or with medication.

The participants lost weight throughout the 16 weeks of gastric balloon therapy:

  • at week 4: the mean weight loss was 5.4kg
  • at week 8: mean weight loss 8.9kg
  • at week 12: mean weight loss 11.5kg
  • at week 16: mean weight loss 15.2kg

Although weight loss decreased overall in the first 12 weeks, the rate of weight loss began to slow down at the end of the first 12 weeks. It then increased again in the last month, when the patients followed a very low calorie ketogenic diet (VLCKD) to boost weight loss.

How did the researchers interpret the results?

The researchers concluded: "The Elipse balloon appears to be a safe and effective weight loss method. Furthermore, the introduction of a VLCKD (very low calorie ketogenic diet) improves weight loss."

They added: "The procedureless nature of the Elipse balloon may make it amenable to a larger population of obese patients not responding to diet treatment and a variety of clinicians (e.g. nutritionists, dieticians and internists) who currently do not have access to endoscopic or surgical weight loss devices."


This research investigated whether treatment with a swallowable gastric balloon is a safe and effective option to help obese people lose weight.

Overall, the study found the gastric balloon led to weight loss when used alongside a low calorie diet, with a mean weight loss of 15.2kg by the end of the 16-week treatment period.

However, the rate of weight loss declined after 12 weeks of treatment, before going up again in the last month with the introduction of a very low calorie diet.

This is an interesting piece of research, but it has a number of limitations.

  • This is a very small study, and the findings would have to be observed on a large scale before it can be decided whether this swallowable gastric balloon is a safe and cost-effective option compared with other gastric balloon procedures.
  • The study only looks at the effects of the gastric balloon after 16 weeks of treatment. The effects of the gastric balloon for long-term weight loss would have to be studied before it's decided whether this could be a sustainable weight loss treatment.
  • Because the study has only been presented as a poster at a conference, only limited information on the findings is currently available. A full research paper would provide more information on the methods and limitations of the study. 

Dr Simon Cork, Research Fellow at the Department of Investigative Medicine at Imperial College London, commented: "This is an interesting study with interesting outcomes for clinical practice. It is a small study (only 38 people); however, in terms of proof of concept this is acceptable.

"It is also noteworthy that weight loss begins to slow down as the trial goes on (until the introduction of a low calorie diet). This is not surprising, but shows that in itself, gastric balloons are not long-term solutions for weight loss.

"Sadly, the weight lost through this balloon will undoubtedly be put back on soon after the balloon is removed. Nevertheless, gastric balloons are still useful for some patients, and the introduction of a device which doesn't require surgery to implant is a positive step forward."

Read more on weight loss and weight loss surgery.

Links To The Headlines

'Gastric band in a pill' can help obese lose two stone. The Daily Telegraph, May 18 2017

Gastric band in a pill provides quick fix for ballooning weight. The Times. May 18 2018

Diet pill balloon can lose you 2st. The Sun, May 18 2017

The balloon you swallow to help you shed weight. Daily Mirror, May 18 2017

Balloons could help patients to avoid gastric band surgery. The Guardian. May 18 2017

'Fat but fit' still at higher risk of heart disease

"The idea that people can be fat but medically fit is a myth," reports BBC News.

The story is based on research from scientists at the University of Birmingham, reported at a medical conference but not yet published.

The researchers used information from a UK database of GP records covering 3.5 million people, to calculate people's chances of getting cardiovascular disease, such as a heart attack or stroke.

They focused on people who were obese based on a body mass index (BMI) over 30, but who did not have the associated risk factors of high blood pressure, diabetes or abnormal fats in their blood.

The researchers wanted to know if this group, sometimes called "metabolically healthy obese" people, had a raised risk of cardiovascular disease compared to people of recommended weight (a BMI of 18.5 to 24.9).

The research found they had a higher chance of heart disease, stroke or transient ischaemic attack (mini stroke) and heart failure, compared to those of recommended weight. However, their risk was not as high as for obese people who also had diabetes, high blood pressure or abnormal fats.

The research is unpublished, which means we can't check the validity of the study. However, it confirms that keeping to a healthy weight is likely to lower your chances of cardiovascular disease, which is not a surprising finding.

Where did the story come from?

The study was carried out by researchers from the University of Birmingham. It was presented at the European Congress on Obesity in Portugal.

Sources of funding were not declared.

Some sections of the UK media seized on the study with glee. "Think you're fat AND fit? There's no such thing!" crowed the Daily Mail, illustrating its article with fat-shaming photographs of overweight people at the gym.

Most of the coverage repeated the line that it is not possible to be overweight and healthy, which is not what the study found.

The study results showed obese people were at an increased risk of certain diseases, but that doesn't mean they will all get these diseases.

What kind of research was this?

This was a prospective cohort study.

This type of study is good at finding links between factors – such as weight, metabolic indicators and cardiovascular disease, in this case – but cannot prove that one causes another.

So the study does not prove that being obese but metabolically healthy causes cardiovascular disease, only that there's a link between the two.   

What did the research involve?

Researchers used electronic health records from 1995 to 2015 from the Health Improvement Network database of UK general practice records.

They looked at records of people aged 18 and over, without cardiovascular disease at the start of the study. People were grouped according to their BMI and whether they had any of three metabolic risk factors: diabetes, high blood pressure or abnormal blood fats.

Researchers then calculated the relative risk for each group of getting one of four cardiovascular disease conditions:

  • coronary heart disease (including angina and heart attack)
  • cerebrovascular disease (including stroke and transient ischaemic attack or TIA)
  • heart failure, where the heart muscle is unable to pump sufficient blood around the body
  • peripheral vascular disease, where blood vessels in the legs narrow and cause pain while walking

They compared the risks of people with recommended weight and no metabolic risk factors with people who were obese and had no, one, two or three metabolic risk factors.

They adjusted their figures to take account of confounding factors including age, sex, smoking and socioeconomic status.

What were the basic results?

Of the 3.5 million people in the study, 766,900 (21.9%) were obese – of whom 518,000 (14.8%) were obese with no additional risk factors (metabolically healthy).

The researchers found that, compared to people of recommended weight, metabolically-healthy obese people were:

  • 50% more likely to get heart disease
  • 7% more likely to get cerebrovascular disease
  • twice as likely to get heart failure

The findings for peripheral vascular disease were mixed. Overall, metabolically-healthy obese people were 9% less likely to get peripheral vascular disease. However, excluding smokers, the risk was 11% higher.

Metabolic risk factors raised the chances of getting any of these conditions, in addition to obesity.

Compared to recommended weight, metabolically-healthy people, those who were obese and had all three risk factors were:

  • 2.6 times more likely to get heart disease
  • 58% more likely to get cerebrovascular disease
  • 3.8 times more likely to get heart failure
  • 2.2 times more likely to get peripheral vascular disease

The researchers say their figures were statistically significant; however they were unable to supply the full data with confidence intervals, so we can't check this.

How did the researchers interpret the results?

The researchers said their study showed that "metabolically-healthy obese individuals are at higher risk" of the diseases studied and that "The priority of health professionals should be to promote and facilitate weight loss among obese persons, regardless of the presence or absence of metabolic abnormalities."

Study author Dr Rishi Caleyachetty added: "So-called metabolically healthy obesity is not a harmless condition and perhaps it is better not to use this term to describe an obese person."


The question of whether someone can be "fat but fit" has been much debated. If you're obese but exercise, eat well and don't have metabolic risk factors, the theory goes, you could be just as healthy as someone of recommended weight. This study suggests that may not be true.

It is definitely worth adopting a healthy lifestyle, whatever your weight. The study found that, the more metabolic risk factors people had, the more likely they were to develop heart disease, cardiovascular disease and so on. Metabolic risk factors do make a difference.

But in this large study, on average, people who were obese with no metabolic risk factors had a higher risk of disease than people of recommended weight with no metabolic risk factors.

The study has some strengths. It is very large, and uses data from records that are thought to be reasonably reliable. However, we need to remain cautious about the strength of the study until we can see the full data. The researchers say the paper is under peer review and is expected to be published in a medical journal.

If you are worried about your weight, talk to your doctor and take a look at our weight loss programme.

Links To The Headlines

It is not possible to be 'fat and fit', major study finds. Independent, May 17 2017

Think you're fat AND fit? There's no such thing! Mail Online, May 17 2017

Being 'fat but fit' is a myth, claims study. Sky News, May 17 2017

Can you be fat and fit? No you can't be both obese and healthy, says study of 3.5 million people. Metro, May 17 2017

No such thing as 'fat but fit', major study finds. Guardian, May 17 2017

'Fat but fit' idea is a medical myth, researchers find. Telegraph, May 17 2017

'Fat but fit is a big fat myth'. BBC News, May 17 2017

Lack of sleep knocks your social appeal, says research

"A couple of bad nights is enough to make a person look 'significantly' more ugly," reports BBC News.

Researchers in Sweden found people rated photographs of strangers as less attractive and healthy when the people in the photographs had less sleep.

The study used photographs of healthy, mainly young, students taken after either two nights of normal sleep (around eight hours a night) or two nights of restricted sleep (around four hours a night).

The photos were rated by 122 strangers, who were asked how much they would like to socialise with the people in the photographs, and how healthy, attractive, trustworthy and sleepy they looked.

The study found that on average, people were 2.1% less likely to want to socialise with people who'd had less sleep.

It's unclear how significant this finding is in real life, or what effect it might have on people not getting enough sleep.

If you're having difficulty sleeping, whether or not other people want to socialise with you may be the least of your worries.

Persistently poor sleep can increase the chances of obesity and diabetes, and worsen conditions like depression and anxiety.

Find out more about getting a good night's sleep.

Where did the story come from?

The study was carried out by researchers from Karolinska Institute and Stockholm University in Sweden and was funded by the two institutions. 

It was published in the peer-reviewed journal Royal Society Open Science on an open access basis, meaning it's free to read online.

BBC News gave a balanced overview of the study, but didn't mention the small size of the effect of sleep deprivation.

What kind of research was this?

This was an experimental psychological study, using volunteers. This type of study can show the effects of experimental conditions on volunteers, but doesn't necessarily tell us what happens to people with sleep problems in real life.

What did the research involve?

Researchers recruited 14 female and 11 male students, mostly in their early 20s but ranging from 18-47 years old. 

All 25 students had their photograph taken twice – once after two nights of sleep restriction and once after two nights of normal sleep.

The photos were viewed by 122 members of the general public from Stockholm, 65 of them women, who gave ratings on a number of questions.

The researchers looked at the results to see if there was a difference between people's ratings of photos taken when people were sleep restricted, or when they'd had normal sleep.

For the photographs after normal sleep, people were told to go to bed for around eight hours, between 10pm and midnight until between 6am and 8am.

Before the sleep deprivation photographs, people were told to go to bed for around four hours, between midnight and 2am until between 4am and 6am.

They used actigraphs (special monitors) to measure activity so the researchers could check the students had followed the instructions properly.

The average difference in hours of sleep between the normal and restricted sleep was 3.5 hours a night, adding up to seven hours less sleep than normal over two nights.

All photographs were taken at the same time of day by the same photographer, with people wearing no make-up and hair scraped back from the face.

Raters were asked to look at 50 photos (two from each person) and say on a scale of one to seven:

  • how much they would like to socialise with them
  • how attractive they were
  • how healthy they looked
  • how sleepy they looked
  • how trustworthy they looked

Students were paid for taking part and raters were offered cinema tickets.

The researchers excluded ratings from people whose ratings showed low variability (less than 0.5 standard deviation between scores on normal sleep and restricted sleep photos) because they say this could indicate "low motivation to adhere to the instructions of the task".

What were the basic results?

People's average ratings were mostly in the middle of the seven-point scale on all questions, with averages between three and five for people who'd had normal sleep.

Raters' scores suggested they were less willing to socialise with people who'd been sleep restricted, but only by 0.15 points on a seven-point scale (around 2.1%).

Compared with average ratings after normal sleep, average ratings on a seven-point scale were:

  • 0.09 points lower for attractiveness
  • 0.11 points lower for health
  • 0.25 points higher for sleepiness

There was no difference in the trustworthiness scores between normal sleep and sleep deprivation.

Analysis showed only about a third of people's reduced willingness to socialise with sleep-restricted people was explained by the findings on attractiveness, health and sleepiness. In other words, something other than attractiveness, health or sleepiness was putting people off.

How did the researchers interpret the results?

The researchers say their study "indicates that restricted sleep affects facial appearance negatively and decreases others' willingness to socialise with the sleep deprived person".

They say it confirms previous findings that people completely deprived of sleep for one or two nights are judged to look less healthy and attractive, and extends the findings to "less substantial and more natural" sleep loss conditions.


Most people who have looked in the mirror after a sleepless night won't be surprised to hear that a poor night's sleep makes you look less attractive and healthy.

It may not be particularly welcome news that your appearance could also put people off talking to you.

But the study results show only a very small impact of sleep deprivation on people's perceptions of appearance.

While the results are statistically significant, it's hard to know how you would notice a 2% drop in a stranger's willingness to socialise with you.

And studies like this, which include only a limited demographic (in this case Swedish students aged around 22, mostly white) may have little relevance to anyone who doesn't fit that profile.

More important are the known health effects of sleep problems. An occasional late night is very different from persistent difficulties in getting to sleep or staying asleep.

Regular poor sleep can raise your risk of diabetes, heart disease and obesity, and is linked to mental health problems like anxiety and depression.

There are plenty of things you can try yourself to increase your chances of getting a good night's sleep. But if you've tried these and you're still struggling to sleep, talk to your GP.

Good ways to sleep well include:

  • regular sleep hours for going to bed and getting up
  • keeping your bedroom calm, cool, comfortable and quiet
  • taking regular exercise, but not late in the evening
  • cutting down on caffeine
  • avoiding too much alcohol, especially late at night
  • relaxing before going to bed with a bath or a good book, or listening to calming music

Read more about getting to sleep.  

Links To The Headlines

Beauty sleep is a real thing, research shows. BBC News, May 17 2017

Links To Science

Sundelin T, Lekander M, Sorjonen K, Axelsson J. Negative effects of restricted sleep on facial appearance and social appeal. Royal Society Open Science. Published online May 17 2017.

Hope for plant-based contraceptive, study claims

"Forget Plan B – try aloe vera, controversial study claims: Scientists insist pills made from dandelions and mangoes can prevent pregnancy without a hit of hormones," reports the Mail Online.

The news is based on a study investigating whether chemicals found in certain plants can reduce sperm's ability to fertilise a woman's egg.

Sperm get a boost of energy from the hormone progesterone as they approach the egg. This activation increases their swimming speed in the female reproductive tract, enabling them to penetrate the egg.

Using donor sperm samples, this research showed how two plant chemicals – pristimerin (found in thunder god vine) and lupeol (found in mango, dandelion root and aloe vera) – were able to prevent sperm activation.

This raises the possibility that these natural substances could act as an alternative to hormone-based contraceptives, which are known to have side effects.

More laboratory research is needed to show if this type of contraceptive method has the potential to be safe and effective before researchers can consider moving on to human trials.

The researchers are currently working on developing a contraceptive patch and pill. But it's likely to be many years before we know if this could lead to a new licensed contraceptive.

Where did the story come from?

The study was carried out by researchers from the University of California.

It was funded by a US National Institutes of Health grant, a Pew Biomedical Scholars Award, an Alfred P Sloan Award, and Packer Wentz Endowment Will.

The researchers declare a conflict of interest in that two of the authors are inventors on a patent application filed by the University of California.

The study was published in the peer-reviewed journal Proceedings of the National Academy of Sciences and is free to read online.

The news stories have broadly reported the story accurately, but don't state that any potential new contraceptive would take years to develop. 

What kind of research was this?

This laboratory study aimed to assess whether it's possible to use plant chemicals to restrict sperm movement, thereby preventing them from moving effectively towards the egg.

The researchers explain how the sperm calcium channel, CatSper, which is found in the tail, is a key part of male fertility.

The female hormone progesterone activates CatSper by binding to a particular receptor (ABHD2), energising the sperm and boosting fertility.

In theory, any chemical that blocks this receptor has the potential to behave like a contraceptive and prevent fertilisation.

This type of research is useful for further understanding how biological mechanisms work and identifying potential new therapies.

But even if it's shown to work in the laboratory, much more testing is needed before we can conclude that this is a safe and effective alternative form of contraception.  

What did the research involve?

Four healthy donors provided sperm samples for this research. The researchers analysed the effects different hormones and substances have on calcium channels (CatSper) and consequently sperm movement. All tests were performed at normal body temperature (37C). 

Sperm samples were exposed to the following hormones:

  • testosterone
  • oestrogen
  • progesterone
  • hydrocortisone (a steroid hormone)
  • pregnenolone sulphate (a steroid hormone)
What were the basic results?

The researchers found testosterone, oestrogen and hydrocortisone had no effect on the mobility of sperm and its ability to penetrate the egg.

They confirmed that progesterone activates the sperm for fertilisation by binding to the ABHD2 receptor. They also found pregnenolone sulphate had a similar effect in activating sperm, likely by binding to the same site.

The researchers then identified two steroid-like plant chemicals, pristimerin and lupeol, which appeared to block the action of the progesterone and pregnenolone sulphate on sperm.

By preventing the action of the other hormones, they reduced the sperm's ability to activate and then penetrate and fertilise an egg. 

How did the researchers interpret the results?

The researchers concluded that their results indicate pregnenolone sulphate and progesterone are the main steroids that initiate sperm activation.

Pristimerin and lupeol, found in plants, can act as contraceptives by reducing sperm movement and preventing fertilisation.  


This laboratory study aimed to investigate a variety of steroid hormones and plant compounds to look at their effect on sperm activation and ability to fertilise an egg.

The researchers confirmed that the hormone progesterone present in the female reproductive tract seems to be needed to activate sperm and make them able to fertilise an egg.

The also found that two plant compounds, pristimerin and lupeol, were able to block the sites on the sperm that are activated by progesterone. This means these two compounds could have a potential contraceptive action.

But it's far too early to say whether new contraceptives could become available as a result of this research. More laboratory research would be needed to show their potential to be safe and effective before considering trials in humans.

For example, at the current stage it's not actually known whether these compounds would incapacitate all sperm and prevent them fertilising an egg.

It's also unclear what method of exposure would be needed (like a pill, patch or vaginal ring) and whether the compounds have toxic side effects.

Most potential new treatments identified at such an early experimental stage don't make it all the way to becoming licensed treatments available to the general public. 

Find out more about contraception.

Links To The Headlines

Plant chemicals hope for 'alternative contraceptives'. BBC News, May 16 2017

Forget Plan B – try aloe vera, controversial study claims: Scientists insist pills made from dandelions and mangoes can prevent pregnancy without a hit of hormones. Mail Online, May 15 2016

Contraceptive pill without side-effects could be created using aloe vera extract, scientists say. The Daily Telegraph, May 15 2017

Links To Science

Mannowetza N, Millera M and Lishkoa P. Regulation of the sperm calcium channel CatSper by endogenous steroids and plant triterpenoids. Proceedings of the National Academy of Sciences of the United States of America. Published online May 15 2017

Can fizzy water make you fat?

“Fizzy water could cause obesity by encouraging you to eat more,” The Daily Telegraph reports.

Researchers aimed to see whether it could be the carbonation in soft drinks – rather than the sugar – that explains the link between soft drinks and obesity.

Overall, they found rats that drank diet or regular fizzy drinks ate more and gained more weight over six months than rats that drank flat soda or water. The weight gain was associated with increased production of the appetite hormone ghrelin, which is produced by both rodents and humans.

The researchers then looked at the effects of carbonated drinks in 20 young men and found they also had higher blood ghrelin levels after drinking fizzy drinks than after flat soda or water.

But we can’t say from the results of this study alone that carbonation or ghrelin production is the full answer to the link between soft drink consumption and obesity.

It is likely that obesity is caused by multiple environmental, social and lifestyle factors, rather than carbonation on its own.

People who consume lots of fizzy drinks may also be more likely to have a less healthy diet and to be doing less exercise. The safest and cheapest bet for refreshment is plain old tap water.

Where did the story come from?

The study was carried out by researchers from Birzeit University in Palestine and was funded by grants from the same institution. 

It was published in the peer-reviewed journal Obesity Research and Clinical Practice.

The coverage of the study in the UK media was accurate.


What kind of research was this?

This animal research aimed to see whether having fizzy drinks could contribute to weight gain.

The authors state that arguably there are many causes of obesity, including environmental, social and genetic factors. They say numerous studies have observed links between obesity and soft drink consumption, mostly believed to be due to the sugar content in these drinks.

But there’s another element to both sugar sweetened and diet fizzy drinks: carbon dioxide. This study  aimed to look at the effects of carbonation.

Animal research is a useful step to see how biological processes may work in humans, as we share many similarities.

That said, we aren’t identical to rodents, so any findings would always need to be validated in human trials. Preliminary attempts at validation were made in this study. There are still likely to be many other issues involved with dietary intake and weight gain.   

What did the research involve?

The study involved groups of male rats who were all fed a standard diet, but given one of four different drinks:

  • tap water
  • regular degassed (flat)
  • soda regular carbonated soda
  • diet carbonated soda

The researchers assessed food consumption, weighed the rats, and analysed blood sugar and cholesterol after six months on the diet.

They also looked at blood levels of the hormone ghrelin, which is released from the digestive system in response to hunger.

After death, the rats’ stomachs were also examined to see how much ghrelin had been produced and their liver was examined for fatty deposits.

In a second part of the study, 20 healthy human male students aged 18-23 were given a light breakfast followed one hour later by each of the four drinks.

The students repeated this experiment on different days so they were all trying the same drinks. They then had blood samples taken to measure ghrelin. Ghrelin is a hormone that’s “used” by the digestive system to simulate feelings of hunger.

What were the basic results?

Rats that drank tap water or flat soda weighed significantly less than those drinking the carbonated drinks. Rats that drank both the diet and sugary fizzy drinks gained a similar amount of weight. Weight gain was slowest in the water-drinking rats compared with all three groups drinking soda.

Rats drinking the fizzy drinks ate significantly more food than those drinking water and flat soda. This was associated with increased blood levels of ghrelin, further supported by evidence of increased ghrelin secretion from the stomach.

There was no difference in blood sugar or cholesterol levels, but those that drank fizzy drinks had more fat in the liver.

In the human volunteers, ghrelin levels were higher after drinking fizzy drinks one hour after food – three-folds higher than after flat soda, and six-folds higher than after water.

How did the researchers interpret the results?
The researchers concluded that, “This study clearly shows discernible effect of the carbon dioxide gas in carbonated drinks on increased food ingestion and heightened risk of weight gain, obesity and fatty liver disease by inducing ghrelin release.”


There seemed to be a clear distinction in this study between fizzy and non-fizzy-drink consumption in terms of weight gain, appetite and ghrelin production.

These findings were further supported by the study in healthy adult volunteers, which similarly showed that the fizzy drinks increased ghrelin production.

But does this mean that carbonation and ghrelin production provide the whole answer to why soft drink consumption is linked with obesity?

But this doesn’t account for the link between weight gain and diet drinks which don’t contain sugar’They suggest carbonation could be the common link between the two.

This is possible. But it may also be that other unhealthy lifestyle factors, which this study didn’t look at, could also be a common link between sugary and diet fizzy drinks..

In real life, people who drink soda lots of fizzy drinks could also be more likely to have a less healthy diet and exercise less.

It could still be argued that even if people drinking soft drinks do eat more unhealthy food, this is caused by the carbonation making them eat more, but this isn’t proven.

Another point to bear in mind is that this research was conducted primarily in rats. Human beings may not have identical biology.

And although the researchers did follow this up with a human study, they only looked at a very small sample of young men. We can’t necessarily apply their results to women or other populations.

Even in the rats, they found though the rats had increased levels of the appetite hormone, there was no effect on the levels of another satiety hormone that tells them they’re full. This means we can’t be certain that ghrelin provides the whole answer to weight gain.

Overall, this study raises an interesting possibility that fizzy drinks could stimulate the appetite and cause weight gain, which is definitely worthy of further research.

The best way to achieve a healthy weight is through eating a balanced diet and exercising regularly And as unexciting as it may seem, water straight from the tap is the best option to quench your thirst. 

Links To The Headlines

Fizzy water could cause obesity by encouraging you to eat more. The Daily Telegraph, May 15 2017

 Fizzy water could make you FAT, reveal scientists…and you could be better off drinking ‘flat’ sugary drinks. The Sun, May 15 2017

Fizzy water could be making you fat – here's how. Daily Mirror, May 15 2017

Links To Science

Eweis SD, Abed F, Stiban J. Carbon dioxide in carbonated beverages induces ghrelin release and increased food consumption in male rats: Implications on the onset of obesity. Obesity Research and Clinical Practice. Published online February 19 2017

Keyhole knee surgery is 'waste of time' review finds

"Keyhole knee surgery for arthritis pain 'is pointless'," the Daily Mail reports.

The headline is prompted by a review of the available evidence around knee arthroscopy (keyhole) procedures for people with degenerative knee conditions such as osteoarthritis – so called 'wear and tear arthritis'.

In spite of the headlines, this conclusion is not particularly newsworthy as it is consistent with current recommendations of UK guideline groups like the National Institute For Health and Care Excellence (NICE) and the British Orthopaedic Association.

One exception raised by the review is that knee arthroscopy is often performed, and recommended by these organisations, for people with mechanical locking or clicking symptoms, often consistent with meniscal tears (tears in wedges of cartilage in the knee joint). Based on the evidence from one key trial last year, the expert panel who did the review conclude there's no evidence for a benefit in these people either.

It remains to be seen whether recommendations in future updates of UK guidelines will alter as a result of these findings.


Where did the story come from?

The guidance was produced by researchers from various international institutions, including McMaster University and University of Toronto in Canada and South Western Sydney Clinical School in Australia. It received no sources of financial support and the authors declare no conflict of interest.

The guidance document is published in the peer-reviewed British Medical Journal and is openly available for online access.

The Daily Mail coverage, while mainly accurate, may be a little misleading as it says these procedures are currently performed "on patients with a common form of arthritis" – implying osteoarthritis. This isn't strictly true as arthroscopy is not currently recommended for people with osteoarthritis; only if there are symptoms of locking.


What kind of research was this?

This was a clinical practice guideline on the role of arthroscopic (keyhole) surgery for degenerative arthritis and meniscal tears.

Degenerative knee arthritis can generally be thought of as osteoarthritis. It is a medical term used to describe people (usually older than 35) with knee pain who may have signs and symptoms of osteoarthritis or meniscal tears, such as locking or clicking.

The menisci are wedges of cartilage in the knee joint, in between the thigh and shin bones. The authors explain how a quarter of people over the age of 50 have some degree of degenerative knee disease.

In this guidance document, an expert panel reviewed current practice and looked at the evidence on knee arthroscopy. They discussed these findings – along with patients with first-hand experience of degenerative knee disease and its treatment – to form recommendations around the use of knee arthroscopy.        


What do the group say about current practice?

The experts explain how the management of people with osteoarthritis (degenerative knee disease) often includes "watchful waiting" to see what happens, alongside exercise and weight loss (if overweight) and use of anti-inflammatory painkillers as needed.

More invasive treatment options that may be considered include steroid injections into the knee joint, arthroscopic knee surgery or knee replacement. There's no fixed consensus on what's best and management will often vary between patients.

However, keyhole approaches appear most common and more than 2 million procedures are performed worldwide each year, at a cost of $3bn per year in the US alone. They are particularly used when there are signs of meniscal tear.


What is the evidence for knee arthroscopy?

The experts considered available systematic reviews on knee arthroscopy. They considered pain, function and quality of life to be the most important and relevant outcomes for patients. In one review, though many of the 25 studies had looked at these outcomes, it was difficult to know what real-life meaning the changes would have (for example, a three-point change on a rating scale).

A key randomised controlled trial from last year found that knee arthroscopy was no better than exercise for people with degenerative knee arthritis with meniscal tear – yet this is often seen as a particular indication for this procedure.

The panel considered the quality and strength of the evidence using a recognised systematic approach (GRADE – Grading of Recommendations, Assessment, Development and Evaluations) to form their recommendations.


What does the group recommend about knee arthroscopy?

They strongly recommend against the use of arthroscopy in nearly all patients with degenerative knee disease based on systematic review evidence. They say that this recommendation applies to patients regardless of imaging evidence of osteoarthritis or the presence of mechanical locking or clicking symptoms (indicating meniscal tears).

The panel say they are confident that knee arthroscopy does not improve long term pain or function. They did find evidence that for a small number of people (less than 15%) arthroscopy gave small improvements in pain or function for a few months, but this wasn't sustained by one year.

They consider that the potential risks of the procedure outweigh any possible short-term benefit. Aside from rare complications, common drawbacks are that it can take weeks for people to fully recover from arthroscopy. Pain, swelling and difficulty putting weight on the leg are common.

Symptoms from degenerative knee conditions often fluctuate, and many can experience improvement over time without intervention.

The panel feel confident that further research is unlikely to alter this recommendation.

The only helpful use of arthroscopy is for people with a truly locked knee they can't straighten. The recommendations also aren't relevant to people with sports injuries or major trauma.



This expert panel review provides compelling evidence against the use of knee arthroscopy for degenerative knee conditions/osteoarthritis. This procedure often has varied and inconsistent use in clinical practice.

As part of their review the researchers also considered what other government organisations currently recommend about the procedure.

NICE already says knee arthroscopy (with washout – flushing the joint with fluid) should not be performed for people with osteoarthritis. The only indication NICE currently gives for the procedure is people who have a clear history of mechanical locking symptoms. But it's not clear whether the person has to have a truly locked knee, or locking and clicking symptoms that come and go.

The British Orthopaedic Society, like NICE, advises against arthroscopy for people with osteoarthritis but does recommend the procedure for people with mechanical locking symptoms. It also explicitly recommends arthroscopy with partial meniscal removal for people with meniscal tears.

Therefore, UK guidelines currently support the advice not to use the procedure for osteoarthritis, but do recommend it for locking/meniscal symptoms. It remains to be seen whether these expert panel findings alter recommendations in future updates of these guidelines.

Links To The Headlines

Keyhole knee surgery for arthritis pain 'is pointless': Warning minor procedure has been oversold as a cure for all problems. Daily Mail, May 11 2017

Links To Science

Siemieniuk RAC, Harris IA, Agoritisas T, et al, Arthroscopic surgery for degenerative knee arthritis and meniscal tears: a clinical practice guideline. BMJ. Published online May 10 2017

Yoga may bring long-term benefits for people with depression

"Yoga can ease depression symptoms, according to the largest study to ever investigate the link," the Mail Online reports.

The study didn't find any benefits from doing yoga at the end of the 10-week study period, but there were improvements in symptoms at a six-month follow-up review. Because of the mixed results, these findings need to be interpreted with caution.

The US study included 122 adults with moderate depression who hadn't responded effectively to antidepressants. They were assigned to 10 weeks of either yoga or health education classes.

The main outcome of interest to the researchers were changes in the participants' symptoms of depression, as measured by depression scores, at 10 weeks.

The researchers didn't find any difference between the groups at 10 weeks. But they did find a difference in terms of symptom improvements between the two groups when they compared the scores from 10 weeks with those after six months.

On their own, the results of this study don't provide firm evidence that yoga is beneficial for depression.

There was no effect on the main outcome the study set out to examine, and participants had responded to advertisements, so likely had an interest in yoga to start with. 

This could mean that they were more likely to be receptive to the idea yoga could have a benefit, so there could have been a placebo effect at work.

These findings don't change current guidelines on the treatment of depression using psychological interventions like cognitive behavioural therapy, as well as antidepressants. 

There is, however, evidence that exercise and practising mindfulness  – the two key tenets of yoga – may help enhance mental wellbeing. 

Where did the story come from?

The study was carried out by researchers from Brown University, the University of California, and the Eyes of the World Yoga Center, all in the US.

It was funded by the US National Institute of Nursing Research and published in the peer-reviewed journal, Psychological Medicine.

The Mail's coverage is generally accurate, but doesn't discuss the study's limitations in any detail.

What kind of research was this?

This randomised controlled trial aimed to see whether yoga is an effective additional treatment for people with depression still experiencing symptoms, despite taking antidepressants.

The researchers report around a third of people don't have an adequate response to treatment with antidepressants, and there's a need for interventions to improve symptoms for people in this situation.

A previous systematic review found people who practise yoga experience more improvement in their symptoms than those who receive usual care.

Hatha yoga, which combines mindfulness along with physical exercise, is the most common type of yoga and the form of yoga assessed in this study.

What did the research involve?

Adults from Rhode Island were recruited to the trial through advertisements.

Eligible participants had to have moderately severe depression, as scored by the well-validated Quick Inventory of Depression Symptomatology (QIDS) scoring system. A score of between 8 and 17 is seen as corresponding to moderately severe depression.

They also had to have no history or symptoms of other mental health disorders, no alcohol use problems, minimal previous experience of yoga, and have been taking a stable antidepressant dose for at least eight weeks.  

Participants were then randomised to either weekly yoga classes (63 people) or health education classes (59) for 10 weeks.

Hatha yoga classes included breathing exercises, meditation, postures, relaxation, and education around home practice.

Classes were available twice weekly, and participants were asked to attend at least once a week. All classes were delivered by registered yoga instructors who met regularly to ensure class consistency.

Health education classes were run along the same schedule as yoga – twice weekly for 10 weeks, with participants encouraged to attend at least once a week.

Instructors followed a manual, and covered general health education around topics such as alcohol, smoking, caffeine, nutrition, sleep, pain management, and preventing chronic diseases.

People were assessed up to the end of the intervention at week 10, and then followed up for a further six months. The main outcome of interest was depression score on the QIDS scale at 10 weeks.

In their analyses, researchers took into account class attendance and baseline characteristics, including additional treatments. Nearly all people continued to take antidepressants throughout the study and 40% attended psychotherapy sessions.

What were the basic results?

People in the yoga group attended an average of 8.9 classes over 10 weeks, and those in the health education group attended seven classes over 10 weeks.

There was no significant difference between the groups in QIDS scores at 10 weeks. Scores improved by an average 3.93 points in the yoga group and 3.15 in the health education group. 

However, the researchers did find a significant improvement when they looked at the whole treatment and follow-up period.

Looking at treatment response (greater than 50% reduction in QIDS score), there was no difference between the two groups at 10 weeks. But by six months follow-up, 51% of the yoga group met response criteria compared with 31% of the health education group.

How did the researchers interpret the results?

The researchers concluded that, "Although we did not see a difference in depression symptoms at the end of the intervention period, yoga participants showed fewer depression symptoms over the entire follow-up period. Benefits of yoga may accumulate over time." 


The study will have to be interpreted in the context of other research into yoga and depression. But taken in isolation, it doesn't provide firm evidence that yoga is beneficial for depression.

The findings are applicable to a very specific population group: people with moderately severe depression who took antidepressants (often alongside other psychological therapy) and had no other mental health illness.

They also hadn't previously practised yoga, but must have had an interest in doing so as they responded to advertisements.

This means the groups by no means represent all people with depression symptoms. 

The study was set up to examine the effect on depression score at 10 weeks. There was no statistically significant difference between the groups.

The main outcome in a study is usually the most reliable, as researchers recruit the number of people they need to detect a difference between groups.

But in this study, researchers calculated they needed 75 people in each group, but weren't able to recruit enough. This means the study was underpowered for the main outcome, never mind any secondary outcomes.

And the researchers compared yoga with general health education classes; they didn't compare yoga with usual care, including standard treatment approaches for depression. 

These findings don't alter the current recommendations for the treatment of depression.

The National Institute for Health and Care Excellence (NICE) guidelines recommend initially considering cognitive behavioural therapy (CBT) or structured group physical activity for people with mild to moderate symptoms.

Antidepressants may be prescribed if people have persistent or more severe symptoms, or a history of episodes of depression.

Regular exercise is recommended for everyone – if you have an interest in yoga, there's no reason why the practice shouldn't be part of your treatment.

But it's most important that you first seek help from your GP if you have symptoms of low mood. Treatments like yoga should be complementary to recommended treatments for depression, not an alternative.

Links To The Headlines

More than half of depression sufferers could see their symptoms improve by over 50% with weekly yoga classes, according to the largest study of its kind. Mail Online, May 10 2017

Links To Science

Uebelacker LA, Tremont G, Gillette LT, et al. Adjunctive yoga v. health education for persistent major depression: a randomized controlled trial. Psychological Medicine. Published online April 6 2017

Life expectancy for people with HIV now 'near normal'

"Young people on the latest HIV drugs now have near-normal life expectancy because of improvements in treatments," BBC News reports.

The report says advances in antiretroviral drug treatments reduce the risks of serious complications.

Researchers used data from 88,504 people with HIV from Europe and North America to track improvements in survival since 1996, when antiretroviral therapy (ART) was introduced.

ART involves using a combination of drugs that helps prevent the virus from replicating inside the body and attacking the immune system.

The researchers calculated that a 20-year-old starting treatment today could live to 67 years.

The improvement in survival for people with HIV is one of the great health success stories of recent times. What was once considered a terminal disease is now seen as a manageable condition.

While this study doesn't tell us the reasons for improved survival, it's reasonable to think medication plays a part.

However, a continuing issue of concern is the study also showed that people with HIV who injected drugs, or who had a low CD4 cell count (a marker for immune system health) had not seen much improvement in life expectancy.

If you are in a high-risk group for contracting HIV, such as being a man who has unprotected sex with other men, or you inject drugs, you should get an HIV test. The sooner treatment can begin, the more effective it usually is in the long-term.


Where did the story come from?

The study was carried out by an international team of researchers led by the University of Bristol in the UK and was funded by the UK's Medical Research Council, Department for International Development and the European Union.

The study was published in the peer-reviewed journal Lancet HIV on an open access basis, so it is free to read online.

The study was widely covered in the UK media, with most reports celebrating the increase in life expectancy to "near normal" levels.


What kind of research was this?

This was an analysis of several cohort studies which collectively reported on what happened to adults with HIV who started taking ART during four time periods, from 1996 to 2013.

The researchers wanted to see whether survival in people taking ART had improved over time.

Cohort studies are good at showing patterns and changes over time, but they don't show cause and effect – so we can see that deaths declined over the study periods, but the study doesn't tell us why that happened.


What did the research involve?

Researchers used data from 18 cohort studies in Europe and North America to track what happened to 88,504 people when they first started treatment for HIV, across four different time periods. They looked to see how many people survived the first year of treatment (usually the highest-risk period) and then how many survived for the two years following.

After adjusting their figures to take account of confounding factors, they compared survival rates for the four time periods, and used this information to calculate estimated life expectancy.

The time periods were:

  • 1996 to 1999 (ART was introduced in 1996)
  • 2000 to 2003
  • 2004 to 2007
  • 2008 to 2010

Researchers took account of a number of confounding factors:

  • people's age and sex
  • whether they injected drugs
  • whether they had AIDS at the start of the study
  • their CD4 cell count (a marker of the health of the immune system) at the start of ART
  • their viral load (the amount of HIV in their blood) at the start of ART

They calculated the first year and the second and third year of ART treatment separately, because mortality is usually higher in the first year. When calculating estimates of life expectancy, they calculated it based on deaths during the first three years of therapy, then excluding the first year, to give a life expectancy for people who survive the first year of treatment.


What were the basic results?

People starting ART for HIV during 2008 to 2010 were much more likely to survive the first three years of treatment than people who started treatment in earlier time periods.

Looking at the total numbers of deaths within the first three years of treatment, 6% of people starting ART between 1996 and 2003 died compared to 3% who started between 2008 and 2010.

However, these overall figures don't take account of confounding factors.

Taking those into account, people who started ART between 2008 and 2010 were 29% more likely to survive the first year of treatment (hazard ratio [HR] 0.71, 95% confidence interval [CI] 0.61 to 0.83), compared to those who started treatment in 2000 to 2003.

The survival chances in all other time periods were similar to 2000 to 2003. Looking at survival in years two and three, the improvement continued – people starting ART in 2008 to 2010 were 20% more likely to survive (HR 0.80, 95% CI 0.66 to 0.97).

The researchers used mortality during the first three years of ART to calculate estimated life spans. They calculated that, for a European 20-year-old starting ART in 2008 to 2010:

  • a woman could expect to live on average to 67.9 years (95% CI 67.2 to 68.7), compared to 85 years in the French general population
  • a man could expect to live on average to 67.6 years (95% CI 66.7 to 68.5), compared to 79 years in the French general population

However, for those who survive the first year of ART, life expectancy goes up by about a decade, because deaths in the first year of treatment bring down the average life expectancy.

This means people with HIV who survive the first year of ART are likely to live about as long as people without HIV.

A 20-year-old with a high CD4 cell count after one year of ART (suggesting a good response to treatment) during 2008 to 2010 could expect to live to 78 (95% CI 77.7 to 78.3).

There were some exceptions. Improvements in survival were not as significant among:

  • people who injected drugs
  • people who had a very low CD4 count at the start of ART

Estimated life expectancy in the US was slightly lower than in Europe – which may simply reflect the lower overall life expectancy in the US. 


How did the researchers interpret the results?

The researchers say their figures show that survival of people living with HIV in the first three years of ART "improved substantially" during the time period studied.

Better survival in the first year of treatment, they say, is "likely" explained by better drug combinations when people start ART. They say improvements in drugs have led to more effective drugs with fewer side effects.

However, they say that response to treatment "only partly" explained the improvement in survival. Other factors may include more options for patients when HIV has developed resistance to initial drugs. They suggest that simpler, one-a-day, pill regimens mean people are more likely to take their medicine correctly.

Also, they say, now that people with HIV are expected to live into old age, they are more likely to be checked and treated for other diseases such as cardiovascular disease, hepatitis C infection, and cancer.



This study is good news for anyone affected by HIV. It shows that people who start on modern HIV treatments can now live almost as long as people without HIV. The study is a demonstration of the enormous transformation in life expectancy for many people with HIV since the 1980s.

However, the study can't tell us why these improvements have come about. We know that drug treatments have improved greatly since 1996, when the study began, so it's reasonable to think that drug treatments play an important role.

However, there are other factors that might be important, such as earlier diagnosis and treatment, quick and effective response to the infections and cancers that HIV leaves people vulnerable to, and greater treatment choice when a drug combination fails.

The study has some limitations. The participants in the study were all treated in high income countries in Europe or North America. Improvements on this scale may not apply to resource-poor parts of the world, where people don't have ready and reliable access to ART.

Also, the life expectancy figures given are only averages. They don't guarantee that people with HIV will live to those ages, any more than average life expectancy for the general population guarantees that's how long you will live.

The researchers note that people who inject drugs, and people whose immune system is already damaged by the time they are diagnosed with HIV, have seen much less improvement.

The challenge is to find ways to extend the benefits seen among those diagnosed and started quickly on treatment, to people who risk being left behind.

Prompt diagnosis and treatment – plus adherence to treatment in the long-term – are key if we are to see continued improvements in HIV life expectancy.

Find out more about testing and treatment for HIV.

Links To The Headlines

HIV life expectancy 'near normal' thanks to new drugs. BBC News, May 11 2017

HIV patients aged 20 diagnosed today will live into their mid-70s: Study highlights progress made in treatment over the past 30 years. Daily Mail, May 11 2017

Modern drugs give HIV patients in Europe and US extra 10 years of life expectancy. The Daily Telegraph, May 11 2017

People with HIV living 10 years longer due to medical advances. The Independent, May 11 2017

HIV patients can expect a normal lifespan as drugs keep virus at bay. The Times, May 11 2017 (subscription required)

Links To Science

The Antiretroviral Therapy Cohort Collaboration. Survival of HIV-positive patients starting antiretroviral therapy between 1996 and 2013: a collaborative analysis of cohort studies. The Lancet - HIV. Published online May 10 2017

Ibuprofen linked to increased risk of heart attacks

"Taking painkillers for just one week 'raises the risk of a heart attack'," the Daily Mail reports. The report is based on a new analysis that found a link between anti-inflammatory painkillers like ibuprofen and heart attack risk.

Researchers looked at data from 446,763 people and found some evidence that all commonly-used non-steroidal anti-inflammatory drugs (NSAIDs) appear to increase the risk of heart attack, and that the risk rises in the first week of use. The study found the risk was highest with higher doses.

However, the study does leave some unanswered questions. Researchers only looked at effects among those prescribed the drugs and not those using over the counter, so they may not be representative of the general population.

And while the study tells us how likely people taking an NSAID are to have a heart attack, compared to people who hadn't used them in the past year, it doesn't give an indication of what the actual baseline risk of a heart attack is in these groups. And this risk varies from person to person.

It also can't prove NSAIDs were the direct cause of heart attack – it didn't take into account all possible influencing factors, such as smoking for example. Also, not all results reached statistical significance and so could have been the result of chance.

If you've been prescribed NSAIDs and are concerned about your heart attack risk, speak to your GP. When treating minor ailments with painkillers, always use the lowest effective dose for the shortest time possible.


Where did the story come from?

The study was carried out by researchers from McGill University and the Centre Hospitalier de l'Université de Montreal, both in Canada, Hospital District of Helsinki in Finland, and Leibniz Institute for Prevention Research and Epidemiology in Germany. It was funded by McGill University.

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

The study was widely covered in the UK media and the majority of the coverage was of a good quality. The Mail, The Daily Telegraph, Sky News, BBC News and The Mirror all carried balanced and accurate reports.

The headline in The Guardian – "Common painkillers may raise risk of heart attack by 100%" – is misleading because the 100% increased risk figure relates to high dose rofecoxib, which is far from being a common painkiller, having been unavailable for 13 years. Also, the 100% figure relates to the upper end of the estimated range of risk.

The Sun's headline – "Taking ibuprofen to treat pain 'for just ONE DAY increases your risk of heart attack by half'," – also overstates the risk, as the figure is for ibuprofen use between one and seven days, not one day only.


What kind of research was this?

This is a meta-analysis, using individual patient data taken from large observational studies. A meta-analysis is a good way to pool data from previous research, and using individual patient data helps balance risks and avoid bias. However, observational studies cannot prove cause and effect, because confounding factors other than the ones measured may be influencing the results.


What did the research involve?

Researchers looked for observational studies based on big patient databases that investigated non-steroidal anti-inflammatory drugs (NSAID) use and heart attack. The studies compared people who'd had a heart attack with those who had not, and used prescribing data to see whether they had been prescribed NSAIDs.

The researchers analysed this data, taking account of a wide range of potential confounding factors. They calculated the risk of having a heart attack after being prescribed each of the five NSAIDs, at different time periods, and different doses.

The methods used were robust and the results from the different studies were similar, which suggests the findings are likely to apply across populations with different baseline risks of heart attack. After excluding inappropriate studies, the researchers asked for access to individual patient data to carry out their analysis. Four studies refused access, leaving them with data from four other studies – two from Canada, one from Finland and one from the UK.


What were the basic results?

The study found mixed results. Recent and current use of any NSAID is linked to a raised risk of having a heart attack, compared to someone who has not used an NSAID in the past year. However, some of these results did not reach statistically significant thresholds – meaning it's possible that risk wasn't increased in these cases. That said, the figures were all in the same direction – tending towards showing an increase in risk.

The raised risk was generally increased with use in the previous year or month, starting in the first week of being prescribed the drugs in the study period. It seemed highest between eight to 30 days – i.e. the first month of taking the drug. Although the risk was still raised after a month, it tailed off. There was some variation in this trend though – some NSAIDs had a higher risk after 30 days and some a lower risk.

The increased risk of heart attack for any dose of NSAIDs in the first week of use, compared to no use in the past year, was:

  • Diclofenac – a 50% increased risk (odds ratio [OR] 1.50, 95% credible interval [CrI] 1.06 to 2.04) (credible intervals are similar to confidence intervals, but are generated by a specific kind of statistical analysis called Bayesian analysis)
  • Ibuprofen – a 48% increased risk (OR 1.48, 95% CrI 1.00 to 2.26]
  • Naproxen – a 53% increased risk (OR 1.53, 95% CrI 1.07 to 2.33)
  • Rofecoxib (a drug that has been withdrawn) – a 58% increased risk (OR 1.58, 95% CrI 1.07 to 2.17)

Higher doses (more than 1,200mg a day for ibuprofen, more than 750mg a day for naproxen and more than 25mg a day for rofecoxib) further increased the risk.

Previous studies had found a lower heart attack risk for naproxen than with other NSAIDs, but that was not apparent in this study.


How did the researchers interpret the results?

The researchers said their study was "the largest of its type," with "broadly generalizable" findings which showed "current use of all studied NSAIDs, including naproxen, was associated with an increased risk of acute myocardial infarction [heart attack]."

They add: "Given that the onset of risk … occurred in the first week and appeared greatest in the first month of treatment with higher doses, prescribers should consider weighing the risks and benefits of NSAIDs before instituting treatment, particularly for higher doses."



This study is a useful addition to our knowledge about the links between NSAIDs and heart attack risk. The study suggests all commonly-used NSAIDs are linked to a similarly-raised risk of heart attacks, that the risk generally rises with the dose, and that it is highest in the first month of treatment.

The researchers did a good job at taking account of potential confounding factors that could have affected the results. Even so, we don't know for sure that the NSAIDs were the direct cause of the problem. For example, if you are prescribed NSAIDs for a painful condition, and have a heart attack two weeks later, it's hard to know whether the cause was the NSAID or the condition itself. They were also not able to take into account some known risk factors for heart attacks such as smoking and body mass index (BMI).

The study doesn't tell us about our own individual risk of heart attack, which is important when thinking about how you might be affected by NSAIDs. If your risk of having a heart attack in the next 10 years is high – say 30% – then a 48% increased chance of heart attack takes it up to just under 45%.

But if you have a low risk of having a heart attack – say 1% – then a 48% increase only takes the risk up to 1.48%. An increase in risk may be statistically significant, but have little clinical significance.

The study findings back up current advice that doctors should consider people's heart attack risk before prescribing courses of NSAIDs, particularly at higher doses.

The research was carried out using data on prescription NSAIDs, so it didn't look specifically at occasional use of over the counter ibuprofen. However, as with all drugs it makes sense only to use them when you need them, and to take the lowest dose that works, for the shortest period of time that you need it.

If you often use painkillers, it may be a good idea to talk to your doctor to see whether there's an underlying problem that needs treating, or ask about alternatives to painkillers, such as physiotherapy.

Read more about treatment options for pain.

Links To The Headlines

Taking painkillers for just one week 'raises the risk of a heart attack': Strongest doses of five types of drug can increase chance by up to half. Daily Mail, May 10 2017

Common painkillers may raise risk of heart attack by 100% – study. The Guardian, May 9 2017

'Heart attack risk' for common painkillers. BBC News, May 10 2017

Common painkillers may increase risk of heart attack. Sky News, May 10 2017

One week of painkillers can increase chances of heart attack, new study finds. The Daily Telegraph, May 9 2017

Painkillers raise your risk of having a heart attack within one week. Daily Mirror, May 10 2017

Taking ibuprofen to treat pain ‘for just ONE DAY increases your risk of heart attack by half’. The Sun, May 10 2017

Links To Science

Bally M, Dendukuri N, Rich B, et al. Risk of acute myocardial infarction with NSAIDs in real world use: bayesian meta-analysis of individual patient data. BMJ. Published online May 9 2017

Review finds no link between dairy and heart attack or stroke risk

"Eating cheese does not raise risk of heart attack or stroke," reports The Guardian. This follows a large review pooling the results of 29 observational studies into the link between dairy consumption and cardiovascular disease; coronary heart disease, as well as all-cause deaths.

The studies included almost 1 million people from around the world and found no increased risk of the factors mentioned related to dairy consumption. They even found a very slightly lowered risk (2%) of cardiovascular disease and all-cause death from eating fermented dairy products such as cheese.

Dairy products are often high in saturated fat, something we should consume small quantities of, as it is linked to increased risk in health outcomes such as heart attacks and stroke. However, they are also high in calcium (which helps strengthen bones), a good source of protein and part of a balanced diet.

In April, the National Osteoporosis Society issued a warning that the perception of dairy products as unhealthy could lead to an increase in osteoporosis cases in the future.

The daily guideline amount of saturated fat is no more than 30g for the average man and 20g for the average woman. If you are concerned about consuming too much saturated fat, opt for low-fat versions of yoghurt, milk, cheese and other dairy products.

If you are vegan you will need to take steps to ensure you get enough calcium in your diet. Read more diet advice for vegans.


Where did the story come from?

The study was carried out by researchers from Reading University, UK, University of Copenhagen, Denmark and Wageningen University and Research Centre, The Netherlands.

The study was published in the peer-reviewed medical journal European Journal of Epidemiology and is openly available to access online.

The study was funded by an unrestricted grant from the Global Dairy Platform, Dairy Research Institute and Dairy Australia. However, the funders are reported to have had no role in the study design or any other study processes. The researchers declared receiving funding from various dairy and food companies as well as one author being a member of advisory boards for a number of large food companies.

The Guardian's reporting of the study was accurate, highlighting that dairy products are an important source of calcium, but are often high in saturated fat – something we should not be consuming too much of.


What kind of research was this?

This was a systematic review which aimed to identify and pool the results of cohort studies that have looked at the links between dairy consumption and health outcomes including cardiovascular disease, stroke and death.

A systematic review is a good way of summarising research in a particular area. Cohort studies are often the best available evidence when looking at whether something such as diet has an effect on long-term health outcomes. However, you can never rule out the possibility that other health and lifestyle factors (confounders) are influencing the results.

Randomised controlled trials, which are seen as the best way to assess evidence, are often hard to conduct: it may be difficult (and often unethical) to randomly assign enough people to dietary patterns and follow them for long enough to observe health outcomes.


What did the research involve?

The authors searched literature databases for prospective cohort studies published up to September 2016. Eligible studies had included a group of healthy adults (>18) and followed them over time to look at the amount of dairy they consumed and incidence of cardiovascular disease, coronary heart disease and death from all causes.

A total of 29 studies involving 783,989 participants were included. Participants had an average age of 57 years, an average BMI of 25.4, and were followed up over time between 5 and 25 years. The majority of studies (17) came from Europe with others from Asia, Australia, and the US.

Portion sizes were standardised and researchers looked at the link for each increasing increment per day:

  • 244g a day for milk
  • 50g a day for yoghurt
  • 20g a day for fermented dairy products (including cheese, yoghurt and soured milk products)
  • 10g a day for cheese
  • 200g a day for total, high-fat and low-fat dairy 

The researchers adjusted their analyses for the following confounding variables:

  • age
  • sex
  • smoking
  • alcohol intake
  • body mass index (BMI)
  • reported physical activity
  • food energy intake

They also took study quality into account.


What were the basic results?

There were a total of 93,158 deaths, 28,419 incidences of coronary heart disease and 25,416 incidences of cardiovascular disease.

Total dairy intake (either high-fat or low-fat), milk intake and yogurt intake were not associated with risk of all-cause death, coronary heart disease or cardiovascular disease.

Cheese (per 10g/day) was not linked with risk of death or coronary heart disease. There was the suggestion of a reduced risk of cardiovascular disease, but this was on the threshold of statistical significance so may just be a chance finding (relative risk [RR] 0.98, 95% confidence interval [CI] 0.95 to 1.00).

Total fermented dairy intake (per 20g/day) was associated with 2% lower risk of both death and cardiovascular risk in a link that just reached statistical significance (RR 0.98, 95% CI 0.97 to 0.99). However, in sensitivity analysis (an analysis of potential uncertainty), excluding a Swedish study of women's results for cheese, there was no longer a significant link.


How did the researchers interpret the results?

The researchers concluded that "this meta-analysis combining data from 29 prospective cohort studies showed there were no associations between total dairy, high- and low-fat dairy, milk and the health outcomes including all-cause mortality, coronary heart disease or cardiovascular disease. The modest inverse associations of total fermented dairy were found with all-cause mortality and cardiovascular disease, but not coronary heart disease. By examining different types of fermented food in relation to CVD, we found marginally inverse association with cheese but not yogurt."



This large meta-analysis of cohort studies demonstrated no increased risk to cardiovascular disease, coronary heart disease or all-cause death from eating dairy products.

The review has strengths in its large size and the fact it was able to analyse different types of dairy product, such as high and low-fat and everyday products such as cheese and yoghurt.

However, there are a number of factors to consider:

  • The results of a systematic review are only as good as the quality of the underlying studies. These are all observational studies and it's possible that unadjusted health and lifestyle factors are having an influence. Different studies adjusted for different variables; for example, some adjusted for overall diet, smoking and total energy intake, others did not.
  • Studies may also have differed in how accurately they measured analysed dairy intake and health outcomes. This may explain some variation in individual study results, and make it difficult to summarise these studies all together.
  • Overall there wasn't good evidence for any link between dairy and these health outcomes. The lowered risk of cheese fell short of statistical significance. The links between fermented products and all-cause death and cardiovascular disease were down to the results of one study. This shows the influence that one study, which may differ in methods from others, can have on the overall results.
  • There are other dairy products such as cream that are very high in fat but were not individually assessed and might have had a more negative effect on health.
  • Only three studies were from Asia, compared to 17 from Europe. The results might therefore be more generalisable to European populations than the rest of the world.

Dairy products such as cheese, milk and butter often contain high levels of saturated fat and salt, particularly the full-fat versions.

Consuming too much saturated fat or salt is known to be bad for us and can increase risk of health outcomes such as cardiovascular disease. However, dairy is also an important source of calcium and consuming it in moderation is part of a balanced diet.

Unless you choose not to eat dairy products as you are a vegan, or due to allergies or intolerances, there is no clinical need to cut an entire food group, like dairy, from your daily diet.

As Aristotle famously said, "everything in moderation". And this is usually a good rule to live by when it comes to healthy eating.

Read more advice about eating a balanced diet.

Links To The Headlines

Eating cheese does not raise risk of heart attack or stroke, study finds. The Guardian, May 8 2017

Links To Science

Guo J, Astrup A, Lovegrove JA, et al. Milk and dairy consumption and risk of cardiovascular diseases and all-cause mortality: dose–response meta-analysis of prospective cohort studies. European Journal of Epidemiology. Published online April 3 2017

Evidence behind reports of new baldness cure is a little thin

"Scientists studying cancer stumble on 'breakthrough' in search for baldness cure," announces The Daily Telegraph, adding that not only does this mean "a cream or ointment may soon cure baldness or stop hair turning grey" but also it could one day ... explain why we age".

Sadly for those of us with grey, or no, hair on top, these claims are arguably premature.

Researchers were actually conducting a study in mice looking into a rare genetic condition called neurofibromatosis, which causes tumours to grow along the nerves, when they discovered the role a protein called KROX20 plays in hair colour.

The KROX20 protein is produced in specific cells within each individual hair follicle. This in turn switches on production of another protein called SCF. This SCF protein is needed to support the mature pigment (colour) producing cells in the hair follicle, and if it is not produced the mice lose their hair colour and become white. If the mice lack the KROX20-producing cells completely, they cannot produce any new hair and become bald.

While the basic biology of cells in different mammals is very similar, researchers are likely to want to perform tests on human cells in the laboratory to confirm the findings apply to humans.

This advance does not automatically mean that researchers are "on the cusp" of curing baldness or grey hair. The research is at an early stage, and it is not yet known whether the loss of hair colour is reversible and, if so, how it might be reversed. 

Where did the story come from?

The study was carried out by researchers from the University of Texas and was funded through various grants from the National Institutes of Health.

The study was published in the peer-reviewed scientific journal Genes & Development.

While it's necessary to explain why a particular piece of research might be important, the predictions of what might happen as a result of this study are premature.

The University of Texas issued a press release about the study and it would appear that this formed the basis of the Telegraph's and the Daily Mail's coverage. Both describe the research in very similar terms to the wording in the press release.

It is the press release which suggests that "The research also could provide answers about why we age in general as hair graying and hair loss are among the first signs of aging".

It is certainly not possible to say at this stage whether these very specific hair-related processes are related more widely to ageing.


What kind of research was this?

This was animal research which has looked at the biology of hair greying and hair loss.

The researchers were actually investigating what seemed to be a completely different topic – neurofibromatosis – which causes benign tumours (neurofibromas) to develop in the covering (called the "sheath") of nerves.

However, they found that one strain of mice that they genetically engineered to study this condition actually developed grey fur early in life. Therefore they carried out more experiments to look at why this was, and what they could learn about hair greying.

This type of research is commonly used to get a very detailed understanding of the biological processes that go on in the body. When researchers have a better understanding of how such a process works it helps them to work out ways they might be able to stop them if required (for example if they normally lead to hair greying or loss) and help people when these processes go wrong.

However, results are very early stage and much more research is needed before any new treatments could be developed.


What did the research involve?

The researchers genetically engineered mice to stop producing a protein called SCF – Stem Cell Factor – in a specific group of cells which also produces a protein called KROX20. They found, to their surprise, that these mice lost all hair colour. This started when they were around 30 days old, and about nine months later the mice's hair was completely white.

The KROX20 protein was known to switch on certain genes during development, including those important in making the fatty coverings (sheaths) of nerves. It is also active in certain cells within the hair follicles. Once researchers discovered its effect on hair colour they did further experiments into what role these cells were playing in hair colouration.

For example, they looked at the levels of pigment (melanin) in the hair over time. They also investigated exactly what type of cells were producing KROX20, and where they were found in the hair follicle. The researchers also looked at what happened if they killed off the KROX20-producing cells at a key point in their hair production cycle.


What were the basic results?

The researchers found that the cells in the hair follicles which produced KROX20 would normally also produce SCF.

This SCF was found to be needed to maintain mature pigment-producing cells (melanocytes) in the hair follicle.

If the KROX20-producing cells did not also produce SCF, the mice's follicles lost mature melanocytes, and their coats lost their colour because no new pigment (melanin) was being deposited into the hair as it grew. This process started early on in the mice's lives – by the time these mice were 11 days old the amount of melanin in the hair was starting to decrease.

The researchers found that the KROX20-producing cells were developing from the same line of cells that produced keratinocytes – a type of cell commonly found in the outer layer of skin (epidermis).

These cells were found initially in only a restricted area of the hair follicle, but gradually they increased in numbers and also spread to other areas in the hair follicle. This included contributing to the formation of the hair shaft.

The researchers also found that if they killed off the KROX20-producing cells in the hair follicle, then the mice grew no new hair.


How did the researchers interpret the results?

The researchers concluded that they had identified a group of "progenitor [cell]s which regulate hair growth and pigmentation", in part by helping maintain pigment-producing cells (melanocytes).



The current study identified a group of cells in the hair follicles of mice which are important both in forming the hair shaft to allow hair growth, and also in maintaining hair colour.

So far this research has been in mice, but the basic biology of cells in mammals is very similar, so it seems likely that the findings would also apply to humans. Researchers are also likely to want to perform tests on human cells in the laboratory to confirm their findings.

The findings represent an advance in what is known about how hair grows and maintains its colour. However, this doesn't automatically mean the researchers are "on the cusp of developing a cream or ointment to cure baldness or stop hair turning grey" as suggested in the Mail.

The research is at an early stage, and the researchers themselves note that they still need to carry out studies to look at whether the loss of hair colour is reversible. Carrying out research takes time, and not every advance in understanding results in successful treatments.

Read more advice about hair loss and possible treatment options.

Links To The Headlines

Scientists studying cancer stumble on 'breakthrough' in search for baldness cure. The Daily Telegraph, May 7 2017

Skin cell discovery could spell cure for baldness and grey hair: Breakthrough found by accident could lead to cream to treat both. Daily Mail, May 8 2017

Baldness breakthrough as scientists finally identify cells which cause hair loss. Metro, May 8 2017

Links To Science

Liao C, Booker RC, Morrison SJ, Le L. Identification of hair shaft progenitors that create a niche for hair pigmentation. Genes and Development. Published online May 2 2017

Concerns about alleged 'harmful' arsenic levels in baby rice cakes

"Almost half of baby rice food products contain illegal levels of inorganic arsenic despite new regulations set by the EU, according to researchers," ITV News reports.

While this may sound shocking, arsenic is a common chemical compound naturally present in the environment.

It's found at very low levels in tap water in this country, but is present in foods that come from places where water contamination is higher.

At low levels, it causes no problems. The concern is whether levels could be high enough to cause health problems and, in the case of babies, developmental issues.

This study included 11 babies from Belfast who had their urinary arsenic levels measured pre- and post-weaning. Arsenic levels were higher post-weaning than pre-weaning, when most babies were eating some baby rice products.

Researchers also sampled baby rice products bought in February 2016, and found arsenic levels exceeded the maximum limit.

However, it was only in January 2016 that the European Commission introduced regulations on the amount of arsenic that should be present in rice.

As a spokesperson for the British Specialist Nutrition Association Limited, the trade group that represents rice cake makers, pointed out: "Research … was carried out using products bought in February 2016. This was one month after the application of the legislative requirements. It is likely that all samples were manufactured before the legislation came into force."

This research involved a very small sample from just one region. And there was no comparison group from elsewhere in the UK.

This means we can't conclude with any certainty that the measured arsenic levels can be directly attributed to rice, or that these levels would have any adverse developmental effects. Further testing of rice products could be useful.

Where did the story come from?

The study was carried out by researchers from Queen's University and Royal Victoria Hospital in Belfast, and Dartmouth College in the US.

Funding was provided by a Marie Curie Intra-European Fellowship within the 7th European Community Framework Programme, and the Metabolic Research Unit at the Belfast Health and Social Care Trust.

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

While some of the headlines could be seen as alarmist, the general tone of the UK's media coverage was generally fair and balanced.

The Guardian is of one of many sources that provided helpful quotes from independent experts, including a spokesperson from the Food Standards Agency, who said:

"We recommend that consumers eat a balanced, varied and healthy diet. Rice and rice products can be part of that, including for young children.

"However, we do advise that toddlers and young children – ages 1-4.5 – should not be given rice drinks as a substitute for breast milk, infant formula or cow's milk.

"This is because of their proportionally higher milk consumption and lower body weight compared to other consumers." 

What kind of research was this?

This small cohort study aimed to assess arsenic metabolites in the urine of babies before and after weaning.

The researchers also analysed the levels of arsenic in rice cakes and other baby foods used in infant weaning to look at the association.

The researchers explain how early-life exposure to inorganic arsenic is of concern because it could impact health and development.

Arsenic in this country is found at low levels in water, so most exposure comes through dietary sources.

Infants and young children may be at greater risk of arsenic exposure because of their higher food consumption per unit of body weight.

Rice and rice-based products have been reported to contain higher levels of arsenic relative to other foods, and are commonly used in weaning.

In January 2016, the European Commission set a maximum level of inorganic arsenic in rice of 0.1mg per kg. But there's limited information on the impact of this regulation.

This study aimed to look at levels in baby rice, rice cakes and rice cereals compared with this standard, and look at child's levels before and after weaning. 

What did the research involve?

This cohort was set up to look at nutrition during pregnancy and then the first few months after birth.

Researchers recruited mothers who were Caucasian non-smokers with a healthy nutritional status from a hospital in Belfast.

Most (70%) were said to be of high socioeconomic status. Their babies included 41 girls and 38 boys born in 2015.

Infants were grouped into their feeding mode before weaning: breastfed (20), formula fed (32) and mixed feeding (27). Pre-weaning urine samples were collected at an average age of 3.4 months.

A small subsample of 11 infants (born September/October 2015) had post-weaning samples taken at an average age of 7.7 months.

An interview with their mothers at that time confirmed that all but one were eating rice-based products as part of their diet.

The researchers measured the arsenic levels in 13 samples of baby rice, 29 of rice crackers/cakes, and 31 samples of rice cereal from nine different manufacturers obtained from 17 shops in the Belfast area in February 2016.

What were the basic results?

The researchers reported levels of two arsenic metabolites (substances created when the metabolism breaks down compounds like arsenic): monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA).

They found that before weaning, infants who were exclusively formula fed had higher urine levels of MMA, DMA and total arsenic than those who were exclusively or partially breastfed.

For example, compared with breastfed infants, formula fed babies had 6.7 times higher levels of MMA, and around double the level of DMA and total arsenic.

Post-weaning urine samples contained higher levels of these metabolites than pre-weaning samples. Urine concentrations were about 7.2 times higher for MMA, 9.1 for DMA, and 4.8 times higher for total arsenic.

Around three-quarters of the baby rice and rice crackers (specifically marketed for babies) analysed exceeded the maximum set arsenic level of 0.1mg per kg, with an average concentration 0.117mg per kg (range 0.055 to 0.177). 

How did the researchers interpret the results?

The researchers concluded that, "Efforts should be made to provide low inorganic arsenic rice and rice-based products consumed by infants and young children that do not exceed the maximum level to protect this vulnerable subpopulation." 


Arsenic is found in the earth's crust and is naturally present in the environment. Certain countries – including India, China and Bangladesh – are known to have higher levels of arsenic in ground water than others.

Water supplies in the UK are low in arsenic, but we may be exposed to arsenic through foods – such as rice and other crops – that have been exposed to contaminated water.

This study shows that babies tend to have higher levels of arsenic metabolites in their urine when exposed to food – including formula milk and rice – and that rice contains higher than recommended levels.

These are important findings, but there are a few points to put this in context:

  • This research used a small sample of infants (particularly the post-weaning sample of 11) and they're all from one region of Belfast with a very specific sociodemographic background (e.g. non-smoking white mothers of high occupational status). These levels may be representative of babies across the country, but we have none for comparison and don't know that for sure.
  • Though nearly all of the 11 babies were given rice products, we can't conclude with certainty that this food was the direct cause of the higher levels.
  • Continued exposure to high levels of inorganic arsenic is known to have toxic effects, possibly increasing the risk of cancer and affecting development. However, this study doesn't give evidence that the arsenic levels in urine observed here would be toxic to the child and could affect their future health. Again, there's no other group for comparison. Many healthy adults today could have had similar (or higher) levels of arsenic metabolites in their urine had they been tested as a baby.

These findings are, nevertheless, important. Europe set a limit on the amount of arsenic that should be present in rice products in January 2016.

Most products tested here exceeded this level, but they were bought in February 2016. It's possible this sampling may have been too close to when the legislation changed, and samples collected now may be different.

Links To The Headlines

Illegal arsenic levels in baby rice food products. ITV News, May 4 2017

Dangerous levels of arsenic found in rice cakes for babies. The Guardian, May 4 2017

Illegal levels of arsenic in 75% of children's baby rice products. Sky News, May 4 2017

Dangerous levels of arsenic found in baby food could stunt growth. The Daily Telegraph, May 4 2017

Dangerously high levels of ARSENIC found in '75% of baby rice sold in UK's major supermarkets'. The Sun, May 4 2017

Unsafe levels of toxic arsenic found in 73% of baby rice snacks – risking the growth, IQ and immune system of infants, finds alarming study. Mail Online, May 5 2017

Links To Science

Signes-Pastor AJ, Woodside JV, McMullan P, et al. Levels of infants' urinary arsenic metabolites related to formula feeding and weaning with rice products exceeding the EU inorganic arsenic standard. PLOS One. Published online May 4 2017

Blood test may lead to targeted therapy for prostate cancer

"A blood test has been developed that could help target treatment for men with advanced prostate cancer," BBC News reports. The test could help identify men unlikely to respond to drugs such as enzalutamide.

Enzalutamide and abiraterone are additional treatments for men for whom standard hormonal treatment has not worked, or has stopped working.

Treatment success varies; some men get little benefit, while others have responses that last many years. The new test – if confirmed – could help doctors know in advance who is likely to benefit.

The blood test looks for extra copies of androgen (male hormone) receptor genes. The drugs block signalling from this gene. Researchers found that men with multiple copies of the gene did worse after treatment with either drug. They did not live as long and were more likely to see their disease return and worsen. The researchers say that if these men can be identified in advance, they could be spared these drugs and offered more suitable treatment.

Making sure a treatment actually has a benefit is important as, aside from wasting NHS money, advanced prostate cancer is almost always fatal. So it would be a much bigger waste if the last few years of a man's live was spent trying out a treatment option unlikely to work, while others such as radiotherapy, could help.

We now need further research to tell us whether selecting patients by this gene test improves treatment results.


Where did the story come from?

The study was carried out by researchers from 24 hospitals or universities in Spain, Italy, the UK and the US, and was funded by Prostate Cancer UK and Cancer Research UK. The study was published in the peer-reviewed journal Annals of Oncology on an open-access basis so it is free to read online.

The study was covered by The Times, ITV News and BBC News. All presented balanced, accurate reports of the results, but didn't mention that further work is needed to find out whether selecting patients based on the test works.


What kind of research was this?

This was an observational study, involving analysis of blood samples from three clinical studies of enzalutamide and abiratone, intended to look for biomarkers such as gene signatures. The research was designed to investigate the importance of certain mutations and numbers of copies of the androgen receptor genes to better understand which treatments will work in men with prostate cancer that hasn't responded to commonly used hormone treatments, such as leuprorelin (Prostap).

This type of study is useful to identify potential tests, but it isn't proof that the test will work to guide treatment and improve patient outcomes. We need clinical trials of the tests to show they work.


What did the research involve?

Researchers looked at the genetic status of men in three trials – two trials of enzalutamide and abiratone in the UK and Italy, with 171 men in total, and one trial of enzalutamide in Spain, with 94 men.

Blood samples taken before treatment and soon after were compared, using two different methods. Researchers classified the men into groups – androgen receptor (AR) gain for those with multiple copies of the AR gene over a certain level, and no AR gain for those under the cut-off point. They then looked to see how the men did after treatment, and compared results for men with AR gain with results for men without AF gain.

All men in the study had previously been treated to reduce their testosterone levels as far as possible (either by hormone drugs or surgery), which is the usual first treatment for prostate cancer. Some had also been treated with chemotherapy. To monitor disease progression and give some idea about men's response to treatment, the men also underwent regular prostate specific antigen (PSA) tests (which tests for a hormone associated with prostate enlargement), computed tomography (CT) scans and bone scans.

The blood samples were analysed by the standard method of DNA sequencing, and by a much simpler, cheaper droplet digital PCR (ddPCR) test, and the results of the two tests compared. The researchers hoped the ddPCR would work as well as sequencing to identify men's AR status, as this test can then be widely used.


What were the basic results?

The ddPCR test performed well against DNA sequencing, meaning it should be a reliable way of finding out men's AR gain status.

In the first two studies:

  • 14% of men who hadn't had chemotherapy and 34% who'd had chemotherapy (with docetaxel) were found to have multiple copies of the AR gene (AR gain).
  • These men were about four times less likely to survive until the end of the trial (hazard ratio [HR] 3.98, 95% confidence interval [CI] 1.74 to 9.10] for pre-chemotherapy patients; HR 3.81, 95% CI 2.28 to 6.37 for post-chemotherapy).
  • Men who had AR gain lived on average nine and a half months after starting treatment, if they'd previously had chemotherapy, compared to 21.8 months for men without AR gain. The researchers were not able to give the equivalent figures for men who'd not had chemotherapy, as the trial was not long enough to establish this. 

In the third study:

  • 12% of men had AR gain (none in this study had previously had chemotherapy).
  • Men with AR gain were 11 times less likely to survive until the end of the trial (HR 11.08, 95% CI 2.16 to 56.95).
  • On average, men with AR gain saw their cancer progress (measured by PSA test) after just 3.6 months, compared to 15.5 months for those without AR.


How did the researchers interpret the results?

The researchers say they have designed a "robust assay [test]" which "is affordable and can be widely implemented in clinical laboratories". However, they say further research is needed before the test can be put into widespread use.

Before changing clinical practice to select patients using the test, they say, "our findings require confirmation in prospective trials where plasma AR CN [copy number] defines treatment selection."



Genetic testing is becoming more common in cancer treatment as a way of tailoring treatment to the individual cancer. It's already used in breast cancer, for example. This test could help identify which men that have not responded to hormone treatment are most likely to benefit from two of the newer prostate cancer drugs.

It is good news, because men could then be spared treatment that is unlikely to help them, and directed towards more suitable treatment options. Also, both of these newer drugs are very expensive, so a suitable test could save the NHS a great deal of money.

Meanwhile, those men who are likely to benefit will take the drug knowing it's likely to help.

However, we're some way off being able to use the test in practice. This research shows that, among a group of 265 men, those with multiple copies of the androgen receptor gene did worse after treatment than those without. That doesn't prove that selecting patients for treatment based on AR gene status will improve outcomes.

We need to see studies that select patients for treatment based on their test results, and follow them up to see how they do, to be sure the test is truly helpful.

Links To The Headlines

Prostate cancer: Blood test could help target treatment. BBC News, May 4 2017

Blood test could help prostate cancer treatment. ITV News, May 4 2017

£50 blood test boosts chances of surviving prostate cancer. The Times, May 4 2017 (subscription required)

Links To Science

Conteducia V, Wetterskog D, Sharabiani MTA, et al. Androgen receptor gene status in plasma DNA associates with worse outcome on enzalutamide or abiraterone for castration-resistant prostate cancer: a multi-institution correlative biomarker study. Annals of Oncology. Published online May 3 2017

Low-gluten diet linked to heart attack risk

"Gluten-free diet can do more harm than good for people without coeliac disease," The Independent reports, as a new study found that the "trendy gluten-free diets loved by Gwyneth Paltrow and Russell Crowe may increase the risk of heart disease".

Gluten is a protein found in grains such as wheat, barley and rye. In people with coeliac disease, it damages the intestines and triggers digestive symptoms such as diarrhoea, meaning they need to follow a gluten-free diet.

Recently there has been increasing interest in the possible health benefits of avoiding gluten among people who do not have coeliac disease, though the long term evidence about its effects in this group is currently limited. Despite this, the gluten-free food market is reported to have made $3.5bn worth of global sales in 2016.

The current study followed more than 100,000 people from 1986 to 2012, assessing their diets and whether they had heart attacks during that time. These people did not have heart disease at the start of the study, and importantly did not have coeliac disease.

Overall, it found that once other risk factors were taken into account, people's consumption of gluten was not related to their risk of heart attack. However, further analyses suggested that lower consumption of gluten specifically from whole grains (wheat, barley and rye) was associated with increased heart attack risk compared to higher consumption from these sources.

Ideally these findings would be confirmed by other studies, but this research will take time. In the meantime, if you don't need to avoid gluten for medical reasons, this study suggests it may be beneficial to continue including whole grains in your diet for their cardiovascular benefits.


Where did the story come from?

The study was carried out by researchers from Columbia University in New York, and Massachusetts General Hospital, Harvard Medical School, Brigham and Women's Hospital, and the Harvard T. H. Chan School of Public Health in Boston. The authors were funded by grants from the American Gastroenterological Association, Massachusetts General Hospital and the National Institutes of Health.

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

The UK media provided reasonable coverage of the study. As you would expect, most of the otherwise academic reporting was given a touch of glamour by listing celebrities associated with gluten-free dieting.


What kind of research was this?

This was a prospective cohort study looking at whether how much gluten a person eats is linked to their risk of developing heart disease over a long period of time.

Gluten is a protein found in wheat, rye, and barley. It causes inflammation and damage to the intestines in people with coeliac disease. People with coeliac disease have an increased risk of heart disease, but eating a gluten-free diet helps to reduce this risk, as well as symptoms.

Eating a gluten free diet has become increasingly popular among people who do not have coeliac disease as a result of concerns that gluten may cause various digestive and other health problems. However, the impact a low gluten diet may have on risk of heart disease in people who do not have coeliac disease has not been studied in long term prospective studies. This is what the current study wanted to assess.

While a randomised controlled trial is generally the best way to test whether a particular factor causes a specific outcome, it would not be feasible to randomly allocate thousands of people to eat gluten or not for a long period of time. Therefore, a large cohort study such as this is the best way to look at this question.

The main challenge with this study type is to try and single out the effect of gluten as opposed to any other factor. Researchers do this by using statistical techniques to try and "remove" the impact of these other factors (known as confounders).


What did the research involve?

The researchers analysed data from two very large cohort studies in the US called the Nurses' Health Study and the Health Professionals Follow-up Study.

The 110,017 participants without coeliac disease who did not have heart disease in 1986 filled out detailed questionnaires about their diet at the start of the study and every four years after that, up to 2010. The researchers followed them up to see who developed heart disease over this period, and whether different levels of gluten consumption affected the likelihood of developing the condition.

The standard diet questionnaire included more than 130 questions about how often a person consumed specified portions of certain foods and drinks. The researchers used the participants' responses to estimate how much gluten they were consuming on average over the study period using a database of nutritional contents of the foods and drinks.

They included gluten from wheat, rye and barley, but did not include the small amounts of gluten which are present in oats or condiments such as soy sauce as they felt these would be negligible. People were then split into five groups with increasing levels of gluten consumption for comparison.

Because people might change their diet as a result of illness, for people who developed diabetes, cancer, or certain heart disease events such as stroke or had surgery to treat heart disease, the researchers only considered their diet before they developed these conditions.

Participants filled out questionnaires about their health every two years, and if they reported having a heart attack their medical records were checked.

Deaths from heart attack were identified from state and national records, or reports from next of kin. Medical and post-mortem records and death certificates were also checked for these individuals. If these record checks confirmed the reported diagnosis, these people were considered as having developed heart disease.

The researchers analysed whether participants who consumed more gluten were any more or less likely to develop heart disease. They took into account many potential confounders that could be related to heart disease risk, including:

  • age
  • race
  • body mass index
  • history of diabetes, high blood pressure or high cholesterol
  • regular use of aspirin and non-steroidal anti-inflammatory drugs
  • current use of statins
  • current use of a multivitamin
  • smoking history
  • physical activity
  • parental history of heart attack
  • menopausal status and menopausal hormone use
  • other dietary factors such as alcohol, red and processed meats, polyunsaturated and trans fats, and fruit and vegetables

In addition, the researchers also looked at what happened if they took into account consumption of whole and refined grains, as these contain gluten, and have been linked to level of heart disease risk.


What were the basic results?

The mean daily intake of gluten at the start of the study was:

  • 7.5g among women and 10.0g among men in the highest consumption group
  • 2.6g among women and 3.3g among men in the lowest consumption group

People with higher gluten intake tended to have:

  • lower alcohol intake
  • smoke less
  • consume less fat overall
  • eat less unprocessed red meat
  • consume more whole grains and refined grains

During the study 6,529 participants (5.9%) experienced a heart attack.

Before taking into account potential confounders, heart attacks were more common in the group with the lowest gluten consumption than in those with the highest consumption.

However, after taking into account known risk factors for heart disease, the difference between the groups was not statistically significant.

When the researchers looked at the impact of consumption of gluten from just refined grains they also found the difference between groups was not statistically significant.

But when they considered the impact of consumption of gluten in whole grains – they found those with highest gluten consumption were 15% less likely to develop heart attacks over follow up (hazard ratio 0.85, 95% confidence interval 0.77 to 0.93).


How did the researchers interpret the results?

The researchers concluded that differences in long term dietary intake of gluten were not associated with risk of heart disease. However, their results suggested that avoiding gluten may reduce consumption of whole grains, and this may lead to increased risk of heart disease.

They recommended that "promotion of gluten-free diets among people without [coeliac] disease should not be encouraged".



This study has found that while overall gluten consumption in people without coeliac disease may not be related to heart disease risk, avoiding whole grains (wheat, barley and rye) in order to avoid gluten may be associated with increased heart disease risk.

This study has several strengths, including its large size, the fact that data was collected prospectively and diet assessed at several time-points, the long period of follow up, and that it took into account a wide range of potential confounders.

As with all studies of this type, it is possible that other factors may affect the results. However, the researchers took into account as many potential confounding factors as they could in their analyses. This increases confidence in the results, but it is still possible that these or other unmeasured confounding factors are having an effect.

The researchers noted that they did not specifically ask participants whether they were intentionally following a "gluten free" diet or consumption of gluten-free substitute foods.

It is important to emphasise that this study was only in people who did not have coeliac disease. People with coeliac disease need to eat a gluten free diet to control their symptoms, and it is thought that this diet may actually contribute to the reduction in risk of heart disease seen after diagnosis in this group. So people eating a gluten free diet for this purpose should not be concerned by the findings in this study.

The study collected data from 1986 to 2012. Diets over this period have changed, and avoidance of gluten is likely to be more common nowadays. It would be interesting to repeat the study now to see if the same results are found. While it would be good to have these findings confirmed by other studies, carrying out similarly large scale and long term research will take time.

Ideally, if you don't need to avoid gluten for medical reasons, then this study suggests it may be beneficial to continue including whole grains in your diet for their cardiovascular benefits.

Find out more about common digestive problems, such as bloating and heartburn, and how to treat them.

Links To The Headlines

Gluten-free diet can do more harm than good for people without coeliac disease, scientists say. The Independent, May 3 2017

Eating a gluten free diet when you're not coeliac could damage your health. Daily Mirror, May 3 2017

Sorry, Gwynnie, gluten-free is not so great: People who avoid grains increase the risk of developing heart disease. Daily Mail, May 3 2017

Gluten-free diet should not be eaten by people who are not coeliac, say scientists. The Daily Telegraph, May 2 2017

Gluten-free diet could raise heart attack risk. The Times, May 3 2017 (subscription required)

Links To Science

Lebwohl B, Cao Y, Zong G, et al. Long term gluten consumption in adults without celiac disease and risk of coronary heart disease: prospective cohort study. BMJ. Published online May 2 2017

Statins side effects 'have been overstated,' says study

"Side effects from statins 'really are all in the mind'," The Times reports. A new study found people taking statins were more likely to report side effects, such as muscle aches, but only if they knew they were taking the drug.

The researchers said this demonstrates the so-called "nocebo effect", the opposite of the placebo effect, where people experience side effects only because they expect to get them.

This is a puzzling but well-established phenomenon. It's common for people to drop out of clinical trials complaining about side effects even though they were only given a placebo, such as a sugar pill.

In this study, researchers analysed data from two phases of a statin trial carried out between 1998 and 2005. They found people taking the statin atorvastatin were more likely to say they had muscle aches if they knew they were taking the drug.

Researchers say reports of side effects from observational studies – where people know they're taking statins – overstate how common the problem is.

They claim this puts many people off taking the cholesterol-lowering drugs, which could result in "thousands" of heart attacks and strokes.

Muscle pain is common, especially in older adults, so it's unsurprising that many older adults who take statins have muscle pain. That doesn't mean statins caused the problem.

If you've been prescribed a statin and are worried about side effects, talk to your GP. Don't stop taking it without getting medical advice first.

Where did the story come from?

The study was carried out by researchers from Imperial College London, Royal London Hospital, the London School of Hygiene and Tropical Medicine, the University of Gothenburg, and the University of Oxford.

It was funded by the pharmaceutical companies Pfizer, Servier Research Group, and Leo Laboratories. 

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

Five of the eight study authors report potential conflicts of interest, including payments from pharmaceutical companies, many of which manufacture statins.

In the main, the UK media mostly reported the study accurately, although uncritically, giving widespread coverage to comments made by the lead researcher calling for side effect warnings to be dropped from the drugs' labelling.

Although the researcher said this wasn't a case of "people making up symptoms, or the symptoms being all in their heads", The Times ran the headline: "Side effects from statins 'really are all in the mind'."  

What kind of research was this?

This was a two-part study. The first part was a double-blind randomised controlled trial (RCT), which is usually the best way to see the effects of a treatment. The trial was called the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT).

However, trials can't always give the best evidence on adverse effects as these can be rare – they sometimes don't have large enough samples or sufficient follow-up to pick them all up. This is why observational evidence is often used.

Because of the success of the trial in reducing heart attacks and strokes, the researchers were told to stop it early so everyone could be offered atorvastatin.

They continued the study as an open-label non-randomised extension, where people were told whether they'd been taking atorvastatin or placebo, and given the option to continue or start taking atorvastatin.

It's fairly unusual to have a trial that includes both a randomised and non-randomised phase, so the researchers wanted to see whether there was a difference in side effect rates reported in the two phases.

What did the research involve?

The ASCOT trial began in the late 1990s. More than 100,000 people (95% white, 81% men) were recruited to take part in an RCT comparing atorvastatin with placebo.

After about three years, the early results showed people taking atorvastatin were less likely to have heart attacks or strokes.

The researchers were then told to stop the randomised part of the study and offer everyone the chance to take atorvastatin, as denying at-risk people an intervention known to be effective in reducing heart attacks or stroke would have been unethical.

They continued to follow people up for another two to three years. In this analysis, the researchers looked at rates of side effects between the two phases of the trial to see if there was a difference.

People weren't asked specifically about muscle aches or three other possible side effects studied: sleep disturbance, erection difficulties, and cognitive difficulty.

Instead, researchers asked about any unwanted effects people noticed since taking the treatment six weeks after entering the trial, then after three months, and then every six months until the study finished.

In this new analysis, researchers compared the rates of the four adverse effects of interest in the RCT, and in the open label follow-up, to see if they differed.

What were the basic results?

During the double-blinded RCT, rates of reported adverse effects were similar or lower among those taking atorvastatin, compared with placebo:

  • muscle pain – reported by 2.03% taking atorvastatin, 2% taking placebo (hazard ratio [HR] 1.03, 95% confidence interval [CI] 0.88 to 1.21)
  • erection problems – reported by 1.86% a year taking atorvastatin, 2.14% a year taking placebo (HR 0.88, 95% CI 0.75 to 1.04)
  • sleep disturbance – reported by 1% taking atorvastatin, 1.46% a year taking placebo (HR 0.69, 95% CI 0.56 to 0.85)

There were too few cases of cognitive problems to do a proper analysis.

During the RCT, half the participants took atorvastatin and half took a placebo. In the extended open label phase, 65% of people chose to take atorvastatin at some point, while 35% never took it.

Those who reported muscle pain in the RCT phase were less likely to opt for atorvastatin in the open label phase.

People who took atorvastatin in this open label phase were more likely to report adverse muscle pains:

  • muscle pain – reported by 1.26% a year taking atorvastatin, 1% a year not taking them (HR 1.41, 95% CI 1.10 to 1.79)

There were no significant differences for the other adverse effects.

How did the researchers interpret the results?

The researchers say their results are "consistent with a nocebo effect, whereby subjective adverse effects (e.g. symptoms reported by patients) can be more likely to be attributed to a treatment thought to cause some particular side effect".

In other words, people are more likely to think a problem like muscle pain is the result of a drug when they know they're taking a drug that's been associated with muscle pain.

The researchers go on to say "widespread media claims" about the adverse effects of statins have led to many people stopping taking them, or not starting them at all.

They say this has "been estimated to result in thousands of fatal and disabling heart attacks and strokes, which would otherwise have been avoided".


This is a complex study that provides a plausible explanation for the difference in reports of adverse effects of statins in RCTs and observational studies, some of which have suggested as many as 1 in 5 people get side effects from statins.

However, we need to be aware of some limitations and unanswered questions:

  • When people knew they were taking statins, they were more likely to report muscle pain than those not taking statins. But they were less likely to report muscle pain than in the first phase of the study, when they didn't know whether they were taking statins or placebo. We don't know why this is.
  • Almost everyone in the study was white European (95%) and male (81%). We don't know if the results hold true for people in other ethnic groups or women.
  • Because people weren't prompted to report concerns about specific adverse events or side effects, it's possible these may have been underestimated. Also, the study only looked at one statin, and at a dose lower than those often used today.

The unanswered questions mean there may be other explanations for the differences in reporting of adverse effects, other than the "nocebo" effect.

NHS guidelines say doctors should consider offering statins to people who have had a prior heart attack or stroke, or to people with a 10% or higher risk of having a heart attack or stroke in the next 10 years.

Statins need to be used with caution in people with a history of liver disease. There's also a very rare risk of a muscle toxicity causing weakness and breakdown of the muscles (rhabdomyolysis), which can cause serious complications.

For this reason people are asked to be aware of muscle symptoms. However, the chances muscle aches or pains are caused directly by statins is very small.  

If you're unsure about the side effects of any of the medicines you're taking, discuss your concerns with your GP first. Don't stop taking medicines without first discussing the decision with a doctor.

Other ways you can lower your cholesterol include sticking to a healthy diet low in saturated fats and high in fibre, and taking regular exercise.  

Links To The Headlines

Statin side-effects only felt by those who believe in them – study. The Guardian, May 2 2017

Tens of thousands die as they're 'too scared to take statins': Experts say side-effects are being overstated. Daily Mail, May 3 2017

Statins myth: thousands are dying because of warnings over non-existent side effects. The Daily Telegraph, May 3 2017

Thousands 'dying from heart attacks and strokes after being scared away from statins'. ITV News, May 3 2017

Side-effects from statins 'really are all in the mind'. The Times, May 3 2017 (subscription required)

Links To Science

Gupta A, Thompson D, Whitehouse A, et al. Adverse events associated with unblinded, but not with blinded, statin therapy in the Anglo-Scandinavian Cardiac Outcomes Trial—Lipid-Lowering Arm (ASCOT-LLA): a randomised double-blind placebo-controlled trial and its non-randomised non-blind extension phase. The Lancet. Published online May 2 2017