NHS Choices

Can exercise offset some of the harms of regular drinking?

NHS Choices - Behind the Headlines -

"Adults who booze regularly but exercise for five hours a week are no more likely to die than teetotallers," the Mail Online reports.

A study suggests exercise may compensate for some, but certainly not all, of the harms associated with excessive alcohol consumption. This latest study looked at deaths from cancer and cardiovascular disease, as well as premature death in general (usually judged to be dying before the age of 75).

Researchers looked at around 10 years' worth of national survey data from UK adults aged over 40. Unsurprisingly, they found links between all-cause and cancer mortality in inactive people. But they also found increasing levels of physical activity generally removed the association with drinking habits. In fact, occasional drinking was associated with a significant reduction in all-cause mortality for the most active of people.

Although the study had strengths in its large sample size and regular follow-up, we can't be sure that any links observed were solely down to the interaction between alcohol and exercise. For example, people who are physically active may also avoid smoking and consume healthy diets. It is difficult to completely control for such influences when analysing data like this.

While regular exercise may mitigate against some of the harms associated with excessive alcohol consumption it certainly won't make you immune. Many world-class sportspeople, such as George Best and Paul Gascoigne, have had both their careers and lives blighted by drinking.


Where did the story come from?

The UK-based study was carried out by an international collaboration of researchers from Canada, Australia, Norway and the UK. The health surveys on which the study was based were commissioned by the Department of Health, UK. Individual study authors also reported receiving funding from the National Health and Medical Research Council and University of Sydney. 

The study was published in the peer-reviewed British Journal of Sports Medicine. 

The media coverage around this topic was generally overly optimistic, highlighting that by exercising, individuals can completely undo the harm caused by excessive alcohol consumption, which is untrue.

In particular, the Mail Online claimed "Adults who booze regularly but exercise for five hours a week are no more likely to die than teetotallers" which could send out the wrong message to the public.


What kind of research was this?

This cohort study analysed data from British population-based surveys: Health Survey for England (HSE) and the Scottish Health Survey (SHS) to investigate whether physical activity is able to moderate the risk between alcohol consumption and mortality from cancer and cardiovascular diseases.

Cohort studies like this are useful for assessing suspected links between an exposure and outcome. However, there are potentially other factors that have a role to play in such associations and therefore the study design doesn't allow for confirmation of cause and effect.


What did the research involve?

The researchers collected data on 36,370 men and women aged 40 or above from Health Survey for England (1994; 1998; 1999; 2003; 2004; and 2006) and the Scottish Health Survey (1998 and 2003). Among other things, the participants were asked about their current alcohol consumption and physical activity.

Alcohol intake was defined by six categories (UK units/week):

  • never drink (lifetime abstainers)
  • ex-drinkers
  • occasional drinkers (haven't drank anything in past seven days)
  • within (previous) guidelines: <14 units (women) and <21 units (men)
  • hazardous: 14-15 units (women) and 21-19 units (men)
  • harmful: >35 (women) and >49 (men)

Frequency and type of physical activity in the past four weeks was questioned and converted into metabolic equivalent task-hour (MET-hours, which are an estimate of metabolic activity) per week according to national recommendations:

  • inactive (≤7 MET-hours)
  • lower level of active (>7.5 MET-hours)
  • higher level of active (>15 MET-hours)

The surveys were linked to the NHS Central Register for mortality data and the participants were followed up until 2009 (HSE) and 2011 (SHS). There were 5,735 recorded deaths; deaths from cancer and cardiovascular disease were of most interest for this study.

The data was analysed for associations between alcohol consumption and the risk of death from all-causes, cancer and cardiovascular disease. The results were then analysed according to levels of physical activity.

Potential confounders (such as sex, body mass index and smoking status) were controlled for.


What were the basic results?

Overall, the study found a direct link between all levels of alcohol consumption and risk of cancer mortality. It also found that increasing levels of physical activity reduced this association with cancer mortality, and also reduced the link with death from any cause.

  • In individuals who reported inactive levels of physical activity (≤7 MET-hours), there was a direct association between alcohol consumption and all-cause mortality.
  • However, in individuals who met the highest level of physical activity recommendations a protective effect of occasional drinking on all-cause mortality was observed (hazard ratio: 0.68; 95% confidence interval (CI): 0.46 to 0.99). It should be noted that this result just skimmed the cut-off point for statistical significance.
  • In this high activity group, there was no link between all-cause mortality and alcohol consumption within guidelines, or even hazardous amounts, but the risk was still increased for those drinking harmful amounts.
  • The risk of death from cancer increased with the amount of alcohol consumed in inactive participants, ranging from a 47% increased risk for those drinking within guidelines to 87% increased risk for those with harmful drinking.
  • In people with higher activity levels (above 7.5 MET hours) there was no significant link between any amount of alcohol consumption and cancer mortality.
  • No association was found between alcohol consumption and mortality from cardiovascular disease, although a protective effect was observed in individuals who reported the lower and higher levels of physical activity (>7.5 MET-hours) and (>15 MET-hours) respectively.


How did the researchers interpret the results?

The researchers concluded "we found evidence of a dose–response association between alcohol intake and cancer mortality in inactive participants but not in physically active participants. [Physical activity] slightly attenuates the risk of all-cause mortality up to a hazardous level of drinking."



This study aimed to explore whether physical activity is able to moderate the risk between alcohol consumption and mortality from cancer and cardiovascular diseases. It found that increasing levels of physical activity reduced the association for death from both all-causes and cancer.

This study has strengths in its large sample size, comprehensive assessments and long duration of follow-up. The findings are interesting, but there a few points to bear in mind:

  • As the authors mention, cohort studies such as this are unable to confirm cause and effect. Though the researchers have tried to account for various potential health and lifestyle confounding variables, there is the possibility that others are still influencing the results. A notable one is dietary habits which weren't assessed. Also, for example, the former drinkers may have quit due to other health issues which may have introduced bias.
  • The study was unable to look at binge drinking levels of alcohol consumption which would have likely had important health implications.
  • Additionally, there is always the possibility with self-reported surveys that the participants either under or over-reported their drinking habits which can increase the chance of misclassification bias.
  • Though having a large sample size, fewer people reported harmful drinking levels, so links within this category may be less reliable.
  • The study has only looked at the link between alcohol and actually dying from cancer or cardiovascular disease. Links may be different if they looked at associations between alcohol and just being diagnosed with cancer or heart disease, for example.
  • The study is also only representative of adults over the age of 40.

Overall, maintaining a healthy lifestyle seems to be the best bet for reducing the risk of any chronic disease, be it through physical activity, balanced diet or reasonable alcohol consumption.

Current alcohol recommendations for both men and women are to drink no more than 14 units per week.  

Links To The Headlines

How exercise undoes the harm from drinking: Adults who booze regularly but exercise for five hours a week are no more likely to die than teetotallers. Mail Online, September 8 2016

Two hours a week of exercise could offset the dangers of alcohol. The Daily Telegraph, September 8 2016

Exercise can cut risk from alcohol-related diseases, study suggests. The Guardian, September 8 2016

Links To Science

Perreault K, Bauman A, Johnson N, et al. Does physical activity moderate the association between alcohol drinking and all-cause, cancer and cardiovascular diseases mortality? A pooled analysis of eight British population cohorts. British Journal of Sports Medicine. Published online August 31 2016

People who regularly groom their pubic hair at risk of injuries

NHS Choices - Behind the Headlines -

"A quarter of Americans are injured and hospitalized by tidying up 'down there'," the Mail Online reports.

The headline is prompted by a survey which asked 7,570 adults about pubic hair removal and "grooming" (such as waxing). The researchers found that removing all pubic hair, and frequent hair removal, were most likely to cause injuries.

Pubic hair removal has become more common in recent years. This could be due to the mistaken assumption that grooming is more hygienic (as we discussed in 2016). Some commentators have also cited the influence of pornography, where shaved genitals are the norm.

The researchers found 66.5% of men and 85.3% of women who responded to their survey had removed or groomed pubic hair at some point in their lives. However, it's not as dangerous as the Mail Online headline suggests – while 25.6% of people reported at least one injury, these were almost all minor and only 1.4% reported injury that required medical attention.

Cuts, burns, rashes and infections were the main problems. Waxing seemed to cause fewer injuries than shaving, although researchers say more study is needed before it can be recommended as a safer option.

Previous research has shown that removal of pubic hair can also make sexually transmitted infections (STIs) such as HPV more likely.

The most effective method of reducing your risk of catching an STI is to always used a condom during sex, including oral and anal sex.


Where did the story come from?

The study was carried out by researchers from the University of California, the University of Texas Dell Medical School and the Washington University School of Medicine, all in the US. It was funded by the Alafi Foundation, the Hellman Foundation and the National Institute of Diabetes and Digestive and Kidney Diseases.

It was published in the peer-reviewed medical journal JAMA Dermatology.

The Guardian carried a balanced and accurate report of the study. In contrast, the Mail Online's reporting was muddled, misleading and sensationalised. For example, the website states: "A quarter of groomers have suffered severe injuries," although the injuries were mostly minor.

The Mail also inaccurately reported that "more than a third of people surveyed by government health researchers" said they'd had five or more injuries – although this figure applies to only one third of the 25% of people injured, not one third of people questioned. The report also includes findings from other studies as if they were part of the new study which could further mislead the reader. 


What kind of research was this?

This was a cross sectional study, using a web-based survey targeted at US adults aged 18 to 65. The researchers contacted more than 10,000 adults in a "nationally representative" sample.

This type of study can give a snapshot view of what people are prepared to say in a survey about their grooming habits. However, it can't guarantee people answer truthfully.

Also, this methodology leaves any results open to accusations of selection bias. People who take the time to complete the survey may not be representative of the general public.


What did the research involve?

Researchers randomly recruited people to take the survey through sampling of the US postal service database. An email request was sent out in January 2014 asking people to take part in the online survey.

The survey asked questions about people's grooming habits, experience, injuries and infections.

To ensure people weren't excluded because of lack of internet or computer access, those without access were provided with internet facilities to complete the questionnaire.

Participants also received a small points-based incentive equivalent to one dollar.

The results were analysed to find out the extent and nature of the problem, and to identify factors that seemed to increase the risk of injury.


What were the basic results?

Almost half of the people contacted declined to take part in the survey. Of the 52.5% of people (7,570) who did take part:

  • 66.5% of men said they had groomed their pubic hair, and 23.7% said they'd been injured while doing it
  • 85.3% of women had groomed their public hair and 27.1% had been injured

The most common problems were:

  • cuts (61.2%)
  • burns (23.0%)
  • rash (12.2%)
  • infection (9.3%)

This may reflect the types of hair removal methods used. Shaving with a non-electric razor was the most common method (47.5%) followed by electric razor (26.9%), scissors (18.4%) and waxing (2.6%).

For women, those who reported waxing as their main method of hair removal were less likely to have repeated frequent injuries (adjusted odds ratio (AOR) 0.11, 95% confidence interval [CI] 0.03 to 0.43). For men (who were less likely to wax) the type of hair removal method made no difference to injury rate.

Women and men who removed all pubic hair regularly (more than 10 times per year) were more likely to report having an injury (women: AOR 2.21, 95% CI 1.53 to 3.19; men: AOR 1.97, 95% CI 1.28 to 3.01).

The position adopted while grooming made some difference to the severity of injury. People were more likely to get an injury that needed medical attention if they carried out hair removal lying on their back (perhaps because they could not see what they were doing) or if other people were carrying out the hair removal.


How did the researchers interpret the results?

The researchers said their research showed that "pubic hair grooming is a widespread practice" and so "injury prevention efforts are necessary". They said their study "may contribute to the development of clinical guidelines or recommendations for safe pubic hair removal."



Pubic hair removal is now common practice, and this study suggests it is not without risk. It seems sensible to find out more about how it can be done safely, with minimal risk of injury.

However, while the study provides useful information about peoples' experiences of pubic hair removal and injury (at least in the US), it doesn't tell us which is the safest method.

Although waxing was linked to fewer repeated injuries among women, previous studies suggest it can be harmful if done incorrectly, leading to severe injury or infection.

Similarly, although frequent removal of all pubic hair is linked to higher risk of injury, we don't know why this is. It may simply be that doing anything regularly means you have more opportunities to make a mistake.

The research has some limitations. It's notable that almost half of people contacted didn't take the survey. It may be that the people who refused to do the survey were less likely to carry out pubic hair grooming or removal, or are more likely to be embarrassed at the thought of answering questions about it.

Because the research relies on people's own reporting of their experience, we don't know how accurate it is. People may be too embarrassed to give truthful answers, may forget minor injuries, or people who suffer major injuries may be more likely to respond to the survey. All of these things could skew the results.

While people may choose to remove their pubic hair for cosmetic reasons, there are no medical benefits to the practice, and it could increase your risk of contracting a sexually transmitted infection, as we reported on last year.

Links To The Headlines

The dangers of pubic hair grooming: A QUARTER of Americans are injured and hospitalized by tidying up 'down there' - and this study reveals the nation's stupidest techniques. Mail Online, August 16 2017

Wax on, wax ouch: pubic grooming has a high injury rate, survey reveals. The Guardian, August 16 2017

Links To Science

Truesdale MD, Osterberg EC, Gaither TW. Prevalence of Pubic Hair Grooming–Related Injuries and Identification of High-Risk Individuals in the United States. JAMA Dermatology. Published online August 16 2017

'Alternative cancer therapies' may increase your risk of death

NHS Choices - Behind the Headlines -

"Cancer patients who use alternative medicine more than twice as likely to die," is the stark message from The Independent. Researchers found that people who chose alternative medicine instead of conventional cancer treatments were much less likely to survive for at least five years.

Conventional treatments included surgery, radiotherapychemotherapy or hormone treatments. The research only applies to people who choose not to have conventional treatments.

Overall, 78% of people having conventional treatment for cancer survived at least five years, compared to only 55% of people having alternative treatment alone. The difference was biggest for breast cancer, where people who chose alternative therapies were more than five times as likely to die within five years as those who chose conventional treatments.

Because this is an observational study, we don't know if other factors might have affected people's survival chances, as well as treatment choice. However, treatment choice seems the most likely explanation.

There are reports that some people find complementary treatments of benefit during cancer treatments. For example, some people have said that acupuncture helped them cope better with the side effects of chemotherapy.

But importantly, the emphasis is very much on the "complementary" and not on the "alternative". Ignoring medical advice on the treatment choices that potentially offer the most benefit could prove fatal.


Where did the story come from?

The study was carried out by researchers from Yale School of Medicine. No funding information was provided. Two of the four researchers had received previous grants from companies involved in conventional cancer treatments, and one received research funding from the organisation 21st Century Oncology.

The study was published in the peer-reviewed Journal of the National Cancer Institute as a "brief communication", meaning not all the study data was published. Some additional data is published online.

Most of the UK media ran reasonably accurate and balanced stories. Several – notably the Mail Online and The Sun – speculated on the types of alternative therapy people might have been using.

For example, the Mail said: "Breast cancer patients are 5.68 times more at risk if they opt for homeopathy." However, the researchers did not record the alternative therapies used, so we don't know whether homeopathy was one of them.

The Mail also refers to "herbs, botanicals, diets or energy crystals." While these are sometimes promoted as alternative treatments for cancer, again, we don't know which of them were used by people in this study.


What kind of research was this?

This was an observational case control study. This means researchers identified people with cancer who chose to use alternative therapies (cases) and compared their outcomes with those of people with cancer who chose conventional treatments (controls).

The controls were matched as far as possible with each case based on age, sex, demographics and type of cancer. Observational studies can show trends and links between factors (in this case between type of treatment and length of survival after cancer diagnosis) but cannot prove that one causes the other.


What did the research involve?

Researchers used data from the US National Cancer Database to identify patients with breast, lung, colorectal or prostate cancer, who opted not to receive conventional cancer therapies, but were recorded as having had "other-unproven cancer treatments administered by non-medical personnel."

These patients were matched with two patients with the same type of cancer, who were similar in other ways, but had opted for conventional treatment. Researchers then looked to see how many people lived for at least five years, comparing those who chose alternative therapies with those who chose conventional cancer treatments.

Researchers only included people who had cancer that had not yet spread from the initial site. This type of cancer is usually treatable by conventional treatments They also excluded people with stage 4 (advanced) cancer, those whose treatment was intended to be palliative rather than curative, and people whose treatment was unknown.

Researchers found 281 people who matched the criteria and who had opted for alternative therapy only. Of these, 280 were matched to 560 people with the same cancer, who chose conventional cancer treatments.

To minimise the effect of confounding factors researchers matched people in the study using these criteria:

  • cancer type
  • age
  • stage of cancer
  • health insurance – in the US people with health insurance tend to receive a better standard of treatment
  • co-morbidities (other illnesses)
  • race
  • year of diagnosis

In addition, when calculating relative chances of surviving five years, the researchers adjusted their figures to account for the effects of medical and demographic factors.


What were the basic results?

Researchers found that people choosing alternative therapies were more likely to be younger, female, have fewer other ailments, a higher cancer stage, a higher income and education level.

Taking all types of cancer together:

  • 78.3% of people having conventional cancer treatment lived at least five years (95% confidence interval [CI] 74.2% to 81.8%)
  • 54.7% of people having alternative therapies lived at least five years (95% CI 47.5% to 61.3%)
  • people were 2.5 times more likely to live for at least five years if they had conventional treatment (hazard ratio [HR] 2.5, 95% CI 1.88 to 3.27)

The type of cancer made a difference, though. This is probably because some cancers can kill quickly without treatment, and treatment is very effective. We can see this in the breast cancer results:

  • 86.6% of people who chose conventional treatment for breast cancer lived at least five years (95% CI 80.7% to 90.7%)
  • 58.1% of people who chose alternative therapies for breast cancer lived at least five years (95% CI 46% to 68.5%)
  • people were 5.68 times more likely to live at least five years if they had conventional treatment for breast cancer (HR 5.68, 95% CI 3.22 to 10.04)

However, for prostate cancer, it made little difference whether people opted for conventional treatment (91.5% lived for at least five years) or alternative treatment (86.2% lived for at least five years).

This is probably because prostate cancer usually grows very slowly in the early stages so few people die.

For the first five to 10 years, there's little difference in those who have conventional treatments and those who have their prostate cancer monitored, with no treatment unless it starts to grow. So, you would not expect to see a difference in a five year study.


How did the researchers interpret the results?

The researchers said: "We found that cancer patients who initially chose treatment with alternative medicine without conventional cancer treatment were more likely to die."

They added: "Improved communication between patients and caregivers, and greater scrutiny of use of alternative medicine for initial treatment of cancer is needed."



The results and conclusions of this study are clear: people who choose conventional treatments for cancer (such as surgery, radiotherapy, chemotherapy and hormone treatments) are likely to live longer than those who choose alternative medicine only.

It's rare for people to choose to ignore conventional treatment completely when faced with a cancer diagnosis. More often, people choose to add complementary therapies to their conventional cancer treatment. This study doesn't apply to people combining conventional and complementary therapies.

There are some limitations to the study to be aware of:

  • As an observational study, it cannot prove that treatment choice (as opposed to other factors) was the sole reason that people who chose conventional treatments lived longer. However, it seems the most likely explanation. The researchers made efforts to balance out other possibly confounding factors. It's also clear from other studies that conventional cancer therapies do work.
  • The study might have misclassified some people who started taking alternative therapies when diagnosed, but switched later to conventional treatments. However, as they would be classified in this study as having taken conventional treatments, this suggests that any switchers would only strengthen the study findings, if they were reclassified as having taken alternative medicine.

People who are diagnosed with cancer and want the best chance of surviving should choose conventional cancer therapies. These give the best chance of helping people with cancer to live longer lives.

Complementary therapies such as acupuncture and tai chi may help some people but they should never take the place of potentially life-saving treatments such as chemotherapy, surgery and radiotherapy.

Links To The Headlines

Cancer patients who use alternative medicine more than twice as likely to die. The Independent, August 15 2017

Cancer patients who rely on herbs, homeopathy or energy crystals over conventional treatment are two-and-a-half times more likely to die within five years of diagnosis. Mail Online, August 15 2017

Cancer patients who shun chemo for alternative therapies ‘are TWICE as likely to die’. The Sun, August 15 2017

Cancer warning: THIS treatment option could double your risk of dying. Daily Express, August 15 2017

Links To Science

Johnson SB, Park HS, Gross CP, Yu JB. Use of Alternative Medicine for Cancer and Its Impact on Survival. Journal of the National Cancer Institute. Published online August 10 2017

'Fat but fit' people may still be at risk of heart disease

NHS Choices - Behind the Headlines -

"Concept of being 'fit but fat' is a myth, researchers say," ITV News reports after a Europe-wide study looked at associations between body weight, metabolic health and heart disease.

The term "fat but fit" is used to describe people who are overweight or obese but don't have any of the symptoms of metabolic syndrome.

This is a common complication of obesity, and symptoms include high cholesterol, high blood pressure and an inability to control blood sugar levels (insulin resistance).

The study involved 17,640 people. Body weight was used to calculate each person's body mass index (BMI) and various tests were used to assess each person's metabolic health. They were then followed for 12 years to look at the development of heart disease.

The findings showed that BMI was an independent risk factor for heart disease, regardless of metabolic health.

Obese people who were metabolically healthy – the "fat but fit" – had a 28% higher heart disease risk than their normal weight, metabolically healthy counterparts.

But metabolic risk factors still seem to carry the highest risk for heart disease. People who were a normal weight but metabolically unhealthy had a more than doubled risk of heart disease. So despite being a normal weight, their risk was actually higher than the "fat but fit".

The good news is that certain lifestyle changes can prevent or reverse metabolic syndrome and reduce your risk of heart disease.

This includes quitting smoking if you smoke, getting regular exercise, eating healthily, trying to achieve a healthy weight, and cutting down on alcohol

Where did the story come from?

The study was carried out by researchers from Imperial College London, University College London, and an extensive number of other institutions across Europe. 

It was primarily funded by the European Union Framework, the European Research Council, the UK Medical Research Council, the British Heart Foundation, and the UK National Institute of Health Research.

The study was published in the peer-reviewed European Heart Journal.

The UK media's reporting of the study was accurate.

What kind of research was this?

This was an analysis of a random sample of people taking part in the large European Prospective Investigation into Cancer and Nutrition study (EPIC).

As the title suggests, EPIC is an ongoing cohort study looking at the links between diet and cancer. Because of the large amount of data the EPIC study gathers, researchers can also use the data to look at other associations by focusing on smaller groups (a sub-cohort).

Within this sub-cohort, known as EPIC-CVD (cardiovascular disease), the researchers compared cases of people who developed heart disease with those who didn't in a case-cohort study.

The aim was to investigate the theory of "metabolically healthy obesity". This is the idea that people who have excess body fat can still be healthy if they don't have other metabolic risk factors like high blood pressure, high cholesterol and poor blood sugar control.

To date, there's been conflicting evidence about whether the metabolically healthy obese have a higher or lower risk of heart disease and type 2 diabetes.

This study aimed to use the large body of data collected from the EPIC-CVD cohort to better look into this.

What did the research involve?

Between 1991 and 1999 EPIC recruited 366,521 women and 153,457 men aged 35-70 from 10 countries across Europe.

The sub-cohort for the EPIC-CVD project consisted of a random sample of 17,640 adults who were free from stroke or heart disease at baseline.

Participants completed questionnaires on medical history, diet and lifestyle at the start of the study.

They gave blood samples to measure total cholesterol and blood sugar, and their blood pressure, weight, height and waist circumference was also measured.

Being metabolically unhealthy or having metabolic syndrome was defined as having three or more of the following at baseline:

  • high blood pressure, use of blood pressure medications, or self-reported history
  • high triglycerides (a type of fat) or use of lipid-lowering medication like statins
  • low HDL (good) cholesterol
  • high blood sugar, use of diabetes medications, or self-reported history
  • high waist circumference

Researchers looked for the new development of heart disease during follow-up, either self-reported or through data from GP and hospital registers and mortality records. Last follow-up ranged from 2003-10, with an average of 12.2 years.

Researchers looked at the link between body fat, metabolic markers and developing heart disease, adjusting for baseline variables of country, gender, age, education, smoking status, alcohol intake, diet and physical activity.

What were the basic results?

There was a total of 13,964 cases of heart disease during the 12-year follow-up, 631 of which were within the sub-cohort.

Almost two-thirds of the sub-cohort was female, with an average age of 54 and an average BMI of 26.1, which is classified as being overweight.

Of these, 16% were obese – 45% of obese people were classed as metabolically healthy and had no features of metabolic syndrome.

BMI was linked with heart disease risk, with each standard deviation increase in BMI increasing risk by 25% (hazard ratio [HR] 1.25, 95% confidence interval [CI] 1.19 to 1.32).

Adjusting for metabolic risk factors of blood pressure, cholesterol and diabetes substantially reduced the link with BMI, showing the importance of these factors. But the link was still statistically significant (HR 1.05, 95% CI 1.01 to 1.10).

Waist circumference was similarly associated with heart disease risk (HR 1.32, 95% CI 1.24 to 1.41). Again, adjusting for blood pressure, cholesterol and diabetes similarly reduced the link so it was on the threshold of significance (HR 1.06, 95% CI 1.00 to 1.13).

Metabolically healthy obese people had a 28% increased risk of heart disease compared with metabolically healthy normal weight people (HR 1.28, 95% CI 1.03 to 1.58).

But metabolic health still seemed to be the most important factor. Normal weight people who were metabolically unhealthy had a more than doubled risk of heart disease than metabolically healthy normal weight people (HR 2.15, 95% CI 1.79 to 2.57).

Metabolically unhealthy obese people had an even higher risk compared with metabolically healthy people of a normal weight (HR 2.54, 95% CI 2.21 to 2.92).

How did the researchers interpret the results?

The researchers concluded: "Irrespective of BMI, metabolically unhealthy individuals had higher CHD [coronary heart disease] risk than their healthy counterparts. Conversely, irrespective of metabolic health, overweight and obese people had higher CHD risk than lean people."

They say that their findings "challenge the concept of 'metabolically healthy obesity', encouraging population-wide strategies to tackle obesity". 


This large, valuable study confirms that – as has long been thought – an increased BMI is linked with an increased risk of heart disease.

It shows that people with an obese BMI had a higher risk of heart disease, even if they didn't have other risk factors like high cholesterol and high blood pressure, proving that body fat is an independent risk factor.

That said, this study does have some limitations. For example, definitions of being metabolically unhealthy aren't entirely consistent with other definitions of metabolic syndrome.

This was also only assessed at the start of the study, and risk factors may have varied among individuals during follow-up.

And not all participants in the centres across Europe were general population samples. They may have included a higher proportion of those with risk factors.

Nevertheless, the study on the whole supports our understanding of the modifiable risk factors for heart disease, and shows that being obese in itself increases your risk, regardless of your metabolic health.       

More importantly, it also shows it's possible to be "not fat but unfit" if your BMI is within the recommended range but you have one or more metabolic risk factors.

The best way to prevent heart disease, reduce your BMI, and prevent or reverse the symptoms of metabolic syndrome are quitting smoking if you smoke, getting regular exercise, eating healthily, trying to achieve a healthy weight, and cutting down on alcohol.

Links To The Headlines

Concept of being 'fit but fat' is a myth, researchers say. ITV News, August 15 2017

'Fat but fit' still risk heart disease. BBC News, August 15 2017

How 'fit but fat' is a myth: Overweight people are still at greater risk of heart problems even if other markers suggest they are healthy. Mail Online, August 15 2017

People who are 'fat but fit' still face higher risk of heart disease, finds study. The Independent, August 15 2017

Links To Science

Lassale C, Tzoulaki I, Moons KGM, et al. Separate and combined associations of obesity and metabolic health with coronary heart disease: a pan-European case-cohort analysis. European Heart Journal. Published online August 14 2017

Reports that antibacterials in pregnancy are 'harmful' unfounded

NHS Choices - Behind the Headlines -

"Warning to pregnant women, don't use antibacterial soap! Chemicals in the products can make children fat and disrupt their development," is the alarming, yet entirely unsupported, headline from the Mail Online.

US researchers wanted to see if pregnant mice exposed to the chemical triclocarban (TCC), previously used in a wide range of soaps and lotions due to its antibacterial properties, could be passed to offspring via the placenta or breast milk.

Researchers added TCC to the mother's daily drinking water and looked at the short and long term development of the offspring.

They found the substance does enter the placenta and, even more so, the breast milk. Exposed offspring had smaller brains and were fatter with female offspring having particularly high fat levels.

The authors of the study say TCC is a common contaminant of wastewater, but humans don't habitually drink wastewater, or come to that, antibacterial lotions.

Even if humans did drink similar amounts of TCC, we can't use the findings of this study to say what the impact would be on human foetuses and new-borns. Therefore we cannot conclude from this study that using antiseptic soap while pregnant makes children fat.

Nevertheless, TCC and the similar chemical triclosan, are already banned in the US and are being phased out of consumer products in Europe, as we reported earlier this year.

Child obesity can be caused by lots of factors so it seems unlikely that a single chemical would make a child "fat".


Where did the story come from?

The study was carried out by researchers from Lawrence Livermore National Laboratory, Livermore, Slippery Rock University and a Californian based bio-tech company called Bio-Rad.

The research was funded by the US Department of Energy by Lawrence Livermore National Laboratory, Laboratory Directed Research and Development (LDRD) funding and National Institutes of Health in the US.

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

While the actual content of the Mail's story was accurate, ensuring readers knew the research involved mice, the headline – "Warning to pregnant women, don't use antibacterial soap!" – was misleading and arguably scaremongering.

We don't know how much or of what substances women would need to consume to match a comparable level of exposure to mice in this study.


What kind of research was this?

This was laboratory research in mice looking at the effects of a substance called triclocarban (TCC) on the offspring of mothers who were exposed to TCC through contaminated drinking water.

TCC is an antibacterial substance often used in products such as soap, as well as in the medical field and is said to be a common contaminant of wastewater. In mouse studies it has been shown to have detrimental effects on the hormone (endocrine) system at certain doses, along with effects on sexual organs and reproduction.

The US Food and Drug Administration (FDA) has banned TCC along with the antiseptic triclosan due to concerns around their safety. Various UK companies are reported to be phasing out their use in antibacterial products.

This type of research is useful to look at the effects that substances can have on animals, including humans, though we aren't exactly the same as mice. Also in real life, humans aren't likely to be drinking water directly dosed with triclocarban.


What did the research involve?

Researchers wanted to see if giving pregnant mice drinking water contaminated with TCC affected the development of baby mice. This was said to be an environmentally-relevant dose similar to that found in the US water supply – but it's not clear if they mean levels found in the wastewater supply rather than drinking water coming out of the tap.

Researchers looked at placental transfer (where the mother transfers oxygen and nutrients to their baby via blood), and breast milk transfer in the short-term and long-term.

Transfer by placenta

To examine exposure in the womb, female mice were given TCC contaminated water from the first day of pregnancy until the 18th day of pregnancy (almost full term). Foetuses and mothers were then assessed for amount of TCC in the system using accelerator mass spectrometry (AMS). AMS is a type of imaging scan used to measure very small concentrations of potentially toxic compounds in the body.

Transfer by breast milk in the short-term

Mice mothers were given standard water until the offspring were born and then TCC contaminated water from the day of birth for the first 10 days of lactation.

The mice babies and mothers were then assessed using AMS analysis.

Transfer by the breast milk in the long-term

Mothers were again given contaminated water from birth for the first 10 days of lactation and then reverted to standard water. The long-term effects on mice babies and mothers were assessed, from three weeks after birth up until eight weeks after birth using AMS analysis.

Control groups not exposed to TCC contaminated water were used as a comparison for each group.


What were the basic results?

TCC was found to transfer from mother to offspring both through the placenta and through breast-feeding.

  • Foetuses at 18 days gestation had 0.005% of the ingested dose per gram in their bodies. Higher concentrations were detected in the foetal tissue (0.011%) and maternal placental tissue (0.007%).
  • Offspring at 10 days after birth had three times higher concentration in their body (0.015% ingested dose per gram) than the foetuses exposed during pregnancy, showing TCC transfers readily through breast milk.
  • There was no significant difference in foetal weight of those exposed to TCC (through placenta) compared to controls.
  • Those exposed through breast milk also did not differ from controls in the short-term (10 days).
  • However, from day 21 to 56 post birth, those exposed to TCC through breast milk had greater weight than controls (11% higher body weight for females and 8.5% for males). However the brain weight of those in the TCC group was reduced.
  • Looking at gene activity also showed that fat metabolism and energy regulation were poorer in female offspring exposed to TCC compared to controls, but not males.


How did the researchers interpret the results?

The researchers conclude that "this study represents the first report to quantify the transfer of an environmentally relevant concentration of TCC from mother to offspring in the mouse model and evaluate bio-distribution after exposure using AMS. Our findings suggest that early-life exposure to TCC may interfere with lipid metabolism and could have implications for human health."



This experimental study in mice demonstrates the ability of TCC, a substance found in some antibacterial soaps, to transfer from mother to baby across the placenta and through breast milk. Moreover, this had signs of developmental effects on new-born mice, reducing brain size. It also increased body weight, which was associated with poorer fat metabolism in the female mice.

This research adds to the body of research suggesting that triclocarban, like the antiseptic triclosan, has potentially harmful effects and should not be used in consumer products.

However, the study was carried out on mice and they are not biologically identical to people. TCC was also given directly through daily drinking water.

The dose given was said to be similar to that found in US water supplies – however, the authors did say it is a common contaminant of wastewater. They didn't say anything about levels in household drinking water supplies. Therefore it is not completely clear from the study how relevant this dose is. Also, the levels in US water supplies may not be relevant to the UK. Even if it is similar to our exposure – through water, soap or otherwise – the effects to human foetus and new-born development might not be as severe, if it has any effect at all.

TCC is being phased out of products. If you are pregnant or breast feeding and are concerned about potential exposure, there are a range of soaps and other products out there that do not contain TCC.

And as we reported at the beginning of June there is evidence that washing your hands with cold water for 30 seconds is just as effective in getting rid of bacteria as antibacterial hand wash.

Links To The Headlines

Warning to pregnant women, don't use antibacterial soap! Chemicals in the products can make children fat and disrupt their development. Mail Online, August 11 2017

Links To Science

Enright HA, Falso MJS, Malfatti MA, et al. Maternal exposure to an environmentally relevant dose of triclocarban results in perinatal exposure and potential alterations in offspring development in the mouse model. PLOS ONE. Published online August 9 2017

Gene editing brings pig organ transplant closer

NHS Choices - Behind the Headlines -

"Gene editing to remove viruses brings transplant organs from pigs a step closer," The Guardian reports after researchers used the new CRIPSR gene editing technique. CRIPSR acts like a set of molecular scissors that can cut out potentially harmful infectious genes.

Despite the difference in size and shape, many of the pig's internal organs are remarkably similar to human organs, making them a candidate for organ donations. The drawback is that some pigs carry what are known as porcine endogenous retroviruses (PERVs).

Retroviruses are a group of viruses that can cause various cancers and immunodeficiency illnesses, including HIV, which affect people. This has been found to make any attempt to use "unedited" pig cells for donation unsafe.

The researchers showed they could use CRIPSR to target the areas of the pig DNA that carried the retroviral code. Using this technique they were able to successfully remove all retroviruses from the pig cells.

These gene-edited cells were used to create pig embryos, which were implanted into surrogate sows. The resulting piglets were free from PERVs.

This research is a promising step forward in the possible use of pig organs to meet the massive shortage of human organ donors. However, there are many more stages of research to go and there are likely to be other practical, ethical and safety issues to overcome before using pigs as organ donors.

Until further progress is made you can help by signing up to the NHS Organ Donation register. You can sign up online, it takes just a few minutes.


Where did the story come from?

The study was carried out by researchers from eGenesis Inc in the US, Zhejiang University, China, and other institutions in China, the US and Denmark. The study was mainly funded by eGenesis Inc. and the US National Institute of Health, with other funding grants awarded to individual researchers.

eGenesis Inc is a US biotech firm working on trying to make animal-to-human organ transplant safe and effective. This technique is known as xenotransplantation.

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

The UK media give balanced coverage of this research by making it clear there were a number of hurdles to be cleared before xenotransplantation could become a reality.


What kind of research was this?

This laboratory study aimed to see whether it was possible to remove porcine (pig) retroviruses, which can infect human cells, from genetically modified pigs.

Retroviruses are a group of viruses that carry their genetic material in ribonucleic acid (RNA) and are named because of the enzyme reverse transcriptase that transforms RNA into DNA. The retrovirus group can cause various cancers, neurodegenerative disorders and HIV.

Pigs show potential as organ donors for humans as their organs are similar in size and function and they can be bred in large numbers. Porcine retroviruses (PERVs) are currently one of the big safety barriers preventing us using pigs as organ donors.


What did the research involve?

The researchers first demonstrated that porcine retroviruses are transferred to human cells. They transferred pig epithelial cells (which line organs and other surfaces in the body) to human embryonic kidney cells. When the human embryonic cells (cells derived from embryos developed from eggs fertilised in the lab) were monitored for four months, the number of porcine retroviruses increased over time. They showed that these viruses had integrated into the human DNA and could be transmitted to other human cells.

The researchers then showed they were able to inactivate all 62 copies of porcine retroviruses from the pig epithelial cells, which safely eliminated virus transmission to the human embryonic cells.

The focus of the current study was to demonstrate that they could achieve the same results and inactivate porcine retroviruses from pig foetal fibroblast (connective tissue) cells.

Firstly they mapped the 25 viruses present in the genetic code of these cells. They then used the technique of "CRISPR Guide RNA" which guides enzymes to cut the DNA at specific locations, effectively editing out the genes carrying the virus.


What were the basic results?

With some modifications to the CRISPR Guide RNA technique, the researchers were eventually able to completely edit out of all retroviruses from the pig fibroblast cells. They also confirmed that the technique did not lead to unwanted alterations elsewhere in the DNA.

They then used these gene-edited fibroblasts to create pig embryos (using a technique called somatic cell nuclear transfer, SCNT). After confirming the resulting embryos were completely free from retroviruses, they were then transferred to surrogate sows.

From about 200-330 embryos per sow transferred across to 17 sows, they produced 37 piglets, of which 15 remained alive up to four months. The piglets from successful pregnancies were confirmed to have no retroviruses in their DNA. They also confirmed there weren't any abnormal structural changes to these piglets.

The researchers are continuing to monitor the longer term effects in these animals.


How did the researchers interpret the results?

The researchers conclude that they have shown porcine retroviruses can be passed from pig to human cells in the laboratory, highlighting "the risk of cross-species viral transmission in the context of xenotransplantation."

To work towards eliminating this risk, they used a technique called CRISPR Guide RNA to produce pig embryos, foetuses and live pigs free from the retroviruses.



This promising research shows that it can be possible to use gene editing techniques to eliminate retroviruses from pigs, removing one of the potential barriers to using genetically modified pigs as organ donors for humans.

There are a few points to note. As the researchers say, though they have shown that pig retroviruses can be passed onto human cells in the laboratory, we don't know what the effects would be in real life. We don't know whether pig retroviruses would be transferred to humans and whether they could cause cancers or immunodeficiency illnesses, for example.

The research is at an early stage. The study has shown that they can produce retrovirus-free piglets but moving onto pig organ donation is another step. While some pig tissues have been in medical use for decades, such as pig heart valves and insulin, there are likely to be various practical, ethical and safety steps to overcome when it comes to transplanting whole large animal organs into humans.

A number of experts responded to the news – highlighting both the positives and negatives.

Prof Darren Griffin, Professor of Genetics, University of Kent, says: "This represents a significant step forward towards the possibility of making xenotransplantation a reality," while Prof Ian McConnell, Emeritus Professor of Veterinary Science, University of Cambridge, cautions: "[Organ transplant] is a huge unmet need of modern medicine. But the use of animal organs such as pig kidneys and hearts is not without serious ethical and biosecurity concerns."

When it comes to organ donation, demand far outstrips supply in the UK. You can help with this problem by signing up to the NHS Organ Donation register.

Links To The Headlines

GM pigs take step to being organ donors. BBC News, August 11 2017

Gene editing to remove viruses brings transplant organs from pigs a step closer. The Guardian, August 10 2017

GM pigs as human organ donors moves a step closer. ITV News, August 11 2017

Links To Science

Niu D, Wei H, Lin L, et al. Inactivation of porcine endogenous retrovirus in pigs using CRISPR-Cas9. Science. Published online August 10 2017

Vitamin B3 found in Marmite not proven to prevent miscarriage

NHS Choices - Behind the Headlines -

"Like it or loathe it, but Marmite could help prevent millions of miscarriages and birth defects around the world," is the overly optimistic headline in The Daily Telegraph.

The news is based on research into just four families who have children with birth defects, with three of the families also having had miscarriages.

Researchers sequenced the families' DNA, and found all the children had similar mutations that prevent the synthesis and circulation of an enzyme called nicotinamide adenine dinucleotide (NAD) in the body.

NAD is used by the body for cell signalling. Vitamin B3, also known as niacin, is thought to stimulate the production of NAD.

Mice bred to have the same mutations, and who also had miscarriages or offspring with defects, were given vitamin B3 supplements. All went on to have healthy babies.

In theory, vitamin B3 supplements might be effective for women who are pregnant or trying to get pregnant and are deficient in B3.

But the researchers didn't look at this – they only looked at rare genetic mutations in four children and replicated them in mice. Pregnancy outcomes in women weren't studied. 

It's certainly too soon to start recommending that all pregnant women start taking vitamin B3 supplements in the same way they're advised to take vitamin D.

If you're worried about vitamin B3, one way of safely upping your intake is by eating things like Marmite (or Vegemite), chicken and green peas.

Unfortunately, there are lots of reasons why miscarriages and birth defects occur, many of which are currently unavoidable.

Where did the story come from?

The study was carried out by researchers from a range of medical and academic institutions across Australia, including the University of New South Wales, the University of Sydney, Macquarie University, the University of Adelaide, and the University of Queensland School of Medicine.

The research was funded by the Australian National Health and Medical Research Council, the Australian Research Council, the Australian National Heart Foundation, the New South Wales Government Office for Health and Medical Research, a Queensland Premier's Fellowship, the Kirby Foundation, the Chain Reaction Challenge Foundation, and the Key Foundation.

The study was published in the peer-reviewed The New England Journal of Medicine.

The UK media were arguably guilty of taking the study's press release at face value, and we suspect some journalists didn't actually read the study itself.

The much quoted statement from the lead author – "This has the potential to significantly reduce the number of miscarriages and birth defects around the world, and I do not use those words lightly" – is currently not supported by the evidence.

This research doesn't necessarily translate into reducing miscarriages in women. Miscarriages and birth defects happen for a range of reasons, not just because of one rare genetic mutation that reduces vitamin B3. 

What kind of research was this?

This two-stage laboratory study first involved genetic sequencing in families who had children born with multiple birth defects that developed when the child was growing inside the womb.

Researchers then looked at similar disease-causing mutations in mice and the effect that increasing vitamin B3 in the diet had on preventing malformations in the growing foetus.

This type of research is interesting as it combines observations and genetic sequencing on humans with laboratory research in mice manipulated to have similar genetic mutations.

Increases in vitamin B3 would still need to be tested in humans with these particular genetic mutations to make sure this isn't just effective in mice.

What did the research involve?

Researchers took four families that each had a child with multiple birth defects and carried out genetic sequencing.

This technique is used to analyse the individual bases (nucleotides) of a person's DNA. It can help spot when a particular gene is altered (mutated) or missing altogether.

Four families – two from Lebanon, one from Iraq and one from the US – who had babies born with multiple birth defects took part in the research. The families from Lebanon and Iraq were related by blood.

The children had various different defects, some of which included short stature and heart, limb, kidney and ear-related deformities. Three of the mothers had also had one or more miscarriages.

Researchers found certain genetic mutations that affect the production of a molecule called nicotinamide adenine dinucleotide (NAD).

This is produced naturally in the body, but can also be supplemented by increasing the amount of vitamin B3 in your diet, as it's also found in vitamin B3.

The researchers replicated the families' genetic mutations in mice, which were then given supplements of vitamin B3 to see if this affected their future offspring.

What were the basic results?

The four families' genetic mutations caused problems encoding two proteins called 3-hydroxyanthranilic acid 3,4-dioxygenase (HAAO) and kynureninase (KYNU).

These are both involved in a pathway that produces NAD. The children with birth defects therefore had reduced levels of circulating NAD in their bodies.

Mice bred to have mutations that reduced the production of HAAO and KYNU, and therefore reduced levels of circulating NAD, also had miscarriages or offspring born with defects.

After the mice were given more vitamin B3 as part of their diet, thereby increasing levels of circulating NAD, all subsequent offspring were born healthy.

How did the researchers interpret the results?

The researchers concluded: "Disruption of NAD synthesis caused a deficiency of NAD and congenital malformations in humans and mice. Niacin (B3) supplementation during gestation prevented the malformations in mice." 


This early-stage laboratory research has pinpointed two potential genes that might be responsible for some miscarriages and birth defects.

As well as identifying a problem, the researchers also managed to find a solution: the effect of these genes can be combatted by increasing vitamin B3 intake.

But treating a very specific and uncommon cause of birth defects in mice is certainly not a sure-fire solution to "significantly reduce the number of miscarriages and birth defects around the world".

We need future research to see if the same effect would happen in humans.

Also, three of the four children included in the study were the offspring of parents who were related by blood. This might mean that the type of genetic mutations studied in this research are more specific to the children of parents who are related.

A vitamin B3 supplement might have less of an effect on other types of mutations, but we can't say at this stage.

Overall, it seems like upping vitamin B3 intake in mothers who are deficient might have the potential to help prevent miscarriage and congenital malformations.

Testing vitamin B3 levels in pregnant women or women trying to get pregnant to see if they're deficient would identify those who might benefit the most.

And eating more foods like Marmite, meats like turkey and chicken, and vegetables like mushrooms and green peas could be one way to get more vitamin B3. Long-term high-dose vitamin B3 supplements should be avoided as this can lead to liver damage.

The National Institute for Health and Care Excellence (NICE) currently recommends pregnant women take folic acid (400mcg per day) and vitamin D (10mcg per day) supplements. Multivitamin supplements aren't recommended as these often contain vitamin A, which can cause birth defects.

You can also reduce your risk of having a miscarriage by avoiding smoking and drinking alcohol, eating a healthy diet, and being a healthy weight.

Links To The Headlines

Why Marmite could prevent miscarriages and birth defects. The Daily Telegraph, August 10 2017

The power of niacin: Common vitamin found in Marmite and meat can prevent miscarriages and birth defects, reveals breakthrough study. Mail Online, August 10 2017

Major breakthrough as scientists discover vitamin B3 found in Marmite could prevent thousands of miscarriages. The Sun, August 10 2017

'Breakthrough' as scientists discover vitamin can cut birth defects and miscarriages. Sky News, August 10 2017

Links To Science

Shi H, Enriquez A, Rapadas M, et al. NAD Deficiency, Congenital Malformations, and Niacin Supplementation. The New England Journal of Medicine. Published online August 10 2017

Saliva 'may speed healing' but 'kissing it better' probably won't

NHS Choices - Behind the Headlines -

"Kissing it better really works: Saliva found to have properties that help speed up the healing process," reports the Mail Online. Researchers in Chile investigated how human saliva may help wounds to heal more efficiently.

They used lab-grown skin cells and fertilised chicken eggs to see how a protein found in saliva, histatin-1, affects the way cells grow, spread and create new blood vessels. They found it encouraged cells to spread and move in a way that promoted the formation of blood vessels (a process called angiogenesis), which aids wound healing in skin.

The experiments help us to understand why wounds in the mouth heal faster, but we don't know that saliva would encourage wound healing on other parts of the body. While parents "kissing it better" might help children when they hurt themselves (possibly due to a placebo effect), that doesn't mean their saliva is helping a grazed knee to heal quicker. The quantity of saliva that would be required is neither a practical nor hygienic solution, but the research could pave the way for new aids to wound healing.

Where did the story come from?

The study was carried out by researchers from the Universidad de Chile and Pontificia Universidad Católica de Chile, and was funded by five Chilean research foundations. The peer-reviewed study was published in The FASEB Journal, which is the journal of the Foundation of American Societies for Experimental Biology.

Aside from the eye-catching but inaccurate headline, the Mail Online article gives a reasonable overview of the research. It includes speculation from the researchers that their work could lead to the development of better treatments to speed up the healing of wounds.

What kind of research was this?

This was a series of laboratory-based experiments using lab-grown skin cells and fertilised chicken eggs to look at biochemical reactions to the introduction of a specific protein found in saliva, histatin-1. While this type of research is important to better understand wound healing, it's a far cry from using naturally produced saliva on human skin wounds.

What did the research involve?

Researchers carried out a series of experiments using a chemically synthesised form of histatin-1.

First, they tested whether this form was biologically active by mixing it with cells infected with candida yeast (a type of fungus that can cause wound infections) to see if histatin-1 slowed the growth of the yeast.

Next, they tested the histatin-1 on skin cells that had been grown and then wounded to see how quickly the wound healed. Further experiments on lab-grown (cultured) skin cells included tests to see how histatin-1 affected the movement of cells, and their ability to spread, grow and stick to a protein-coated plate.

A further test was carried out on fertilised chicken eggs. The membrane around the embryo (called the chorioallantoic membrane) makes it easy to see the growth of new blood vessels. The researchers made a break in the membranes and introduced histatin-1 to some of them to see whether it affected the growth of new blood vessels.

Finally, some of the experiments were repeated with natural saliva from donors, and again with saliva that had the histatin-1 reduced or removed.

What were the basic results?

Experiments on cultured skin cells found:

  • Histatin-1 slowed the growth of the yeast Candida albicans, showing that the protein was biologically active.
  • Histatin-1 increased the area of the wound that had healed, depending on cell type. For the most common outer-skin cell (keratinocytes), it increased the area from 14.9% healed to 25.4%, and from 31.4% to 46.1% for cells that line blood vessels.
  • More cells treated with histatin-1 moved to the area of the damaged skin cells, more spread around the damaged area and more adhered to protein-coated glass plates.
  • Histatin-1 did not encourage the growth of more cells – it just affected the way in which they behaved.

Experiments using the chicken-egg membrane found that histatin-1 encouraged the formation of new blood vessels, with the effect comparable to other substances known to do this.

One further experiment found that using human saliva from donors encouraged cell movement, while saliva that had histatin-1 removed did not.

How did the researchers interpret the results?

The researchers said their study shows "histatin-1 is a proangiogenic factor [something that encourages the formation of new blood vessels] that promotes endothelial cell adhesion and spreading" and it will "help [in] understanding the mechanisms underlying the novel roles of histatin-1".

They said histatin-1 promotes cell movement as a "crucial step" in the formation of new blood vessels and that this has "important consequences for future research".


This complex study helps us understand the biological mechanisms behind wound healing in the mouth and the role of saliva in promoting wound healing. As well as keeping the mouth moist and reducing levels of harmful bacteria, saliva contains a protein that encourages the movement of cells in ways that help wounds to heal.

It's possible this might lead to the development of new wound-healing treatments in future; however, this study didn't look at future uses – it simply helps us better understand how the body heals itself.

Before any new treatment could be developed, further studies in cell lines and in animals, followed by extensive studies in humans, would be needed to ensure that any treatment was safe and effective. That's a long way off.

Next time you bite your tongue or the inside of your cheek, just imagine the proteins in your saliva working away to help to heal the wound as quickly as possible.

But it's best not to imagine any more than that. While kissing your child's grazed knee may have a powerful placebo effect, we'd recommend reaching for some antiseptic cream and a plaster too.

Links To The Headlines

Pucker up... kissing it better really works: Saliva found to have properties that help speed up the healing process. Mail Online, August 9 2017

Links To Science

Torres P, Díaz J, Acre M, et al. The salivary peptide histatin-1 promotes endothelial cell adhesion, migration, and angiogenesis. The FASEB Journal. Published online July 27 2017

'Exercise pill' could potentially help people with heart failure

NHS Choices - Behind the Headlines -

"Pill that mimics effects of going to the gym could transform lives of heart failure patients," the Daily Mirror reports. While the news sounds promising, it is important to make clear the research involved rodents, not people.

Heart failure is when the heart is unable to pump blood around the body properly. It fails to meet the body's demand for oxygenated blood, leading to symptoms such as breathlessness and fatigue.

One of the causes of heart failure is cardiomyopathy, which is when the heart muscle has become stretched, thickened or stiff.

Researchers wanted to see if a protein called cardiotrophin 1 could help stimulate the growth of new muscle cells.

The study found the protein promoted heart cell growth, similar to the way exercise increases heart strength. The effect of the protein was also reversible, as are the effects of exercise.

While this is very exciting, given there is currently no cure for heart failure, the research is still only early-stage so it could be years before a drug becomes available. And this would only happen if it managed to pass clinical trial stages in people.

If you have been diagnosed with heart failure, making healthy lifestyle choices such as stopping smoking, eating healthily and moderating alcohol intake can prevent complications. You may also be referred to a cardiac rehabilitation programme, which usually involves specialised exercise classes.

Read more about living with heart failure.


Where did the story come from?

The study was carried out by researchers from Ottawa Hospital and the University of Ottawa in Canada, and Fate Therapeutics Inc. in San Diego, US.

The work was funded by grants from the Canadian Institutes of Health Research, the Ontario Research Fund, the Heart & Stroke Foundation of Canada and Fate Therapeutics.

Fate Therapeutics is a biotech company. One of the study's authors has served on the company's scientific advisory board.

The study was published in the peer-reviewed medical journal Nature on an open-access basis, meaning it is freely available to read online.

The UK media's reporting of the research was generally accurate, although the Daily Express failed to make it clear that the research was conducted in mice.

And neither the Express nor the Mirror made clear that promising results in rodents often do not carry over to humans.


What kind of research was this?

This was experimental research conducted in a laboratory on mice and rats with heart failure. It looked at the effect of a protein called cardiotrophin 1 on the heart muscles following heart failure.

Early-stage experimental research such as this is very important in finding potential new drugs that could go on to benefit patients in a way that is not currently available. However, it is a potentially long process before such drugs can be accessed by people with heart failure.


What did the research involve?

Researchers wanted to see whether delivering the protein human cardiotrophin 1 (hCT1) over a 14-day period to mice with heart failure would alter their heart structure and could be a potential treatment for heart failure.

Heart muscle can grow in either a healthy or detrimental way. Healthy growth, usually caused bv regular exercise, is reversible. Reversibility is a good thing in this circumstance as the heart needs to adapt to changing circumstances.

When it grows in a detrimental way, the extra heart muscle growth is irreversible and does not improve heart function. This can then result in heart failure.

The researchers aimed to see if they could stimulate healthy, reversible heart muscle growth in rats and mice using hCT1 protein.

They also wanted to study the effect of a decongestant called phenylephrine, usually used for blocked noses, on rodent hearts. Phenylephrine has been linked to detrimental increases in heart muscle.

They assessed the mice and rats after two weeks of treatment by looking at echocardiograms of the hearts to see any changes.

The treatment was then stopped and echocardiograms carried out six weeks later to see if the effects were reversible. An echocardiogram is when an ultrasound scanner is used to assess the structure of the heart and surrounding blood vessels while also analysing how well the blood is flowing.

Additionally, the researchers carried out experiments on the heart cells of mice to see whether the hCT1 protein changed the structure of cardiac muscle cells.


What were the basic results?

They found that both phenylephrine and hCT1 stimulated heart muscle growth. However, hCT1 had a better ability to control this process and produced structural changes to the heart similar to those induced by exercise. This was in contrast to the phenylephrine treatment, which caused the heart muscle cells to grow wider, but without any positive effects.

After hCT1 treatment was stopped, the heart growth had reversed by six weeks – in a similar way to when exercise is stopped. But the phenylephrine-induced growth was found to be irreversible, which runs the risk of causing heart failure.

Also, the hCT1 protein reduced the loss of function and unhealthy growth associated with right heart failure (where the right-hand side of the heart loses some or all of its pumping ability).


How did the researchers interpret the results?

The researchers concluded they have demonstrated that giving mice the protein cardiotrophin 1 produces "beneficial remodeling of the heart. The cardiac adaptations elicited by cardiotrophin 1 display the essential characteristics and benefits that are associated with endurance exercise adaptation, all of which are fully reversible when cardiotrophin 1 protein delivery is discontinued."



The protein hCT1 caused heart muscles to grow in a more healthy way in rodents with heart failure. When treatment stopped, the heart went back to its original condition – something that does not happen when the heart grows in a dysfunctional way.

There is currently no cure for heart failure and treatment is only available for keeping symptoms under control. Therefore, this very promising early-stage research with potential for developing a drug for people with heart failure, has huge implications.

However, it is important to remember that as this is experimental laboratory research, there are many more stages and hurdles to clear before a drug could become available. Something that works for rats and mice will not necessarily work for humans as we are anatomically different and biological processes do not happen in exactly the same way. It may also cause future side effects that were not apparent in these short-term laboratory experiments.

If you have been diagnosed with heart failure, follow your doctor's advice on how you can relieve your symptoms, reduce your risk of complications and improve your overall quality of life.

Read more about treating and living with heart failure.

Links To The Headlines

Pill that mimics effects of going to the gym could transform lives of heart failure patients. Daily Mirror, August 9 2017

Heart disease: 'Exercise pill' that mimics effects of visit to the gym could improve lives. Daily Express, August 9 2017

Links To Science

Abdul-Ghani M, Suen C, Jiang B, et al. Cardiotrophin 1 stimulates beneficial myogenic and vascular remodeling of the heart. Cell Research. Published online August 8 2017

Software used to screen social media photos for depression signs

NHS Choices - Behind the Headlines -

"The images you put up on Instagram could be used to diagnose if you're depressed," the Mail Online reports.

Researchers attempted to see if computer-driven image recognition could diagnose depression based on the form and content of people's posts on Instagram, a social media photo sharing site.

They looked at more than 43,000 images from 166 people, who also completed a survey about their mood.

The researchers found people who reported having a history of depression were more likely to post images that were bluer, darker and less vibrant.

The computer programme was able to correctly identify 70% of the participants with depression, getting it wrong 24% of the time.

These results were compared with a separate independent study, which estimated that GPs only correctly diagnose 42% of cases.

This is a proof of concept study into what is often referred to as "machine learning", where sophisticated algorithms assess massive amounts of data to see if they can begin to spot patterns in the data that humans can't.

The researchers suggest social media could become a useful screening tool. But aside from whether the science stacks up, there are ethical and legal implications that would need to be considered before this could happen.

If you've been feeling persistently down and hopeless in the last few weeks and no longer take pleasure in things you used to enjoy, you may be depressed. Contact your GP for advice.

Where did the story come from?

The study was carried out by researchers from Harvard University and the University of Vermont, and was funded by the National Science Foundation and the Sackler Scholars Programme in Psychobiology.

It was published in the peer-reviewed journal EPJ Data Science.

There was wide coverage of the story in the media, which was generally accurate – but none highlighted any of the study's limitations.

The media also failed to point out that although the researchers say their 70% detection rate is better than GPs, the GP detection rate was taken from a study that looked at GPs making a depression diagnosis without using any standard assessments. This means we're unable to verify the accuracy of this figure.

What kind of research was this?

This case-control study compared the Instagram posts of people who reported a history of depression with the posts of those who did not.

Although this is an interesting concept, this type of study isn't able to prove cause and effect.

For example, we don't know whether the individual preferences for colour, mood or genre had changed over time in either group – more people in the depression group may have happened to always prefer the colour blue, for example.

What did the research involve?

The researchers recruited 166 adults aged between 19 and 55 using Amazon's Mechanical Turk (MTurk) crowdwork platform. This is an online service where participants receive small rewards for taking part in regular surveys or similar tasks.

They completed an online survey about any history of depression and agreed to let researchers have access to their Instagram posts for computer analysis.

A total of 43,950 photos were compared for 71 people with a history of depression and 95 healthy controls.

The researchers chose to measure differences in the following features of Instagram posts:

  • hue – colour on the spectrum from red (lower hue) to blue/violet (higher hue)
  • brightness – darker or lighter
  • vividness – low saturation appears faded, while high saturation is more intense or rich
  • use of filters to change the colour and tint
  • presence and number of human faces in each post
  • number of comments and likes
  • frequency of posts

They then compared these features between the two groups and ran various computer programmes to see if they could predict who had depression based on 100 of their Instagram posts.

They compared their predictions with those made by GPs using data from a previous independent meta-analysis, which found GPs are able to correctly diagnose 42% of people with depression without using any validated questionnaires or measurements.

The Center for Epidemiologic Studies Depression Scale (CES-D) questionnaire was used as a screening tool for depression.

This uses a scale of 0-60 – it's generally considered that a score of 16 or more indicates a likely diagnosis of depression. People with a score of 22 or more were excluded from this study.

To see if humans are able to identify factors that computers cannot, the researchers also asked a sample of online users to each rate 20 randomly selected photographs on a scale of 0-5 on the following measurements:

  • happiness
  • sadness
  • interest
  • likeability

In all, 13,184 images were rated, with each image being rated by at least three people.

What were the basic results?

The computer programme identified 70% of the people with depression. It incorrectly identified 24% of people as having depression who did not.

The results were much less accurate for predicting depression before it had been diagnosed.

According to the computer-generated results, people in the depressed group were more likely to post:

  • photos that were bluer, darker and less vibrant
  • photos that generated more comments but fewer likes
  • more photos
  • photos with faces
  • photos without using filters

If they did use filters, they were more likely to use "inkwell", which converts photos to black and white, whereas the healthy controls were more likely to use "valencia", which brightens images.

The human responses to the photos found people who were in the depression group were more likely to post sadder and less happy images. Whether the images were likeable or interesting didn't differ between the groups.

How did the researchers interpret the results?

The researchers concluded: "These findings support the notion that major changes in individual psychology are transmitted in social media use, and can be identified via computational methods."

They say this early analysis could inform "mental health screening in an increasingly digitalised society". They acknowledge that further work on the ethical and data privacy aspects would be required.


This study suggests that a computer algorithm could be used to help screen for depression more accurately than GPs – using Instagram images.

But there are several limitations that need to be considered when analysing the results:

  • As only people with a CES-D score of between 16 and 22 (on a scale of 0-60) were included, this is likely to have ruled out those with moderate to severe depression.
  • There were a small number of participants.
  • Selection bias will have skewed the results – it only includes people who like to use Instagram and are willing to allow researchers access to all of their posts.
  • Many potential participants refused to take further part in the research once they realised they'd have to share their posts.
  • It relied on self-reporting of depression rather than formal diagnoses.
  • The data is all from US participants, so may not be generalisable to the UK.
  • The 100 posts from people with depression were analysed if they were within a year (before and after) of the diagnosis. As we don't know how long people may have had symptoms for before diagnosis and whether their symptoms had improved, it's difficult to make any accurate conclusions.
  • We don't know their lifelong preferences for colours or genre when posting images.
  • And, most importantly, the figure quoted that GP diagnostic accuracy was only at 42% was based on meta-analysis of studies where GPs were asked to diagnose depression without using questionnaires, scales or other measurement tools. This doesn't give a very realistic representation of depression diagnosis in normal clinical practice. As such, it can't be assumed that this model would be an improvement over standard methods for depression screening or diagnosis.  

Though the results of this study are interesting, it's unclear what benefits or risks may be attached to any future use of screening tools for depression using Instagram or other social media.

If you're concerned that you're depressed, it's best to contact your GP – there are a variety of effective treatments available.

Read more about seeking advice about low mood and depression.

Links To The Headlines

Can you tell which of these pictures reveals you are on the verge of depression? How the images that you post on Instagram reveal more than you realise about your state of mind. Mail Online, August 8 2017

A blue mood can colour Instagram posts, study finds. ITV News, August 8 2017

Posting lots of photos on social media? It could be a sign of depression. The Daily Telegraph, August 8 2017

Links To Science

Reece AG, Danforth CM. Instagram photos reveal predictive markers of depression. EPJ Data Science. Published online August 8 2017

Alcohol linked to an increased risk of skin cancer

NHS Choices - Behind the Headlines -

"Drinking just one glass of beer or wine a day could give you skin cancer, scientists have warned," the Mail Online reports.

Researchers pooled the results of previous studies and found a small, but significant, association between alcohol consumption and non-melanoma skin cancers. The most common of these types of cancer are squamous cell and basal cell carcinoma.

While this news is obviously a cause for concern, non-melanoma skin cancers are far less aggressive than malignant melanoma, a type of skin cancer that can spread to other parts of the body. With prompt diagnosis and treatment, non-melanoma skin cancers are often curable.

The review gathered the results from 13 studies and found that 10g of alcohol per day was linked with a 7% increase in risk of basal cell and 11% increase in risk of squamous cell carcinoma. 10g of alcohol per day is equivalent to one unit of alcohol, such as a glass of wine.

However, these findings come with several caveats. The individual studies differed in terms of the alcohol categories they compared and whether they took account of the various factors that may influence the links.

Even if alcohol does have a direct effect, these are relatively small risk increases. For example, if a person had a 10% lifetime risk of a squamous cell cancer, an 11% risk increase would only increase this risk to 11%.

People drinking responsibly within current alcohol recommendations (no more than 14 units a week for men and women, spread over at least three days) should not be concerned.


Where did the story come from?

The study was carried out by researchers from Chan School of Public Health in Boston and other institutions in the US, Taiwan and South Africa. The study was funded by the US National Institute of Health. It was published in the peer-reviewed British Journal of Dermatology.

While both The Mail Online and the Daily Mirror's coverage was broadly accurate, headlines suggesting an increase in risk without putting it into context could cause undue alarm.

Also, the Mail's sub-headline: "A daily glass of wine increased the risk of melanoma, the deadliest skin cancer" was the finding of an earlier study, not this review.


What kind of research was this?

This was a systematic review that aimed to pool the available literature looking at the link between alcohol intake and risk of non-melanoma skin cancer. This includes squamous cell and basal cell carcinoma, which are slower growing and less aggressive than malignant melanoma. Like melanoma, ultraviolet (UV) light is a risk factor for developing these cancers, though dietary and alcohol links have also been suggested.

A systematic review is the best way of gathering the evidence to date, though the results are only as good as the size and quality of the underlying studies.


What did the research involve?

The authors searched two literature databases to identify English language observational studies (cohorts or case controls) that had looked at the link between alcohol intake and squamous and basal cell carcinomas.

Studies were assessed for quality and researchers pooled risk data for the two types of cancer. They looked at the effect of increasing alcohol intake, ideally by 10g increments of ethanol per day. One 150ml glass of 12% wine contains around 14g of alcohol.

Thirteen studies met inclusion criteria. One came from the UK and others from the US, Italy, Finland, Denmark, Turkey, Yugoslavia and Australia. They were a mix of population-based and hospital-based observational studies. The studies differed in terms of the high- and low-alcohol categories they compared and the confounding factors they took into account.


What were the basic results? Basal cell carcinoma

Six studies were pooled, which found that every extra 10g of ethanol consumed per day (a small glass of wine) was linked with a 7% increase in risk of this type of cancer (relative risk 1.07, 95% confidence interval 1.04 to 1.09). However, the peak for risk was only 9g of alcohol per day, with little increase in risk above that amount.

There was considerable variation in the results of the individual studies. The positive result mainly came from the three US studies, with the two European studies and single Australian study in this group finding no statistically significant link.

Squamous cell carcinoma

Only three studies were pooled. A 10g increase in ethanol consumption per day was linked with an 11% increase in risk of this type of cancer (relative risk 1.11, 95% confidence interval 1.06 to 1.16). There was minimal difference in the results of the three studies.


How did the researchers interpret the results?

The researchers conclude that their study "found evidence that alcohol drinking is positively associated with both [basal cell] and [squamous cell] carcinoma risk in a dose-dependent manner. These results should be interpreted with caution due to potential residual confounding. Nonetheless, because alcohol drinking is a prevalent and modifiable behaviour, it could serve as an important public health target to reduce the global health burden of [non-melanoma skin cancer]."



These findings should be interpreted with care before concluding that an alcoholic drink per day increases your risk of skin cancer.

There are several important cautions:

  • These are only observational studies. It wouldn't be possible to randomise people to different alcohol intake and follow them to look at cancer development. And with observational studies, many other health, sociodemographic and lifestyle factors may be influencing the link between alcohol intake and cancer development. The studies differed considerably in terms of the influencing factors they took account of, with some adjusting for various confounders, some adjusting for only age and gender, and some taking none into account. Therefore we cannot be sure that alcohol is having a direct and independent effect on cancer risk.
  • The individual studies differed in the alcohol intake they compared. For example, some compared all drinkers with non-drinkers, others compared intake of more or less than one glass a week, and others compared "above average" intake with none. This makes it very difficult when pooling the studies to be sure what intakes you are comparing – especially given the additional limitation that alcohol intake will have been self-reported, so may be inaccurate.
  • The relative risk increases are very small at only 7% and 11%. We don't know from this paper what the absolute risk of these cancers was – in other words, what proportion of all people actually developed these cancers during the follow-up time. A small increase in a small risk still results in a small risk. For example, if a person had a 10% baseline risk of squamous cell carcinoma, an 11% relative risk increase would only raise that baseline risk to 11%.

Overall, this study provides a good summary of the available literature on the links between alcohol intake and non-melanoma skin cancer, but we can't be certain of the size and strength of these links.

People drinking responsibly within current alcohol recommendations should not be concerned.

Finally, being "sun smart" and avoiding excessive exposure to sunlight (as well as artificial sources of UV light) should help reduce your risk of both non-melanoma and melanoma skin cancers.

Read more advice about sun safety.

Links To The Headlines

How that nightly tipple could lead to skin cancer: Just one alcoholic drink a day can raise risk of one type by 11%. Mail Online, August 7 2017

Booze skin cancer warning as one drink a day 'can raise risk of disease by 11 per cent'. Daily Mirror, August 7 2017

Links To Science

Yen H, Dhana A, Okhovat JP, et al. Alcohol intake and risk of nonmelanoma skin cancer: a systematic review and dose–response meta-analysis. British Journal of Dermatology. Published online July 26 2017

Diabetes drug may be helpful for Parkinson's disease

NHS Choices - Behind the Headlines -

"A drug commonly used to treat diabetes could help those living with Parkinson's disease," The Guardian reports. A small study suggests a drug called exenatide may have a modest beneficial effect on motor (movement) symptoms in people with Parkinson's disease.

Exenatide is known as a GLP-1 agonist, used to help regulate blood sugar levels in people with diabetes. Previous, early-stage research also suggests it may help protect nerves against damage, which is the root cause of Parkinson's.

The study looked at changes to people's movement ("motor") ability when given either an injection of exenatide or a placebo injection. The people in the study had their motor ability assessed by a well-validated scoring tool before taking the drug, at various points during the trial, and 12 weeks after they were last treated.

At the final measuring point, people who had received exenatide had shown a small improvement in their motor scores, while people in the placebo group had got worse. However, the difference between those changes was modest. People receiving exenatide did not report any significant improvement in quality of life.

Nonetheless, it is an interesting finding warranting further research into the longer-term effects of giving exenatide to people with Parkinson's disease.

It could be the case that a repurposed GLP-1 agonist specifically designed to treat Parkinson's would provide more benefit.


Where did the story come from?

The study was carried out by researchers from University College London, the Leonard Wolfson Experimental Neuroscience Centre in London and the National Institute of Aging in Baltimore. It was funded by The Michael J Fox Foundation for Parkinson's Research and the Department of Health National Institute for Health Research Biomedical Research Centres.

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

Overall the UK media covered the research well, though the headlines tended to overstate the impact of the drug on symptoms and the significance of these very early findings.

The Mail Online's assertion that the drug could "halt" Parkinson's was particularly optimistic as the results only indicated a slight change in motor symptoms and no change in any other symptoms.

BBC News' headline "First hints Parkinson's can be stopped" is a more realistic appraisal of the research.


What kind of research was this?

This study was a randomised controlled trial (RCT) comparing people given the diabetes drug exenatide with those who were given a placebo. During the study, neither the people who were in the trial nor their doctors knew which drug they had received, so the RCT was double-blinded – the best way of assessing an intervention. Although the study was quite small, the researchers were still able to find some differences between the two groups of people at the end.

The main aim of the study was to see whether exenatide had a beneficial effect on people's motor scores 12 weeks after completing the 48-week course of drugs.


What did the research involve?

The researchers recruited 62 people to the study and randomised them to receive either exenatide (32 people) or a placebo drug (30 people). Both drugs were given to people in the form of injections, which they used themselves. People took the injections for 48 weeks while carrying on their normal medication, and then stopped the injections while continuing to be studied for an additional 12 weeks.

People were eligible to take part in the study if they:

  • were aged 25-75 years
  • had idiopathic Parkinson's disease (where the cause is unknown)
  • were taking "dopamine boosting" (dopaminergic) drugs such as Levodopa, where the effects start to wear off before the next dose is taken
  • were considered able to self-inject the drug
  • were at Hoehn and Yahr stage 2.5 or less during treatment (the Hoehn and Yahr scale is a five point scale used to describe the severity of symptoms, so participants were no more than halfway through disease progression)

People who had dementia, diabetes, or a body mass index (BMI) below 18.5 were not allowed to join the study.

The researchers took various measurements of people before, during and after the study, including the Movement Disorders Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS); which consists of five different sections, or parts, assessing different sets of symptoms.

The main measure they looked at was the MDS-UPDRS 3 score, which measures motor ability on a scale of zero (no symptoms) to 132 (very severe). They were particularly interested in how people scored after the 12-week period of no injections at the end of the study. Each assessment was performed first thing in the morning before they had taken their usual dopaminergic medication and then one hour after taking their dopaminergic medication.

The data was analysed on the basis of what drug people were supposed to have taken, regardless of whether they continued on that treatment for the whole of the study. This is an appropriate way of analysing this kind of data.


What were the basic results?

At 60 weeks, before taking their daily dopaminergic medication:

  • In the group receiving exenatide, people had an average improvement in MDS-UPDRS 3 shown by a reduction from 32.8 to 31.9 (change 1.0, 95% confidence interval [CI] 2.6 to 0.7).
  • Motor scores of the people in the placebo group had on average worsened, from 27.1 to 29.2 (change 2.1, 95% CI 0.6 to 4.8).
  • There was an average difference between the two groups of 3.5 (95% CI 6.7 to 0.3), meaning that people in the placebo group overall had worse motor scores than those receiving exenatide.
  • There were no statistically significant results in any other part of the MDS-UPDRS score such as MDS-UPDRS 1 which assesses mood, or MDS-UPDRS 2 which looks at how badly daily activities of life have been affected.

After taking their daily dopaminergic drugs:

  • The scores on the MDS-UPDRS 3 improved in the exenatide group to 19.9 and in the placebo group to 14.5.
  • There were no differences between the two groups on any other part of the MDS-UPDRS either at 48 or 60 weeks.


How did the researchers interpret the results?

The researchers highlighted the benefit on motor scores of taking exenatide, but acknowledged that there was no difference in scores between the two groups in the other parts of the MDS-UPDRS while taking the drug. They also noted no difference was observed between the two groups of people when looking at their mood, cognition, non-motor symptoms, dyskinesia (involuntary movements like tremors) and quality of life.
The researchers also noted some small differences at the beginning of the study between the two groups. People in the exenatide group were slightly older, had higher baseline MDS-UPDRS 3 scores, and had lower Levodopa equivalent doses than people in the placebo group.

While RCTs try to match different groups as much as possible, this can be harder in trials with smaller populations, such as this one.



This research shows some interesting early findings, though the magnitude of effect was very small compared to the improvements in symptoms with current dopaminergic drugs. The study was well conducted but did have some limitations:

  • The number of people taking part was quite small. This may have meant it was hard to detect any other benefits or harms of taking the drug other than the effects on motor scores.
  • The period of time people were given the drug and followed up meant that longer-term effects could not be measured.
  • The benefit of the drug observed so far might not be big enough to make a difference to people's day-to-day lives, but this may change with a longer or larger study.

Overall, this well-designed piece of research indicates that it would be worth carrying out further studies of longer-term outcomes in bigger populations.

It could well be the case that a repurposed version of exenatide, or similar GLP-1 agonist, could prove more successful.

Links To The Headlines

Diabetes drug could help those living with Parkinson's disease, research reveals. The Guardian, August 4 2017

First hints Parkinson's can be stopped. BBC News, August 4 2017

Type 2 diabetes drug could combat Parkinson's: Test results suggest treatment could stop the disease in its tracks. Mail Online, August 4 2017

Cheap diabetes drug exenatide helps Parkinson’s patients move. The Times, August 4 2017 (subscription required)

Links To Science

Athauda D, Maclagan K, Skene SS, et al. Exenatide once weekly versus placebo in Parkinson's disease: a randomised, double-blind, placebo-controlled trial. The Lancet. Published online August 3 2017

Gene editing used to repair diseased genes in embryos

NHS Choices - Behind the Headlines -

"Deadly gene mutations removed from human embryos in landmark study," reports The Guardian. Researchers have used a gene-editing technique to repair faults in DNA that can cause the often-fatal heart condition, hypertrophic cardiomyopathy.

This inherited heart condition is caused by a genetic change (mutation) in one or more genes. Babies born with hypertrophic cardiomyopathy have diseased and stiff heart muscles, which can lead to sudden unexpected death in childhood and in young athletes; often because they don't realise they have the condition and so put their heart under strain when exercising.

In this latest study researchers used a technique called CRISPR-cas9 to target and then remove faulty genes. CRISPR-cas9 acts like a pair of molecular scissors, allowing scientists to cut out certain sections of DNA. The technique has attracted a great deal of excitement in the scientific community since it was released in 2014. But as yet, there have been no practical applications for human health.

The research is at an early stage and cannot legally be used as treatment to help families affected by hypertrophic cardiomyopathy. And none of the modified embryos were implanted in the womb.

While the technique showed a high degree of accuracy, it's unclear whether it is safe enough to be developed as a treatment. The sperm used in the study came from just one man with faulty genes, so the study needs to be repeated using cells from other people, to be sure the findings can be replicated.

Scientists say it is now important for society to start a discussion about the ethical and legal implications of the technology. It is currently against the law to implant genetically altered human embryos to create a pregnancy, although such embryos can be developed for research.


Where did the story come from?

The study was carried out by researchers from Oregon Health and Science University and the Salk Institute for Biological Studies in the US, the Institute for Basic Science and Seoul University in Korea, and BGI-Shenzen and BGI-Quingdao in China. It was funded by Oregon Health and Science University, the Institute for Basic Science, the G. Harold and Leila Y. Mathers Charitable Foundation, the Moxie Foundation and the Leona M. and Harry
 B. Helmsley Charitable Trust and the Shenzhen Municipal Government of China. The study was published in the peer-reviewed journal Nature.

The Guardian carried a clear and accurate report of the study. While the reports from ITV News, Sky News and The Independent were mostly accurate, they over-stated the current stage of research, with Sky News and ITV News saying it could eradicate "thousands of inherited conditions" and the Independent claiming it "opens the possibility for inherited diseases to be wiped out entirely." While this may be possible, we don't know whether other inherited diseases might be as easily targeted as this gene mutation.

Finally, the Daily Mail rolls out the arguably tired cliché of the technique leading to "designer babies", which seems irrelevant at this point. The CRISPR-cas9 technique is only in its infancy and (ethics aside) it's simply not possible to use genetic editing to select desirable characteristics – most of which are not the result of one single, identifiable gene. No reputable scientist would attempt such a procedure.


What kind of research was this?

This was a series of experiments carried out in laboratories, to test the effects of the CRISPR-Cas9 technique on human cells and embryos.

This type of scientific research helps us understand more about genes and how they can be changed by technology. It doesn't tell us what the effects would be if this was used as a treatment.


What did the research involve?

Researchers carried out a series of experiments on human cells, using the CRISPR-cas9 technique first on modified skin cells, then on very early embryos, and then on eggs at the point of fertilisation by sperm. They used genetic sequencing and analysis to assess the effects of these different experiments on cells and how they developed, up to five days.

They looked specifically to see what proportion of cells carrying faulty mutations could be repaired, whether the process caused other unwanted mutations, and whether the process repaired all, or just some of, the cells in an embryo.

They used skin cells (which were modified into stem cells) and sperm from one man, who carried the MYBPC3 mutation in his genome, and donor eggs from women without the genetic mutation. This is the mutation known to cause hypertrophic cardiomyopathy.

Normally in such cases, roughly half the embryos would have the mutation and half would not, as there's a 50-50 chance of the embryo inheriting the male or female version of the gene.

The CRISPR-cas9 technique can be used to select and delete specific genes from a strand of DNA. When this happens, usually the cut ends of the strand join together, but this causes problems so can't be used in the treatment of humans. The scientists created a genetic template of the healthy version of the gene, which they introduced at the same time as using CRISPR-cas9 to cut the mutated gene. They hoped the DNA would repair itself with a healthy version of the gene.

One important problem with changing genetic material is the development of "mosaic" embryos, where some of the cells have corrected genetic material and others have the original faulty gene. If this happened, doctors would not be able to tell whether or not an embryo was healthy.

The scientists needed to test all the cells in the embryos produced in the experiment, to see whether all cells had the corrected gene or whether the technique had resulted in a mixture.

They also did whole genome sequencing on some embryos, to test for unrelated genetic changes that might have been introduced accidentally during the process.

All embryos in the study were destroyed, in line with legislation about genetic research on embryos.


What were the basic results?

Researchers found that the technique worked on some of the stem cells and embryos, but worked best when used at the point of fertilisation of the egg. There were important differences between the way the repair worked on the stem cells and the egg.

  • Only 28% of the stem cells were affected by the CRISPR-cas9 technique. Of these, most repaired themselves by joining the ends together, and only 41% were repaired by using a corrected version of the gene.
  • 67% of the embryos exposed to CRISPR-cas9 had only the correct version of the gene – higher than the 50% that would have been expected had the technique not been used. 33% of embryos had the mutated version of the gene, either in some or all of their cells.
  • Importantly, the embryos didn't seem to use the "template" injected into the zygote to carry out the repair, in the way the stem cells did. They used the female version of the healthy gene to carry out the repair, instead.
  • Of the embryos created using CRISPR-cas9 at the point of fertilisation, 72% had the correct version of the gene in all their cells, and 28% had the mutated version of the gene in all their cells. No embryos were mosaic – a mixture of cells with different genomes.

The researchers found no evidence of mutations induced by the technique, when they examined the cells in a variety of ways. However, they did find some evidence of gene deletions caused by DNA strands splicing (joining) themselves together without repairing the faulty gene.


How did the researchers interpret the results?

The researchers say they have demonstrated how human embryos "employ a different DNA damage repair system" to adult stem cells, which can be used to repair breaks in DNA made using the CRISPR-cas9 gene-editing technique.

They say that "targeted gene correction" could "potentially rescue a substantial portion of mutant human embryos", and increase the numbers available for transfer for couples using pre-implantation diagnosis during IVF treatment.

However, they caution that "despite remarkable targeting efficiency", CRISPR-cas9-treated embryos would not currently be suitable for transfer. "Genome editing approaches must be further optimised before clinical application" can be considered, they say.



Currently, genetically-inherited conditions like hypertrophic cardiomyopathy cannot be cured, only managed to reduce the risk of sudden cardiac death. For couples where one partner carries the mutated gene, the only option to avoid passing it onto their children is pre-implantation genetic diagnosis. This involves using IVF to create embryos, then testing a cell of the embryo to see whether it carries the healthy or mutated version of the gene. Embryos with healthy versions of the gene are then selected for implantation in the womb.

Problems arise if too few or none of the embryos have the correct version of the gene. The researchers suggest their technique could be used to increase the numbers of suitable embryos.

However, the research is still at an early stage and has not yet been shown to be safe or effective enough to be considered as a treatment.

The other major factor is ethics and the law. Some people worry that gene editing could lead to "designer babies," where couples use the tool to select attributes like hair colour, or even intelligence. At present, gene editing could not do this. Most of our characteristics, especially something as complex as intelligence, are not the result of one single, identifiable gene, so could not be selected in this way. And it's likely that, even if gene editing treatments became legally available, they would be restricted to medical conditions.

Designer babies aside, society needs to consider what is acceptable in terms of editing human genetic material in embryos. Some people think that this type of technique is "playing God" or is ethically unacceptable because it involves discarding embryos that carry faulty genes. Others think that it's rational to use the scientific techniques we have developed to eliminate causes of suffering, such as inherited diseases.

This research shows that the questions of how we want to legislate for this type of technique are becoming pressing. While the technology is not there yet, it is advancing quickly. This research shows just how close we are getting to making genetic editing of human embryos a reality.

Links To The Headlines

Deadly gene mutations removed from human embryos in landmark study. The Guardian, August 2 2017

Human embryo editing breakthrough is a ‘major advance’ towards controversial treatments for babies. The Independent, August 2 2017

Scientists edit genes in human embryos to prevent inherited diseases. Sky News, August 2 2017

Ethical concerns over dawn of the designer baby: Campaigners warn breakthrough that removed faulty DNA could lead to creation of 'superior' children with genes modified to improve appearance or intelligence. Mail Online, August 3 2017

Human embryos edited to stop disease. BBC News, August 2 2017

Links To Science

Ma H, Marti-Gutierrez N, Park S, et al. Correction of a pathogenic gene mutation in human embryos. Nature. Published online August 2 2017

Kitchen sponges may be a 'bacteria hotspot' – but no need to worry

NHS Choices - Behind the Headlines -

"Study finds just a sugar-cube sized piece of kitchen sponge can contain 54 BILLION bacterial cells," the Mail Online reports. A German study sampled 14 different kitchen sponges and found they contained far more bacteria than expected.

Genetic analysis revealed the used sponges contained billions of bacteria, from 362 species-like groups called "operational taxonomic units" (OTUs).

However, it's not clear that any would be harmful in the context of someone's typical exposure to a kitchen sponge, despite 5 of the 10 most common OTUs found being bacteria from "risk group 2" (RG2) – a classification including bacteria that may cause disease in certain circumstances.

For example, researchers found high levels of the Acinetobacter strain of bacteria. This can cause potentially serious infections – but only if it penetrates deep inside the body, or infects traumatic wounds or burns.

People associate bacteria with germs. But we are all covered in bacteria, inside and out, and so are our homes. Most are either harmless or actually play a useful role in biological processes, such as digestion. Only a few cause diseases, so the fact kitchen sponges harbour bacteria is not as alarming as it sounds.

The researchers found that methods to clean sponges, such as heating them in microwaves to kill bacteria, don't work particularly well. They suggest replacing sponges weekly rather than cleaning and re-using them.

Where did the story come from?

The study was carried out by researchers from Justus-Liebig University Giessen, Furtwangen University and the German Research Centre for Environmental Health, all in Germany. It was funded by the Institute of Applied Research (IAF) of Furtwangen University and published in the peer-reviewed journal Nature Scientific Reports on an open-access basis, so it can be read online free of charge.

The Mail Online carried a reasonably accurate report of the research. However, it made much of the fact that some of the bacteria identified came from RG2, a class that includes "bacteria that cause typhoid fever, the plague, cholera and food poisoning". While this is correct, the researchers did not find any of the actual bacteria that cause these conditions in the sponges tested.

What kind of research was this?

This was a genetic analysis of a small sample of kitchen sponges to assess the number, variety and density of bacteria living on and within them.

This type of study can investigate the amount and type of bacteria present in the sponges. However, it can't tell us where the bacteria came from or how they may have affected the health of the people using the sponges.

What did the research involve?

Researchers collected 14 used kitchen sponges from houses in a German town, along with information about how regularly sponges were changed and whether they were specially cleaned to remove bacteria. The type, number and density of bacteria within the sponges were assessed using the latest genome sequencing techniques and a microscopy visualisation technique.

Most previous studies of bacteria in kitchens and kitchen accessories – such as dishcloths and sponges – used bacterial culturing, which can only detect species that can be grown on culture plates in the laboratory. This study used a genetic sequencing technique, called 454-pyrosequencing, of 16S RNA genes to find a much larger range of bacteria, including those that are difficult or impossible to culture in the laboratory.

Laser scanning microscopy was used on fixed samples of sponge to visualise the numbers and density of bacteria.

The researchers grouped the bacteria into OTUs, which was a way of classifying closely related bacteria so they could then divide them into types that might cause infection.

They also checked to see if cleaning the sponges using special processes, such as microwaving them, affected the number or types of bacteria found.

What were the basic results?

The researchers found billions of bacteria on the sponges' surfaces and the walls of their interior spaces. Among these, gene sequencing identified 362 OTUs, the majority of which were related to the gammaproteobacteria phylum (a group of classes that share distinctive characteristics).

The 10 most frequently found OTUs were responsible for almost 70% of all the gene sequences found on the sponges, and 5 of these 10 fell into the "German Technical Rule for Biological Agents Risk Group 2", suggesting they may have the potential to cause disease in humans.

The researchers didn't find any signs of salmonella, proteus or campylobacter, which are known to cause food poisoning and would be concerning to see in a kitchen or similar environment.

Imaging showed that most of the bacteria were still growing at the time of analysis. The highest density of bacteria recorded was 54 billion bacterial cells in a 1cm cube of sponge.

How did the researchers interpret the results?

The researchers concluded that "kitchen sponges harbour a higher bacterial diversity than previously thought" but "human pathogens [disease-causing bacteria] might represent just a minority" of the bacteria found.

They added: "Sponge sanitation methods appear not sufficient to effectively reduce the bacterial load and might even increase the shares of RG2-related bacteria."

Instead of attempting to clean sponges, they suggest "a regular (and easily affordable) replacement of kitchen sponges, for example on a weekly basis".


There's no need to panic about the results of this study. Bacteria are everywhere, so it's no surprise to find them growing in kitchens. The researchers say sponges, being porous and usually damp, represent ideal conditions for bacteria to grow.

The study found that one of the most dominant types of bacteria came from the Moraxella family. These bacteria are often found on human skin, so it's likely they got onto the sponges from people's hands. Moraxella are also linked to the unpleasant smell sometimes found after laundry has taken longer to dry, so they seem to be common in the household environment. 

The study has a few limitations. As only 14 sponges from one area of Germany were tested, we don't know if the results would apply to households in other parts of the world.

The researchers say the relation of the ONU gene sequences to RG2 species provides "only a weak indicator for the pathogenic potential of the identified bacteria" and that they are "not aware of any case in which an infection from these bacteria was explicitly reported from a domestic environment". The technology is not yet precise enough to show that any specific bacteria found growing in sponges causes disease.

However, we do know poor kitchen hygiene can lead to infections, especially when preparing uncooked food, such as salad or raw chicken. Bacteria-laden sponges, if used to wipe down surfaces, could spread pathogenic bacteria around and make infection more likely. You might want to consider simply replacing your sponge regularly, instead of rinsing it in hot water or zapping it in the microwave.

Read more advice about Food safety and home hygiene.

Links To The Headlines

You'll never do the dishes in the same way again: Study finds just a sugar-cube sized piece of kitchen sponge can contain 54 BILLION bacterial cells. Mail Online, August 2 2017

Links To Science

Cardinale M, Kaiser D, Lueders T, et al. Microbiome analysis and confocal microscopy of used kitchen sponges reveal massive colonization by Acinetobacter, Moraxella and Chryseobacterium species. Scientific Reports. Published online July 19 2017

Could discovery of 'fat switch' cure obesity?

NHS Choices - Behind the Headlines -

"Obesity cure possible after discovery of fat 'switch'," is the somewhat premature headline in The Daily Telegraph.

Researchers have identified a "biological switch" that controls when fat cells convert fat into energy for the body. But the headline fails to make it clear that this discovery was in mice, not humans.

Current thinking is that fat cells start off as "beige", where they're essentially in a neutral state. They can then be converted into either white or brown fat cells.

White fat cells store energy and can contribute towards obesity. Brown fat cells are primed to burn energy by warming the body.

It's possible for white fat cells to be converted into brown fat cells – by fasting, for example – in a process known as browning. In some cases, brown fat cells can switch back to being white fat cells again.

This study looked at this process in mice and found a mechanism that controls this switch. It involved an area of the brain called the hypothalamus and a protein called TCPTP, which acts on insulin receptors.

Researchers found the switch was stuck in obese mice and they were in energy-storing mode all the time, promoting weight gain.

But we don't yet know if the switch would be the same in humans, and to what extent it contributes to obesity.

Interfering with neural pathways in the brain could have unintended consequences, so any drugs developed to target the process would need thorough testing to make sure they're safe.

For now, the best way to achieve a healthy weight is to stay active and eat a balanced diet.

Where did the story come from?

The study was carried out by researchers from Monash University in Australia, and the Department of Neuronal Control of Metabolism in Cologne, University Hospital Cologne, the University of Cologne, and the National Center for Diabetes Research, all in Germany.

The research was funded by the NHMRC of Australia, the Diabetes Australia Research Trust, and the National Imaging Facility.

It was published in the peer-reviewed journal Cell Metabolism.

The UK media coverage of this research was generally accurate, although The Guardian failed to mention anywhere in their article the research was conducted in mice.

Any talk of a cure for obesity being found, as suggested by The Daily Telegraph, is premature.

The study's results can't be directly linked to human biology. There's no way of knowing yet if fat control mechanisms in human brains work in the same way.

What kind of research was this?

This experimental research was carried out in mice to understand the mechanism behind the storage or expenditure of energy in normal and obese mice, as well as during feeding or fasting stages.

This kind of research is very useful for showing how biological mechanisms might potentially work in humans.

But the research is at a very early stage, and there's a long way to go before therapies or treatments might be available for humans.

What did the research involve?

The researchers looked at brain scans, blood tests and metabolic measurements in mice to examine how the mechanisms in a part of the brain called the hypothalamus work in response to feeding and fasting, and see how these might potentially work in humans.

The hypothalamus is responsible for regulating a number of essential biological processes, including appetite, and regulating body temperature.

The specific area in the hypothalamus the researchers were interested in was the insulin receptor TCPTP.

The researchers looked at the mice's ability to use energy just after a meal and store energy in between meals by preventing or allowing the action of insulin.

Insulin levels rise after eating as blood glucose levels rise, causing the brain to send signals to start "browning" fat so energy is expended. When insulin levels lower, energy starts to be conserved again.

The researchers looked at beige fat cells and their ability to switch between white fat cell-like states (energy storage) and brown-like states (energy expended).

They also looked at the mechanism that controls these beige fat cells, how this mechanism changes according to eating or fasting patterns (and therefore insulin levels), and whether there are any differences in this mechanism in obese mice.

What were the basic results?

The researchers found beige fat cells' ability to switch between energy storage versus expenditure was important in a feeding versus fasting context.

They found this was co-ordinated by the hypothalamus and the action of TCPTP on insulin receptors in this area of the brain.

Hypothalamic TCPTP was increased during the fasting phase, which prevented insulin signalling, resulting in less browning of the white fat cells and therefore less energy expenditure.

Hypothalamic TCPTP decreased during the feeding phase, increasing insulin signalling and resulting in more browning of the white fat cells and more energy expended.

The ability to suppress the hypothalamic TCPTP as a result of feeding didn't work as effectively in obese mice.

Removing hypothalamic TCPTP in obese mice restored browning of the beige fat cells after feeding, increasing energy expenditure once more to promote weight loss.

Mice without hypothalamic TCPTP didn't become obese when overfed.

How did the researchers interpret the results?

The researchers concluded: "Our studies indicate that the energy expenditure specifically associated with feeding in chow-fed lean mice is reduced in diet-induced obesity.

"The promotion of feeding-induced energy expenditure may provide an approach by which to combat obesity." 


This early-stage research suggests there is potentially a mechanism by which energy expenditure and storage is controlled in normal-weight mice versus obese mice.

Removing a protein called hypothalamic TCPTP, which acts as the "switch" for fat storage, promoted weight loss in obese mice.

This might give us some insight into how weight loss could be promoted in obese humans by turning this switch off.

But at this stage, this is just a hypothesis – we can't assume the same is true for humans. Many therapies and procedures that appear promising at the outset aren't always successful in humans.

Given the major disease burden caused by obesity, finding ways to reduce its prevalence is a crucial area of research.

For now, the best way to achieve a healthy weight is to stay active and eat a balanced diet.

Links To The Headlines

Obesity cure possible after discovery of fat 'switch'. The Daily Telegraph, August 1 2017

Brain 'on switch' for burning fat after meal discovered by scientists. The Independent, August 1 2017

'Switch' in brain of obese people stays on all the time, researchers say. The Guardian, August 1 2017

Researchers find switch in the brain that tells the body to start burning fat after a meal. Mail Online, August 2 2017

Links To Science

Dodd GT, Andrews ZB, Simonds SE, et al. A Hypothalamic Phosphatase Switch Coordinates Energy Expenditure with Feeding. Cell Metabolism. Published online August 1 2017

More older adults 'may benefit from taking statins,' study reports

NHS Choices - Behind the Headlines -

"Nearly all men over 60 and women over 75 eligible for statins, analysis suggests," The Guardian reports.

This is the finding of a study that aimed to see how many people in England would qualify for statin use if the 2014 NICE guidelines for statin therapy in adults were followed.

Statins are drugs designed to lower cholesterol, and in turn reduce the risk of a person developing a cardiovascular disease (CVD). The drugs are crucial for preventing another event occurring in people who already have CVD.

In 2014, the National Institute for Health and Care Excellence (NICE) produced guidelines that recommended that statins should also be prescribed for people with a 10% risk of developing CVD in the next 10 years.

The health watchdog selected a risk assessment tool called QRISK2 to estimate a person's risk of CVD based on a number of factors, such as body mass index (BMI), smoking history and whether family members had developed CVD.

This study cross-checked the NICE guidelines on statins with data from the 2011 Health Survey for England.

It found all men over 70 and all women aged 65-75 could potentially be offered statins based on the CVD risk associated with their age alone, regardless of how healthy they were.

Currently, around four million people are being treated with statins, so this would mean treating an extra seven million people.

It's not clear whether this would add to the NHS budget or actually save money in the long term by reducing the number of people who go on to develop CVD.

If you're concerned about your CVD risk, talk to your GP about the pros and cons of treatment.

Other ways to reduce your risk of CVD include stopping smoking, being more active, drinking less alcohol, eating more healthily, and achieving or maintaining a healthy weight.

Where did the story come from?

The study was carried out by an international team of researchers from the Harvard TH Chan School of Public Health in the US, and the University of New South Wales and the University of Melbourne in Australia.

The researchers were funded by the Swedish Society of Medicine and Gålöstiftelsen, and the HCF Research Foundation.

They also used data from the Health Survey for England, which was funded by the Department of Health and the Health and Social Care Information Centre.

The study was published in the peer-reviewed British Journal of General Practice.

Coverage of the study in the UK press was mixed.

Some papers accurately reported the results of the research, providing useful information from independent experts, who discussed how statins fitted into the bigger picture of preventing CVD.

Other outlets were less helpful, focusing more on other aspects of the debate on whether or not people should take statins.

The Times' headline "Give statins to almost all men over 60, GPs are told" is misleading as it implies that the study made definitive recommendations on public health policy, which it did not.

What kind of research was this?

The aim of this study was to see how many people in England would qualify for statin use if the 2014 NICE guidelines for statin therapy in adults were followed.

This cross-sectional study took a sample of people at a single point in time.

The researchers used data taken from the Health Survey for England (HSE), which is carried out every year to look at health and health-related behaviour in a sample of adults and children.

The information provided by that survey was used to calculate people's risk of CVD to see whether or not they would be eligible for statins.

The researchers then used their findings to estimate how many people in the whole English population might be offered the drugs.

What did the research involve?

The 2014 NICE guidelines say that people who don't have a history of CVD and who have a risk of 10% or more of having CVD in the next 10 years should be offered statins to reduce their risk.

A person's CVD risk is based on the results of a computer-based tool called QRISK2, which uses information about people's lifestyle and health to make predictions about their future health.

The researchers first looked at the QRISK2 tool to see how the results of the tool varied according to what information was provided about the various risk factors it looks at. They then explored how the tool classified people's risk using data from the HSE study.

The researchers took data from a single year of the HSE in 2011. The people from that year who were eligible for this study:

  • were aged between 30 and 84 years old
  • had provided a blood sample
  • had answered questions about lifetime history of CVD
  • didn't have data missing that would be needed for the QRISK2 tool

In total, 2,972 people were included in the study. The researchers calculated a QRISK2 result for each of the study participants.

They then compared the results with the general population to estimate how many people in the whole of England might be eligible for statins.

The analysis carried out was suitable for this type of study. But the decision to exclude people who had data missing on some risk factors could introduce bias in the results if these people were different from the people included in the study.

What were the basic results?

The researchers estimated that all men over the age of 70 and all women aged 65-75 could potentially be offered statins, as all people in those groups would have a QRISK2 score of 10% or more.

This result applied even if they were otherwise healthy. For people with other risk factors, the age at which they might be offered statins would be lower. 

If the NICE guidelines were completely implemented, 11.8 million adults aged 30-84 could be offered statins to reduce their risk of CVD.

How did the researchers interpret the results?

The authors noted that the QRISK2 tool puts a lot of emphasis on age, which means older adults are likely to have statins recommended to them by this tool even if they don't have many other risk factors for CVD.

They also discussed some of the pros and cons, both for individuals and for the health service, of more people being prescribed statins.

For example, they estimated that if the NICE guidelines were followed, 290,000 CVD events might be prevented.

But more resources would be needed in the health service to properly screen, treat and monitor the patients who were offered statins.

Of the 9.8 million people without previous CVD who would be eligible for statins, 6.3 million aren't currently taking them.

The researchers stated that statin therapy should only be started following discussion between the doctor and patient, particularly if the main or only risk factor a person has is their age.


The study was an interesting analysis of how many more people in England could be eligible to receive statins than those currently receiving them.

It didn't make any recommendations about acting on these findings. The study was also unable to follow people over time to see whether statins might have made a difference.

And the study did have some limitations:

  • Because it only looked at people at one point in time, we don't know whether the people who were considered at risk of CVD actually went on to develop it.
  • The researchers were only able to use one year of data from HSE, as this was the only year that had the information they needed about people's history of CVD.
  • Using more data may have detected trends, as CVD risk has changed in the population over time.
  • The study assumed that people in the HSE population were representative of the general English population when estimating how many adults could be offered statins. Although the HSE study is designed to try to be representative, there may be situations the survey population doesn't match the general population for a specific risk factor or condition.

It's best to talk to your GP if you think you'd benefit from taking statins or you're already taking them but have questions.

If you can't take statins or don't want to take them, other ways you can lower your cholesterol include stopping smoking, being more active, drinking less alcohol, eating more healthily, and achieving or maintaining a healthy weight.

Links To The Headlines

Nearly all men over 60 and women over 75 eligible for statins, analysis suggests. The Guardian, August 1 2017

Statins should be made available for majority of over 60s, study claims. ITV News, August 1 2017

The statins divide: Harvard experts urge for the pill to be given to all men at 60 and women from 75 but other GPs warn they are being 'needlessly doled out'. Mail Online, August 1 2017

Statins: Almost every older person should be given potentially life-saving drugs, study finds. The Independent, August 1 2017

Give statins to almost all men over 60, GPs are told. The Times, August 1 2017 (subscription required)

Links To Science

Ueda P, Lung TW, Clarke P, Danaei G. Application of the 2014 NICE cholesterol guidelines in the English population: a cross-sectional analysis. British Journal of General Practice. Published online July 31 2017

Calls for GPs to offer HIV screening in high-risk areas

NHS Choices - Behind the Headlines -

"Offering routine HIV tests to people when they register with new GP surgeries in high-risk areas is cost-effective and could save lives," The Guardian reports.

The news comes from the findings of a large trial in the London Borough of Hackney.

Researchers wanted to see if offering HIV screening to new patients registering with GP surgeries would detect more people with the disease.

Based on the data from the trial, the researchers found screening led to HIV diagnosis in four times the number of people diagnosed without screening.

The researchers' calculations suggested that screening would provide good value for money when looking at the additional quality of life and lifespan it provided over more than 30 years.

They calculated it would cost the NHS £4 million a year to roll out the screening programme to all local authority areas with high rates of HIV.

Certain groups of people are at higher risk of contracting HIV – including men who have sex with men, and straight African men and women – and are advised to have regular tests.

If you're concerned you might have HIV, you can get tested free of charge on the NHS. Home testing kits are also available.

These days, HIV isn't usually a life-limiting condition if it's diagnosed and treated early. Read more about HIV testing

Where did the story come from?

The study was carried out by researchers from the London School of Hygiene and Tropical Medicine, University College London, Queen Mary University of London, NHS City and Hackney, Homerton University Hospital NHS Foundation Trust, and the University of Warwick in the UK, as well as the University of British Columbia in Canada.

The research was funded by NHS City and Hackney, the UK Department of Health, and the National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care.

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

The UK media's coverage of the story was mostly accurate, although some of the headlines aren't specific enough.

For example, the Mail Online reported that, "HIV tests should be given to everyone who registers with a GP, an NHS-funded study has recommended". 

But the study only recommends routine screening in parts of the country where there's a known prevalence of around 2 confirmed cases of HIV in every 1,000 adults.   

What kind of research was this?

This cost-effectiveness study looked at the impact of GP-based screening for HIV in adults in areas where HIV rates are relatively high.

Cost-effectiveness studies look at the impact of an intervention over a specified period of time, and calculate how much these cost compared with an alternative – in this case, not providing screening.

These types of studies are useful for decision makers, who need to decide which interventions offer good value for money.

This approach is also a good way to get up-to-date information about the impact of a potential screening programme.

But like all cost-effectiveness studies, some assumptions have to be made about what will happen in the future.

It's impossible to say for sure if these assumptions will turn out to be accurate – this only emerges in the years to come.

What did the research involve?

The researchers used the results of a randomised controlled trial (RCT) in Hackney (RHIVA2) that compared HIV screening when they registered with a GP with doing nothing at all.

Forty GP surgeries took part, with half offering screening to newly registered patients and half not offering screening. Screening was carried out using a rapid finger prick test.

The trial was carried out over 28 months, and HIV diagnosis rates were recorded in the screening practices (20 practices with 44,971 new registrants) and control practices (20 practices with 38,464 new registrants).

In the screening practices, all newly registered patients were given the test as part of registration unless they specifically asked not to have it.

Costs and impacts were projected for a 50-year period. The cost of either providing or not providing GP-based screening was then estimated.

The researchers also estimated health outcomes in the borough if people were or weren't offered screening. For example, they looked at how people's HIV progressed and how this would impact their quality of life and lifespan, and how many people they would pass the infection on to.

Where possible, the researchers used information collected in the RHIVA2 trial in their cost-effectiveness modelling.

If they didn't have the information they needed, they looked for other reliable sources or made assumptions based on what we already know.

They assumed that:

  • people have a long life expectancy after diagnosis because of effective treatment and care
  • after diagnosis, people are less infectious as a result of anti-retroviral therapy
  • after diagnosis, people permanently reduce their number of sexual partners by 25%
  • HIV prevalence in Hackney would stay constant

The researchers used their cost-effectiveness model to calculate how much more the GP-based screening programme would cost.

Health professionals use a measurement known as quality adjusted life year (QALY) as part of their assessment of whether an intervention is cost-effective. 

One QALY means one extra year of perfect health a person gains because of that intervention. For any intervention, researchers can calculate how much extra that intervention costs for each additional QALY it provides across the whole population.

The researchers also looked at:

  • how long it would take for GP-based screening to reach this cost-effectiveness threshold
  • the extra cost per death prevented over a 50-year period
  • the extra cost per case of HIV prevented
What were the basic results?

Over 28 months, GP practices that screened newly registered patients identified 32 people living with HIV who hadn't been diagnosed previously, compared with 14 in the control GP practices.

The key findings were:

  • The overall HIV diagnosis rate was four times higher in the screening group than control group – 0.30 per 10,000 patients per year (95% confidence interval [CI] 0.11 to 0.85) compared with 0.07 per 10,000 patients per year (95% credible interval [CrI] 0.02 to 0.20).
  • The total cost of the GP-based screening intervention was estimated to be £127,724.
  • The estimated average cost per HIV rapid test performed was £25.
  • The average cost per additional patient newly diagnosed because of screening was £7,096.

Based on the trial's findings, other UK data and the assumptions the researchers made, they calculated that:

  • It would take 33 years for screening to become cost-effective based on the commonly used UK threshold – that is, to reach an additional cost of £30,000 per QALY gained.
  • Over a 40-year time period, the cost per QALY would reduce to £22,201 per QALY gained (95% credible interval, CrI, £12,662 to £132,452).
  • By 50 years, cost per QALY would be well below the cost-effectiveness threshold at £16,543 per QALY gained (95% CrI £9,616 to £109,026).

Over the 40-year time period, the additional cost of screening per death prevented would be £372,207 (95% CrI £268,162 to £1,903,385), and £628 874 per HIV transmission prevented (95% CrI £434,902 to £4,740,724). 

How did the researchers interpret the results?

The researchers predicted that screening for HIV in areas of the UK with a high number of new cases will be cost-effective in the medium term.

They said that, "Although anti-retroviral therapy as a prevention intervention is very effective, and treatment coverage in the UK is high, the estimated number of people living with undiagnosed HIV remains substantial and the number of people living with HIV continues to increase.

"Patients should be diagnosed and treated earlier to effect meaningful reductions in transmission, along with ensuring that for those with a negative HIV test other prevention interventions, such as condom use and pre-exposure prophylaxis, are accessible and promoted."


The results of this study suggest it seems to be cost-effective to screen new patients for HIV when they register at a GP practice in areas where HIV is particularly prevalent.

This conclusion is based on projections making use of a wide range of data from the UK, and making certain assumptions about HIV prevalence over time and the behaviour of people who've been newly diagnosed with HIV.

The researchers used good methods, and their recommendation to roll out screening in areas where there are high rates of HIV is consistent with current National Institute for Health and Care Excellence (NICE) guidelines.

Studies like this help decision makers decide which interventions offer good value for money.

But the drawback with these types of studies is they rely on assumptions – and it's not possible to say for certain whether these assumptions are correct.

Other points to bear in mind about this study include:

  • The researchers may have over- or underestimated the cost-effectiveness of screening by assuming HIV rates in Hackney would stay the same and that people newly diagnosed with HIV would permanently change their sexual behaviours.
  • Injecting drug users weren't included in the modelling because reusing needles (which carries HIV risk) is in decline in the UK and HIV is uncommon in this group. But this might vary between regions.
  • The areas with similar HIV rates to Hackney the researchers suggest could potentially benefit from screening might have populations with different characteristics and sexual behaviours.
  • The analyses suggest the cost-effectiveness value for screening could fall within quite a wide range, including some values that suggest screening wouldn't be cost-effective at all.

These findings are in line with current UK guidelines, giving further weight to the recommendation that these measures are adopted and promoted in areas with high rates of HIV.

If you're concerned that you may have been exposed to HIV, contact your GP. Testing is free on the NHS. Home testing kits are also available from pharmacies.

Regular testing is recommended for men who have sex with men, and also sexually active straight people from Africa.

Read more about getting an HIV test.

Links To The Headlines

HIV tests for GPs' new patients could save lives and money, says study. The Guardian, July 30 2017

HIV tests for new GP patients 'can aid early diagnosis'. BBC News, July 31 2017

HIV screening in high risk areas could save lives and money – study. Sky News, July 31 2017

HIV tests 'should be offered to everyone in high risk areas when they enroll with new GP'. The Daily Telegraph, July 30 2017

Give every new patient an HIV test, GPs are told: Routine check would save lives by spotting the virus earlier. Mail Online, July 31 2017

Call to make family doctors test all patients for HIV. The Times, July 31 2017 (subscription needed)

Links To Science

Baggaley RF, Irvine MA, Leber W, et al. Cost-effectiveness of screening for HIV in primary care: a health economics modelling analysis. The Lancet HIV. Published online July 30 2017

Reports that frequent drinking prevents diabetes are inaccurate

NHS Choices - Behind the Headlines -

"Drinking a moderate amount of certain drinks such as wine three to four times a week reduced diabetes risk by about 30%," The Guardian reports. That was the main reported finding of a Danish study looking at the impact of alcohol on diabetes risk.

Researchers looked at a group of more than 70,000 people who had completed a survey about their health and lifestyle in 2007-2008, which included questions about their drinking habits. They then checked whether any of the participants had been diagnosed with diabetes (either type 1 or 2) about four years after completing the survey, and looked at survey data for these people.

The researchers noticed a pattern that suggested people who developed diabetes were less likely to have drunk alcohol moderately and frequently compared with those who did not develop diabetes. The researchers reported that the lower risk for diabetes was associated with 14 units per week for men and seven units for women (current recommendations are that men and women shouldn't regularly drink more than 14 units per week).

However, the study had various weaknesses, which means it cannot conclusively show that drinking frequently and moderately protects against diabetes. For example, people were only asked about their drinking habits and other lifestyle choices at a single time point. Also, the study doesn't tell us whether those habits changed over the period in which people were monitored for diabetes.

Even if an association does exist, there are far healthier ways to reduce your diabetes risk, such as achieving or maintaining a healthy weight.


Where did the story come from?

This study was an analysis of data from the general Danish population that had been recorded in a previous cohort study. This particular piece of research was carried out with no specific funding, but the survey data had been funded by the Ministry of the Interior and Health, and the Tryg Foundation. It was published in the peer-reviewed journal Diabetologia.

The suggestion that regularly drinking alcohol may be good for you was met with glee by the UK media. The limitations of the study, or the lack of a definitive cause and effect, were not reported fully.

However, some sources carried sensible advice from independent experts, such as Dr Emily Burns, the head of research communications at Diabetes UK, who was quoted in The Guardian as saying: "While these findings are interesting, we wouldn't recommend people see them as a green light to drink in excess of the existing NHS guidelines, especially as the impact of regular alcohol consumption on the risk of type 2 will be different from one person to the next."

There were several reports that wine was particularly beneficial because it has "a role in helping to manage blood sugar", but this was based only on the authors' comments rather than on the results of the research.


What kind of research was this?

This cohort study assessed people for diabetes in 2012 about four years after their lifestyles had been assessed in 2007-2008. The researchers aimed to examine whether there was any association between alcohol drinking patterns and the risk of developing diabetes in people who did not already have the condition. They looked at the amount that people drank, how often they drank, and what types of alcohol were consumed.

The study benefitted from involving a large number of people in the Danish population, which meant a range of drinking patterns were found, and there were sufficient numbers of cases of diabetes to look for associations.

However, a major weakness of the study was that it only looked at alcohol drinking patterns at a single point in time. And people's drinking habits are known to change over time according to their circumstances, preferences and other health issues.

The researchers did attempt to take into account other confounding factors (such as diet and exercise) that may have influenced the results, but these factors may not have been recorded in enough detail to be useful, and other factors might not have been recorded at all.


What did the research involve?

The researchers identified 70,551 people from the Danish Health Examination Survey (an ongoing nationwide study) who were eligible to participate. These people had already completed a questionnaire in 2007-2008 about their lifestyle and health. People had to meet the following criteria to be selected for participation:

  • no existing diagnosis of diabetes at the start of the study
  • not pregnant and haven't recently given birth (within the last six months)
  • have provided at least some information about their drinking habits in the questionnaire

Information about drinking patterns was collected from questionnaires that people completed by themselves on how often they drank, whether they ever binged and how often this happened, and how much they drank different types of drinks (beers, wines or spirits).

The researchers also looked at information that had been collected at the start of the study on the following confounding factors:

  • age
  • sex
  • body mass index
  • education
  • smoking status
  • diet
  • leisure-time physical activity
  • high blood pressure (current or previous)
  • family history of diabetes

A diagnosis of diabetes was recorded using the Danish National Diabetes Register, which uses five different sources to detect diabetes cases, but does not distinguish between type 1 and type 2. During the course of the study the researchers carried out a "sensitivity analysis", where they excluded two of the diabetes cases because of concerns the data was unreliable.

The participants were followed up in the study until it ended in December 2012, unless they emigrated, died or developed diabetes before then. The researchers carried out an analysis that looked at the risk of developing diabetes over time, taking into account different risk factors. They used appropriate statistical methods for dealing with missing data.


What were the basic results?

During the course of the study, 859 men and 887 women developed diabetes. When looking at the average amount that people drank over the course of a week, they found that the lowest risk of diabetes was observed in:

Frequency of drinking

After adjusting for other factors, the researchers reported the consumption of alcohol on three to four days a week was associated with a lower risk of developing diabetes for men: HR 0.73 (95% CI 0.59 to 0.94) and for women: HR 0.68 (95% CI 0.53 to 0.88).

The researchers also looked at binge drinking and found no clear link between binge drinking and risk of diabetes.

Type of alcohol

Researchers noticed a number of patterns in terms of what types of alcohol people drank.

Men who drank 1-6 glasses of beer a week were found to have lower diabetes risk than those who did not.

In contrast, women who regularly drank spirits seven or more times a week had an increased risk of diabetes compared with those who drank spirits once a week or less. However, the researchers failed to take into account that some people drink a mixture of different types of alcohol either on a single occasion or over a week.


How did the researchers interpret the results?

The authors concluded that "light to moderate" alcohol consumption was associated with a lower risk of diabetes when compared to no alcohol consumption at all. They also noted that frequent consumption was associated with the lowest risk, even after taking into account the amount people drank on average during a week.

They noted that the strengths of their study included its size, the fact that they distinguished between people who currently didn't drink from those who had never drunk at all, and that their results were consistent even when they adjusted various conditions.  



Although this study found an interesting association between alcohol drinking habits and risk of developing diabetes, this study does not present strong enough evidence to recommend adopting a particular drinking pattern to reduce diabetes risk.

This study had a number of limitations that weaken confidence in the results:

  • People were only asked about their drinking habits and other risk factors at a single time point. The study doesn't tell us whether those habits changed over the period in which people were monitored for diabetes. Most studies related to alcohol consumption also run the risk that people are not always completely accurate when describing what and how much they drink.
  • The way diabetes cases were recorded for the study did not distinguish between type 1 and type 2 diabetes, even though these conditions have different causes and treatments.
  • The study only followed people up for an average of just under five years, whereas a condition like diabetes may develop due to risk factors experienced over a longer period.
  • The information collected on diet may have been too simplistic to properly allow an understanding of how nutrition may also affect the diabetes risk of the people in the study.
  • Although the researchers excluded people from the study if they already had a diagnosis of diabetes at baseline, they didn't exclude people if they had other chronic health conditions, some of which may contribute to diabetes risk. The only other condition that was considered in the analysis was high blood pressure.

Overall, it is unclear whether the link between moderate alcohol drinking and diabetes is real. It is not proof that starting to drink more, especially for those who do not currently drink, is useful in preventing diabetes. There are other risks, such as liver damage, to consider when drinking frequent or large volumes of alcohol above recommended limits.

If you are concerned that you might be at risk of developing diabetes, speak to your GP about the ways that lifestyle change can reduce your risk.

Links To The Headlines

Regular alcohol consumption could cut diabetes risk, study finds. The Guardian, July 28 2017

Drinking a few times a week 'reduces diabetes risk'. BBC News, July 28 2017

Drinking alcohol three to four days a week 'could reduce risk of diabetes'. The Independent, July 28 2017

Drinking wine three times a week 'cuts diabetes': Risk can be reduced by nearly a third by consuming alcohol 'little and often'. Mail Online, July 28 2017

Drinking most days may protect against diabetes - new study. The Daily Telegraph, July 28 2017

Drinking alcohol regularly could cut diabetes risk - and red wine is your 'healthiest' option. Daily Mirror, July 28 2017

Links To Science

Holst C, Becker U, Jørgensen ME, et al. Alcohol drinking patterns and risk of diabetes: a cohort study of 70,551 men and women from the general Danish population. Diabetologia. Published online July 27 2017

Questions over advice to finish courses of antibiotics

NHS Choices - Behind the Headlines -

"Should you finish a course of antibiotics?" asks BBC Online. The question is prompted by a new review suggesting concerns around antibiotic treatment are driven by fears of under-treatment, when we should instead be concerned about over-use.

Patients have always been advised to finish their course of antibiotics even if they're feeling better. The reasons given are that this will stop the infection from returning, as well as reduce the risk of the bacteria becoming resistant to the antibiotics.

The researchers behind this review challenge these established ideas by suggesting that shortening the course of antibiotic treatment could be just as effective and that "finishing the course" could actually be making the problem of antibiotic resistance worse.

As interesting as this review is, it's important to be aware of the type of research this was. It is a narrative review, which means it was a review that discusses evidence about a particular topic.

It is unclear how the authors picked the evidence that informed this piece. Reviews of this type are always vulnerable to accusations of "cherry-picking", where researchers include evidence that supports their argument while ignoring evidence that doesn't.

Guidelines on prescribing are not set in stone and are constantly being revised. It could be the case that this review leads to a change in recommendations. But until any changes are announced, it is a good idea to take your antibiotics as prescribed, even if you are feeling better.


Who produced this review?

This narrative review was written by researchers from several UK institutions, including Brighton and Sussex Medical School, the University of Oxford and the University of Southampton. It was published in the peer-reviewed British Medical Journal and is free to read online (PDF, 1Mb).

Generally the UK media's coverage was accurate and balanced. The majority of reporting referred to the review as an "opinion piece" and highlighted the importance of people continuing to follow doctors' advice to complete a prescribed antibiotic course.


What is antibiotic resistance?

Antibiotic resistance can build up after bacteria have become repeatedly exposed to antibiotics. The bacteria change or adapt so they are no longer affected by the antibiotic. This renders antibiotics ineffective against infections they were previously able to treat.

It has been widely accepted that stopping antibiotic treatment early encourages bacteria to develop antibiotic resistance. As a result, current medical advice is to finish taking a prescribed course of antibiotics as recommended by a healthcare professional, even if you start to feel better.


What does this review say?

This review challenges current medical advice by suggesting that concerns around antibiotic treatment are driven by fears of "under-treatment", where the course of antibiotics doesn't last long enough to clear any infection, when the concern should be more about over-use.

The authors of the piece make the point that when antibiotics were first used during the 1940s, there was little awareness of the problems of antibiotic resistance, so the concept of "over-use" was never even considered.

In summary, the review raises the following points:

  • Only a limited number of studies have investigated the minimum treatment period needed for antibiotics to be effective. There is little or poor evidence to support the idea that shorter treatments would lead to an increased risk of antibiotic resistance or treatment failure. The authors do, however, acknowledge that some trials have found that for certain conditions, shorter treatment has compromised recovery.
  • Always prescribing a fixed number of days for a course of antibiotics can potentially overlook individual patient characteristics, such as the fact that some patients may respond differently to the antibiotics. For example, a patient's previous antibiotic exposure is not necessarily considered.
  • It is difficult to test the theory that a shorter antibiotic course may be just as effective as a longer one, because the importance of completing a full course of antibiotic treatment is so deeply embedded in both doctors and patients.
  • Public health education around antibiotics needs to highlight that antibiotic resistance is the result of the overuse of antibiotics by patients, and that it cannot be prevented by completing a course. Simpler messages should be issued, such as, "stop when you feel better."


What evidence is this based on?

The researchers of this narrative review say they have used data from randomised controlled trials (RCTs) and observational cohort studies to inform the points made. However, there is no clear methodology so we don't know how the evidence was chosen and whether it was systematic in manner. So the reviewers run the risk of being accused of picking the evidence to support their hypothesis.

When testing a hypothesis like this, a systematic review or meta-analyses would have been the best approach to reviewing the evidence.



This narrative review challenges current medical advice that patients should complete their course of antibiotics, by suggesting that concerns around antibiotic treatment are driven by fears of under treatment, when we should instead be concerned about over use.

Professor Peter Openshaw, President of the British Society for Immunology and Professor of Experimental Medicine at Imperial College London commented:

"It could be that antibiotics should be used only to reduce the bacterial burden to a level that can be coped with by the person's own immune system. In many previously healthy patients with acute infections, letting them stop the antibiotics once they feel better has considerable appeal. However, there are clearly circumstances where antibiotics should be given for extended periods."

"Ideally, there should be clinical trials to support the duration of therapy but in the meantime it should be up to the prescriber to recommend how long to continue treatment."

Professor Mark Woolhouse, Professor of Infectious Disease Epidemiology at the University of Edinburgh, said:

"The article underlines that educating not only patients but also doctors is essential to changing current prescribing practices. It is very clear that prescribing practices do need to change; there is every indication that current volumes of antibiotic usage are too high to be sustainable. We need to start to use antibiotics more wisely before it's too late. The longer we delay, the worse the resistance problem will become."

This review raises some interesting points and the guidelines around antibiotic treatments may change in the future. However, for now it's best to stick with current advice to complete the full antibiotic course as prescribed.

Links To The Headlines

Rule that patients must finish antibiotics course is wrong, study says. The Guardian, July 26 2017

You SHOULDN'T always take full course of antibiotics: Experts now say taking drugs after you feel well may encourage risk of superbugs. Mail Online, July 27 2017

Should we really complete course of antibiotics? Sky News, July 27 2017

'Don't finish the course of antibiotics' - experts turn medical advice on its head. The Daily Telegraph, July 27 2017

Links To Science

Llewelyn MJ, Fitzpatrick JM, Darwin E, et al. The antibiotic course has had its day (PDF, 1Mb). BMJ. Published online July 26 2017

Eye screening linked to fall in sight loss in people with diabetes

NHS Choices - Behind the Headlines -

"The proportion of diabetics who go blind or suffer sight loss has almost halved since a new national retinopathy screening programme started in 2007," BBC News reports. The screening programme was in fact launched in 2003 but rolled out to all diabetic people over the age of 12 by 2007.

The main risk to vision for people with diabetes is diabetic retinopathy, a condition where high blood sugar levels damage the retina, leading to sight loss and even blindness.

Because of this, an NHS screening programme for people with diabetes in England and Wales was launched in 2003.

This latest study looked at patient data from Wales to assess whether the programme had been successful in preventing cases of sight loss arising from diabetic retinopathy.

Results suggest that it has been. The number and rate of people with diabetes who went on to have a Certificate of Visual Impairment decreased from 2008 to 2014.

This shows the potential of screening for diabetic retinopathy to prevent future sight loss, but detailed interpretation of the results is difficult without data from before the screening programme. The reduction could also be down to other factors, such as general increased awareness of diabetes and improvements in care.

If you have diabetes, whether type 1 or type 2, it's important to get your eyes checked once a year. If you haven't received a letter inviting you to a screening appointment in the past year, contact your GP.

Where did the story come from?

The study was carried out by researchers from Swansea University, Cardiff University, Cardiff and Vale University Health Board, Moorfields Eye Hospital and King's College London, all in the UK. The authors did not declare any competing interests.

It was funded by the Wales School of Primary Care Research and the Diabetes Research Unit Cymru.

The study was published in the peer-reviewed BMJ Open on an open-access basis, meaning it's freely available to read online.

The BBC reporting of the story was generally accurate, although the headline declaring "Diabetic sight loss cut by screening" is not necessarily correct, as there are a number of potential reasons for the reduction in sight loss in people with diabetes. 

What kind of research was this?

This was a retrospective analysis of data. This means the researchers looked back at data on the number of new certifications for visual impairment and blindness over a period of eight years to examine any trends – in this case, related to diabetic retinopathy.

This type of research is good at identifying possible associations. However, it cannot determine cause and effect, and therefore cannot prove that the implementation of screening directly caused a reduction in the number of people with visual impairment from diabetic retinopathy.

Diabetic retinopathy is related to type 1 and type 2 diabetes, as having high blood sugar levels damages the retina. It can lead to sight impairment (SI) and severe sight impairment (SSI) if not detected and treated early, and is therefore high on the public health agenda.

Diabetic retinopathy is one of the most common causes of sight loss among people of working age.

What did the research involve?

This was a retrospective analysis of data on the number of new certifications of SI and SSI where the main cause was diabetic retinopathy or maculopathy (diabetic eye disease affecting the central part of the retina). The data came from Wales, for the period 2007 to 2015.

The screening programme for diabetic retinopathy was launched in Wales in 2003 and, by the end of 2006, all people over the age of 12 in Wales known to have diabetes were offered an appointment for screening. This study aimed to see if earlier detection through screening was associated with a fall in cases of SI and SSI.

The level of sight impairment was assessed by looking at the clarity of vision (visual acuity) as well as the field of vision (for example, was there tunnel vision).

Researchers also looked at the population in Wales and the number of people with diabetes as recorded by relevant health statistics.

What were the basic results?

In Wales in 2014-15, there were 339 fewer new certifications for SI and SSI from any cause than there were in 2007-8. Specifically:

  • The rate of SI and SSI combined reduced from 3.6 (95% confidence interval [CI] 3.0 to 4.3) per 100,000 in 2007-8 to 2.8 (95% CI 2.2 to 3.4) per 100,000 people in 2014-15.
  • The rate of SI alone reduced from 2.1 (95% CI 1.7 to 2.7) per 100,000 in 2007-8 to 1.6 (95% CI 1.3 to 2.2) per 100,000 people in 2014-15.
  • The rate of SSI alone reduced from 1.4 (95% CI 1.0 to 1.8) per 100,000 in 2007-8 to 0.9 (95% CI 0.7 to 1.2) per 100,000 people in 2014-15.

Overall, the number of sight loss certifications due to diabetic retinopathy fell by 22 over this period, after an initial increase in 2008. In detail:

  • The number of new certifications for SI and SSI combined caused by diabetic retinopathy increased from 108 in 2007-8 to 140 in 2008-9.
  • The number then fell year on year from 2008-9 to 2014-15 to a total of 86, a 20.4% reduction from the original number of 108.
  • During the same eight-year period (2007-8 to 2014-15), the number of people with diabetes increased by 52,229, from 131,119 to 183,348.
How did the researchers interpret the results?

The researchers concluded: "Findings from this analysis provide positive and useful epidemiological information to assist in the future monitoring of diabetic eye disease in order to provide the basis for assessing the benefit or otherwise of changes in the management of diabetes and diabetic retinopathy/maculopathy."

They added that the analysis "highlights the positive benefits of introducing a community-based screening programme for the early detection of sight-threatening diabetic retinopathy".


The results indicate that since the introduction of the screening programme for diabetic retinopathy in Wales, the total number and rate of new certifications of sight impairment and severe sight impairment have decreased. This is despite an increase in the number of people diagnosed with diabetes.

The study shows a promising trend and highlights the possible benefit of such screening. However, there are some important considerations:

  • Reporting of visual loss currently requires a consultant ophthalmologist to complete a Certificate of Vision Impairment, and this isn't compulsory.
  • Patients may be reluctant to be registered as visually impaired/blind, so true numbers and rates might be underestimated.
  • Screening isn't the only thing that could have led to the decrease in certifications. It may also have been due to increased awareness of diabetes, improved referrals to specialists and better overall diabetes management, rather than the screening.

Everyone with diabetes aged 12 or over should be invited to have their eyes screened once a year.

You should receive a letter from your local Diabetic Eye Screening Service inviting you to attend an appointment. The letter will include a leaflet about diabetic eye screening.

Contact your local screening service or your GP if you haven't received a letter and your appointment is overdue.

Links To The Headlines

Diabetic sight loss cut by screening, research shows. BBC News, July 26 2017

Links To Science

Thomas RL, Luzio SD, North RV, et al. Retrospective analysis of newly recorded certifications of visual impairment due to diabetic retinopathy in Wales during 2007–2015. BMJ Open. Published online July 24 2017


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