NHS Choices

'Poo in a pill' may help treat C. difficile infection

NHS Choices - Behind the Headlines - Mon, 13/10/2014 - 12:00

“Capsules containing frozen faecal material may help clear up C. difficile infections,” BBC News reports.

While the prospect may sound stomach-churning, swallowing somebody else’s "poo" may help treat symptoms such as chronic diarrhoea, which can be life-threatening. 

The headline is based on new research on 20 people with recurrent diarrhoea caused by C. difficile that was not cured with standard antibiotics.

C. difficile is a bacterium that is normally present harmlessly in the gut, but in people who have received courses of antibiotics, there can be an overgrowth of this bacteria, resulting in persistent, often severe, diarrhoea.

The research team gave the patients 30 capsules of frozen faecal matter containing gut bacteria from four healthy donors, in an effort to replace the illness-causing bacteria with non-harmful varieties.

No serious side effects were reported in the small group, and diarrhoea was cured in 14 of the 20 people assessed over an eight-week period. All six non-responders were retreated and four were then cured, taking the total to 18 out of 20 no longer suffering from diarrhoea. Self-reported health scores of the participants also improved.

Larger and longer clinical trials will now need to take place to prove it works, and the treatment’s safety needs to be thoroughly investigated. This treatment concept definitely falls into the “don’t try this at home” category.

The results also have a very specific application to recurrent C. difficile infection and do not relate to other causes of diarrhoea, or other digestive conditions.

 

Where did the story come from?

The study was carried out by researchers from Massachusetts-based hospitals and was funded by the hospital departments themselves. One of the authors declared receiving funds to conduct a clinical trial related to the treatment of C. difficile (not the current study). The study builds on previous research, published in 2012, involving mice

The study was published in the peer-reviewed medical journal JAMA and has been published on an open access basis, so is free to read online.

BBC News reported the story accurately, including warnings to tempted readers not to make their own "home brew” faecal capsules as a way of tackling diarrhoea, which could be dangerous.

The Independent’s claim that these frozen capsules are a definitive cure for C. difficile is premature, given the small size of the study.

It is important to note that these findings are specific only to people hospitalised with C. difficile-related diarrhoea. This is a specific cause of diarrhoea, which is completely different from the diarrhoea and vomiting bugs of the winter season, which are usually caused by viruses. Similarly, diarrhoea may not always be caused by infection at all. For example, inflammatory bowel diseases or bowel cancer can cause diarrhoea. As such, the study has a specific application, and does not relate to "diarrhoea treatment” in general.

 

What kind of research was this?

This was a feasibility study looking at whether it was possible to treat severe diarrhoea caused by a specific gut bug (C. difficile) using frozen faecal matter (poo) capsules from unrelated donors.

C. difficile is a bug that is normally present harmlessly in the gut, but in people (usually hospitalised) who have received courses of antibiotics, there can be an overgrowth of this bacteria, resulting in diarrhoea that can sometimes be severe and even life-threatening.

The rationale for faecal bacterial transplant is that the introduction of “normal” gut bacteria from a healthy donor should rebalance the system, curing the illness.

Faecal transplants have been carried out before, but using fresh donor stools and infusions. This raises a number of problems and complexities, which the researchers sought to address by developing an easy-to-take pill instead.

Feasibility studies are small studies aiming to show whether a new idea might work and to get an idea of its safety. These early studies normally involve a small number of people. If it does seem to work and appears safe, then larger, more methodologically robust studies can occur. These studies aim to establish better proof that the technique is both effective and safe. Feasibility studies on their own do not prove this; they are a stepping stone to more robust investigations.

 

What did the research involve?

This study recruited 20 people who had had at least three episodes of mild to moderate C. difficile infection and failed to get better with standard treatment, or who had at least two episodes of severe C. difficile infection requiring hospitalisation. Their average age (median) was 64.5 years, but ranged from 11 to 89.

Researchers created capsules containing frozen faecal matter, including bacteria, from four healthy volunteers. All 20 participants were given 15 of these capsules on two consecutive days and followed for up to six months to see if their symptoms resolved and if they had any side effects.

The main outcomes of interest were:

  • resolution of the diarrhoea without recurrence up to eight weeks
  • safety and side effects

Secondary outcomes included self-reported wellbeing and daily number of bowel movements.

 

What were the basic results?

The main results were:

  • No serious side effects were reported.
  • Resolution of diarrhoea (up to eight weeks without recurrence) occurred in 14 of the 20 patients (70%) after a single treatment course of the capsules.
  • The remaining six participants had a second treatment round, leading to a further four resolutions. This took the total of successful treatments to 18 out of 20 (90%) with one or two treatments.
  • Patients needing a second treatment to obtain resolution of symptoms had generally lower pre-treatment self-reported health scores.
  • Daily number of bowel movements decreased on average from five (interquartile range [IQR] three to six) the day prior to treatment to two (IQR one to three) at day three, and one (IQR one to two) at week eight.
  • Self-ranked health scores significantly improved on a scale of one to 10 from five before treatment (IQR five to seven) to eight after treatment (IQR seven to nine).

 

How did the researchers interpret the results?

The researchers concluded that, “This preliminary study among patients with relapsing C. difficile infection provides data on adverse events and rates of resolution of diarrhoea following administration of FMT [faecal microbiota transplantation] using frozen encapsulated inoculum from unrelated donors. Larger studies are needed to confirm these results and to evaluate long-term safety and effectiveness.”

 

Conclusion

This study showed it was possible to resolve diarrhoea symptoms in people with recurrent and treatment-resistant C. difficile diarrhoea using frozen capsules of someone else’s faeces. The pill form used is an improvement on previous methods, which require fresh stools and more complex delivery mechanisms.

The study was a small feasibility study, meaning it does not provide robust proof that the technique is yet effective or safe. It did not, for example, have a control group, so we don’t know how many people would have got better on their own. Larger, more robust, clinical trials are needed to prove its effectiveness and safety before it is known whether the experimental pill could have the potential to be developed into a new treatment.

Nonetheless, the study did show that the capsules appeared feasible, initially safe and somewhat effective, so further trials will no doubt follow to develop the technique further.

This study specifically investigated diarrhoea caused by C. difficile, so it is not currently known whether rebalancing a person’s gut bacteria using a pill containing bacteria from another person could have wider applications to other bugs and gut infections.

A final unanswered question is how many people would actually be willing to use the treatment. Given the potential severity of the condition it aims to treat, and the likely tasteless nature of the pill, uptake could be high. Nevertheless, the prospect of ingesting somebody else’s "poo" may be too hard to swallow for some.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Faecal capsules 'may help stop gut infection'. BBC News, October 12 2014

Capsules can cure C difficile – but don't ask what's in them. The Independent, October 12 2014

Links To Science

Youngster I, Russell GH, Pindar C, et al. Oral, Capsulized, Frozen Fecal Microbiota Transplantation for Relapsing Clostridium difficile Infection. JAMA. Published online October 11 2014

Categories: NHS Choices

Fruit juice link to high blood pressure not proven

NHS Choices - Behind the Headlines - Mon, 13/10/2014 - 10:54

"Does drinking fruit juice give you high blood pressure?," the Mail Online asks, as an Australian study found people who reported a daily intake of fruit juice tended to have slightly higher blood pressure. This finding, the researchers argue, is likely down to the high sugar content of fruit juices.

But this and other headlines exaggerated the results of a small, potentially unreliable and unrepresentative study.

In fact, the study showed there was a link between daily fruit juice consumption and central blood pressure in a group of 130 largely healthy 50 to 70 year olds.

People who drank juice daily had a systolic pressure (the upper figure in a blood pressure reading) 3 to 4mmHg higher than those who drank juice rarely or occasionally. But there was no link when measuring blood pressure in the arm using standard measures. 

The media reports focus on the possibility that the slight raise in blood pressure could increase a person's risk of a variety of blood pressure-related diseases, such as a heart attack. But it's unclear whether this small difference would have a meaningful impact on health.

As both juice consumption and blood pressure were assessed at the same time, the study does not prove that fruit juice caused the raised blood pressure. There could be other dietary or physical activity factors accounting for this link, or there could be reverse causation (people drank fruit juice because they were worried about their blood pressure).

Overall, this study alone does not provide evidence that fruit juice increases blood pressure or, by proxy, raises the risk of heart attack or angina. 

Nonetheless, it is important to note that fruit juice is high in sugar, so it's recommended you drink no more than 150ml a day for the sake of your teeth – and to help keep your calories down.

 

Where did the story come from?

The study was carried out by researchers from Swinburne University of Technology and Monash University Australia, and was funded by Swisse Wellness, a company that sells vitamins, supplements, "superfoods" and skincare products, but – notably – not fruit juices.

It was published in the peer-reviewed medical journal Appetite.

The UK media usefully noted the large amount of sugar present in fruit juice, but the Daily Express' statement that fruit juice is a "health danger" that is "putting millions at risk" – while attention-grabbing – is highly subjective. It also doesn't reflect the results of the study, which does not prove fruit juice is a danger.

 

What kind of research was this?

This was a cross-sectional study looking at the link between regular fruit juice consumption and blood pressure.

The authors outline that, "Despite a common perception that fruit juice is healthy, fruit juice contains high amounts of naturally occurring sugar without the fibre content of the whole fruit."

They say, therefore, that regular fruit juice consumption, like soft drink consumption, represents a source of excess sugar in the modern diet.

Excess sugar intake, the team say, is linked to higher blood pressure, obesity and being overweight, and raises the risk of developing a number of associated diseases, such as cardiovascular disease and stroke.

The researchers point to previous research suggesting a link between higher sugar consumption and higher blood pressure, but wanted to investigate the specific role of fruit juice in this relationship.

As this was a cross-sectional study, it cannot prove fruit juice causes higher blood pressure. There may be other explanations and factors at play, such as dietary, physical activity or other lifestyle habits.

It also cannot exclude the possibility of reverse causality, where people with high blood pressure may be consuming more fruit juice because of health concerns, rather than vice versa.

Ultimately, a randomised control trial would be needed to prove that fruit juice – or any other food or drink item representing a source of excess sugar – causes sustained blood pressure increases.

 

What did the research involve?

The researchers asked a group of 160 adults (aged 50 to 70) about their food and drink habits over the past year. On the same day, the team took their blood pressure using two different measures.

One was the standard blood pressure measurement of the upper arm using a blood pressure cuff (brachial blood pressure), and one estimated pressure in the main blood vessel taking blood from the heart, called central, or aortic, blood pressure.

To do this, a probe was used to measure the waveform of blood in the wrist artery. This information was fed into special software that estimated central pressure.

The main analysis looked for links between fruit juice consumption categories and the one-off blood pressure readings at one or both sites.

Fruit juice consumption was categorised as follows:

  • rare – combined those who never drank juice with those consuming no more than three times a month
  • occasional – those consuming juice once a week up to five to six times a week
  • daily – once or more a day

The researchers used two measures of blood pressure (central and brachial), as there is debate about which is best to use in terms of predicting future disease risk.

To be included in the study, people had to be free of major neurological and psychiatric illness, cardiovascular disease, currently be a non-smoker, and have no history of alcohol or drug abuse.

The main analysis was adjusted to reduce the influences of the following confounders:

  • age
  • gender
  • height
  • weight
  • mean arterial pressure
  • heart rate
  • cholesterol and blood pressure treatments

 

What were the basic results?

There were no differences found between the standard blood pressure measure in the arm and the different juice groups, but differences were found for central blood pressure.

Those who consumed fruit juice daily, versus rarely or occasionally, had significantly higher central systolic blood pressure (the upper of the two-figure blood pressure measurement – in a measure of 140/80, 140 is the systolic blood pressure).

They also had higher readings for central pulse pressure and other measures looking at the heart rate and blood pressure wave forms (central augmentation pressure, central augmentation index and lower pulse pressure amplification).

Central systolic blood pressure was 3 to 4mmHg higher for those who consumed fruit juice daily rather than rarely or occasionally.

 

How did the researchers interpret the results?

The researchers concluded that, "more frequent fruit juice consumption was associated with higher central BPs [blood pressures]".

 

Conclusion

This cross-sectional study found a link between regular fruit juice consumption and slightly increased central blood pressure in a group of 130 largely healthy 50 to 70 year olds. People who drank juice daily had a systolic pressure (the upper figure) 3 to 4mmHg higher than those who drank juice rarely or occasionally.

However, when measuring the blood pressure in the standard way, using an inflatable cuff around the arm, there was no link. 

The media reports focus on the possibility that the slight raise in blood pressure could increase a person's risk of a variety of blood pressure-related complications. But it is unclear whether the small difference in systolic pressure would have had clinically significant meaning for the individual.

Similarly, it is not clear why only one of the blood pressure measures was affected and not both, if indeed there was a real link between fruit juice and blood pressure.

Also, the link was only found with systolic blood pressure (arterial pressure when the heart contracts) and not for diastolic (arterial pressure when the heart relaxes), when both figures are equally relevant in terms of the clinical significance of raised blood pressure.

This might be caused by some of the additional limitations in the study, which all introduced error and uncertainty into the findings. These limitations include:

  • relying on people's ability to accurately recall their food and drink habits over the last year, which may be inaccurate
  • being able to estimate central blood pressure accurately
  • only measuring blood pressure once, which is less reliable than measuring it many times on different days to get an average reading
  • all participants were 50 to 70 years old, and the effects in other age groups were not tested
  • it was not clear how long established the juice drinking habits were – we only know about consumption in the previous year

Furthermore, the analysis made no adjustment for other sources of sugar in the diet. Given that fruit juice was being investigated because it represented a source of additional sugar in the diet, this is an important omission.

Without knowing about other sources of sugar, it is difficult to tell how important fruit juice was in the bigger picture, or how much of a person's overall sugar intake was from juice. The role of other sugary drinks or foods is likely to be very important, but was not accounted for in the analysis.

The lack of information on other dietary and physical activity patterns also makes it difficult to exclude the possibility of reverse causality. Based on this cross-sectional analysis, it could equally be possible that people with raised blood pressure could be drinking more fruit juice in addition to other healthy lifestyle changes, rather than that fruit juice is causing the high blood pressure.

So, on its own, this study does not justify a change in fruit juice drinking habits relating to blood pressure, as the risk is unproven. A more robust study design would be needed to properly prove whether this was the case.

However, it serves to remind us that fruit juice contains a lot of sugar, something many people may not be fully aware of. Some juice drinks can contain as much sugar, and sometimes more, than a can of coke.

Any high-sugar food or drink should be consumed in moderation as part of a wide and varied diet, rich in unprocessed fruit and vegetables, and generally low in sugar.

Being aware of the sugar content of food is one of many simple ways to maintain a healthy weight and minimise your risk of developing weight-related diseases now or in the future.

Find out more about how sources of added sugar can sneak into your diet.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Does drinking fruit juice give you high blood pressure? New study finds a regular morning glass of orange juice significantly raises health risk. Mail Online, October 11 2014

Health danger in FRUIT JUICE: Millions put themselves at risk by drinking a glass DAILY. Daily Express, October 11 2014

Links To Science

Pase MP, Grima N, Cockerell R, Pipingas A. Habitual intake of fruit juice predicts central blood pressure. Appetite. Published online September 30 2014

Categories: NHS Choices

Is a cure for type 1 diabetes 'within reach'?

NHS Choices - Behind the Headlines - Fri, 10/10/2014 - 12:25

"Type 1 diabetes cure within reach after breakthrough," The Independent reports after researchers have managed to "coax" human stem cells into becoming insulin-producing cells.

Type 1 diabetes is an autoimmune condition where the body's own immune system destroys the insulin-producing cells of the pancreas. Insulin is a hormone that plays a vital role in regulating blood glucose levels.

There is currently no "cure" for type 1 diabetes and no way to replace these destroyed cells, making the person reliant on lifelong insulin injections.

This study aimed to see if it would be possible to develop these insulin-producing cells from stem cells in the laboratory. 

The researchers demonstrated they were able to successfully produce large numbers of functioning stem cell-derived cells that looked structurally similar to normal pancreatic cells, and produced insulin in response to glucose in the same way.

The function of these cells was demonstrated both in the laboratory and when transplanted into live mice, including mice genetically engineered to have diabetes.

The findings are positive, but the research is still in the very early stages. Further development will be needed to see whether stem cell-derived pancreatic cells could function normally in people with type 1 diabetes.

There is also the question as to whether the transplanted cells could also be targeted by the body's immune system.

Overall, it is too early to know whether there could one day be a complete "cure" for type 1 diabetes.

 

Where did the story come from?

The study was carried out by researchers from Harvard University and was funded by the Harvard Stem Cell Institute, the National Institute of Health, Helmsley Charitable Trust, the JPB Foundation and personal contributions.

It was published in the peer-reviewed scientific journal, Cell.

The UK media's reporting of the study was accurate, but talks of a "cure" for type 1 diabetes are premature.

As the authors of the study acknowledge themselves, "Much work remains to be done to achieve any of these therapeutic, disease-modelling, drug discovery or tissue engineering goals."

 

What kind of research was this?

This was a laboratory study that aimed to develop a generation of insulin-producing pancreatic beta cells from stem cells. 

Type 1 diabetes is an autoimmune condition where the body's own immune system for some reason destroys beta cells, making the person reliant on lifelong insulin injections. There is currently no "cure" for type 1 diabetes and no way to replace these destroyed cells.

As the researchers say, the discovery of human pluripotent stem cells (hPSC) offers a great deal of potential for medical innovation. This is because hPSCs can be converted into other specialist cell types, such as insulin-producing cells.

This then opens up the possibility of generating replacement cells and tissues in the laboratory, which could be used for disease treatment.

This study examines whether hPSCs in the laboratory could be instructed (via manipulation of signalling pathways) to develop into functioning pancreatic beta cells.

 

What did the research involve?

The researchers first cultured different pluripotent stem cell lines and trialled various different laboratory approaches. This was so they could make these differentiate into functioning cells that had the genetic characteristics of pancreatic beta cells.

The stem cell-derived pancreatic beta cells were then incubated in glucose solution to see if this stimulated them to produce insulin. A sequence of further glucose challenges (tests that see how the cells respond to glucose) at increasing concentrations then followed.

The researchers then compared these results with those of normal adult beta cells.

They got further confirmation of the cells' functioning by looking at changes in calcium levels within the cells, as beta cells sense changing glucose levels through calcium signalling. This helps them regulate blood glucose levels as required.

The structure of the stem cell-derived pancreatic cells was then more closely analysed in the laboratory.

As the next stage of the experiment, the stem cell-derived pancreatic cells were then transplanted into live mice with a suppressed immune system.

Two weeks after transplantation, these mice then had various glucose challenges, with blood samples taken to check their blood glucose and insulin levels. This was again compared with transplantation of normal adult beta cells.

Finally, they looked at the effects of transplanting these cells into genetically engineered "diabetic" mice.

 

What were the basic results?

Overall, 75% of the stem cell-derived pancreatic beta cells responded to high glucose challenges, which was similar to that for normal adult beta cells.

The amount of insulin secreted in response to glucose per stem cell-derived cell was also similar to that of normal beta cells. The cellular calcium response to glucose was also similar between the stem cell-derived cells and the normal cells.

The researchers further demonstrated that the structure and protein expression of the stem cell-derived cells was similar to the normal pancreatic cells.

When the stem cell-derived pancreatic cells were transplanted into the mice, the mice successfully secreted insulin into the bloodstream within two weeks.

In the glucose challenge, 73% of the mice with these transplanted cells (27 of 37 animals) showed increased blood insulin levels. This was in comparison to 75% (9 of 12) of those transplanted with normal pancreatic cells.

As a final stage, when transplanted into "diabetic" mice, the stem cell-derived pancreatic cells helped stop the rapidly worsening increasing blood sugar normally observed in these animals. By four months after transplantation, only one out of six of these diabetic mice had died.

 

How did the researchers interpret the results?

The researchers concluded that functional pancreatic beta cells can be generated from human pluripotent stem cells in the laboratory.

The results demonstrate that they function similarly to normal adult beta cells, both in the laboratory and in the live mouse model.

 

Conclusion

This is promising early-stage research into the possible generation of insulin-producing pancreatic beta cells from stem cells in a laboratory.

The researchers demonstrated that they were able to successfully produce large numbers of functioning stem cell-derived cells that looked structurally similar to normal beta cells and produced insulin in response to glucose in the same way.

The successful function of these cells was demonstrated both in the laboratory and when transplanted into mice, including mice genetically engineered to have diabetes.

There is currently no "cure" for type 1 diabetes and no way to replace these destroyed cells. This stem cell research, which holds promise for a possible generation of replacement pancreatic cells, is therefore encouraging.

However, research is still in the very early stages, with studies only having been carried out on a small number of live mice.

Much further development is needed to see whether it could be possible to perform human trials to see whether stem cell-derived pancreatic cells could function normally in people with type 1 diabetes.

Various questions still need to be answered, including whether the transplanted cells could also be targeted by the body's immune system.

Overall, the research is promising, but it is too early to know whether there could one day be a complete "cure" for type 1 diabetes.

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

Type 1 diabetes cure within reach after breakthrough that could spell end of insulin injections for millions. The Independent, October 9 2014

Cure for Type 1 diabetes imminent after Harvard stem-cell breakthrough. The Daily Telegraph, October 9 2014

Type 1 diabetes breakthrough using stem cell research raises hope for cure. The Guardian, October 10 2014

Could this stem cell breakthrough offer an end to diabetes? Expert promised his sick son he'd find a cure. Daily Mail, October 10 2014

Scientists close to a non-insulin cure for diabetes. The Times, October 10 2014

Links To Science

Pagliuca FW, Millman JR, Gürtler M, et al. Generation of Functional Human Pancreatic β Cells In Vitro. Cell. Published online October 9 2014

Categories: NHS Choices

Antibiotic resistance continues to rise

NHS Choices - Behind the Headlines - Fri, 10/10/2014 - 11:29

"Antibiotic resistance continues to rise," BBC News reports as, despite warnings, the number of antibiotic prescriptions in the UK continues to soar, as do new cases of resistant bacteria.

Other news reports take different slants on the story, with The Daily Telegraph blaming the rise on hospitals and out of hours GPs.

The news follows the publication of a new report by Public Health England on the English surveillance programme for antimicrobial utilisation and resistance (ESPAUR), which reports the change in antibiotic prescribing and resistance over recent years.

The report highlights a number of key findings, including a year on year increase in antibiotic prescribing in England, with the majority of antibiotic prescribing taking place in general practice. There also seems to be variation across the UK, with areas with higher antibiotic prescribing also having higher rates of resistant infections.

Public Health England hopes this report will enable general practices and hospitals to compare their data with regional and national trends. They could then see if their rates are higher than other areas, and investigate why and if they can reduce these. This will also provide a baseline measure from which to track changes in both prescribing and resistance in England.

 

What is antimicrobial resistance?

Antimicrobial resistance is a global health threat.

Antimicrobials are drugs used to treat an infectious organism, and include antibiotics (used to treat bacteria), antivirals (for viruses), antifungals (for fungal infections) and antiparasitics (for parasites).

When antimicrobials are no longer effective against infections they were previously effective against, this is called antimicrobial resistance. Regular exposure to antimicrobials prompts the bacteria or other organisms to change and adapt to be able to survive these drugs.

As the report says, the problem has been around for decades, but in the past it was seen as less of a problem as new antibiotics were regularly being developed. 

However, nowadays fewer new antibiotics are being developed, meaning we have fewer options and stronger and stronger drugs in our antibiotics armoury have to be used to treat common infections once they become resistant. This means we are now facing a possible future situation where we will be without effective antibiotics.

 

What does the report say about current antimicrobial resistance in England?

The report highlights the following:

  • There has been an increase in the number of bloodstream infections between 2010 and 2013, and an increase in the number of cases where resistance was identified. For example, during this three-year period the number of bloodstream infections caused by E. coli increased by 12%.
  • The proportion of E. coli bacteria with resistance to antibiotics increased between 2001 and 2006-07 and then decreased, but has risen again between 2010 and 2013. Roughly around one in five infections involving E. coli bacteria in 2013 were resistant to a commonly used antibiotic (ciprofloxacin), an 18% increase from 2010. Around 1 in 10 infections were resistant to the stronger antibiotics (third-generation cephalosporins and gentamicin), a 27-28% increase.
  • Looking across England there is variation in resistance, with ciprofloxacin resistance ranging from 25% in London to 12% in Cumbria, Northumberland and Tyne and Wear. Cephalosporin resistance ranged from 15% in London to 6% in Devon, Cornwall and the Isles of Scilly, and gentamicin resistance ranged from 15% in London to 5% in Durham, Darlington and Tees. 
  • There have been increases in bloodstream infections caused by some bacteria (K. pneumoniae), while others (S. pneumoniae and Pseudomonas) have shown a decline. With all infections there appears to be a notable variation in resistance rates in different geographical regions.
  • A particular focus was looking at antibacterial resistance to carbapenems – very strong antibiotics widely considered to be "antibiotics of last resort". The data indicates these antibiotics currently remain effective for the treatment of more than 98% of blood infections caused by E. coli or K. pneumonia. But, as the report says, this should not lead to complacency. Despite the small proportion of bacteria resistant to carbapenems, there has still been a year on year increase in the number of bacteria able to produce enzymes capable of destroying this antibiotic.

 

What does the report say about current antimicrobial prescribing in England?

The report highlights the following trends in antimicrobial prescribing:

  • Between 2010 and 2013, total antibiotic prescribing increased by 6% – general practice prescribing increased 4%, prescribing to hospital inpatients increased by 12%, and other community prescriptions (such as by dentists, out of hours prescribers, nurses, and other non-medical prescribers) increased by 32%.
  • In 2013, 27.4 out of every 1,000 inhabitants in England were taking a prescribed dose of antibiotics each day, with 79% of these prescriptions occurring in general practice, 15% in hospital and 6% being other community prescriptions (predominantly dentists).
  • The highest combined general practice and hospital antibiotic prescriptions were in Merseyside, with 30.4 per 1,000 inhabitants per day taking antibiotics, more than 30% higher than Thames Valley, with the lowest prescription rates (22.8 per 1,000 inhabitants per day). The highest prescription rate from general practice alone was Durham, Darlington and Tees (26.5 per 1,000 inhabitants per day), which was more than 40% higher than London (18.9 per 1,000 inhabitants per day). It was suggested the lower GP prescribing in London may reflect different healthcare access and delivery in the capital, where there may be a shift in prescribing to local hospitals and private healthcare providers.
  • Overall, the antibiotic use per 1,000 inhabitants per day is thought to be an underestimate of total consumption, as it does not include private prescriptions, which are not recorded as part of ESPAUR at present. The reasons for the increase in consumption are unknown, but may represent changes in the number of patients presenting to medical care with infections requiring antibiotics, or it could be overprescribing of antibiotics by doctors (or dentists). The report says the increase in other community prescriptions needs to be explored to assess whether general practice prescribing is being displaced to out of hours treatment centres.
  • In 2013, 66 different antibiotics were prescribed in both general practice and hospital settings, with a top 15 of these antibiotics accounting for 98% of GP prescriptions and 88% of hospitals. These top antibiotics include penicillins, tetracyclines and macrolides (such as erythromycin). Over the past four years, prescribing of penicillins has increased by 3% and macrolides by 6%.
  • Generally, in general practice the prescription of broad spectrum antibiotics (that are less specific to particular bacteria and cover a wide range of different bacteria) has decreased over recent years, while in hospital the prescription of broad spectrum antibiotics has increased.
  • Comparing the UK with other EU countries, we are said to be in the mid-range for community prescriptions of antimicrobials. But for antibiotics prescribing in hospitals, the UK had rates that were more than twice the average (median) in the EU. However, this may relate at least in part to different prescribing and recording of prescription practices in UK hospitals.

 

What is being done to help?

As the report highlights, antibiotic prescribing and antibiotic resistance are inextricably linked, and overuse and incorrect use of antibiotics are major drivers of resistance.

The Chief Medical Officer for England highlighted the problem of antimicrobial resistance in the 2013 annual report, which led to the UK cross-government five-year (2013-18) antimicrobial resistance strategy.

This is the first report from the English surveillance programme for antimicrobial utilisation and resistance (ESPAUR). Their key aims are to develop surveillance systems to measure both antimicrobial prescribing and resistance, and to measure the impact of antimicrobial prescribing on antimicrobial resistance and patient and public safety.

The data in this report provides national and regional surveillance of antibiotic resistance and antibiotic use trends from 2010 to 2013. Public Health England cautions these are just single snapshots of data, so will require further investigation. They say further validation and exploration of the findings is needed.

The report highlighted that when comparing the maps of antibiotic prescribing and resistance across regions, areas with high prescribing in general have higher resistance levels. Primary and secondary care organisations are advised to audit their own prescription data to compare with regional and national trends.

Knowledge that their consumption is higher than national trends, and assessment of the reasons for this, should help them develop strategies to improve their prescribing as needed.

This information will provide a baseline measure from which to track changes in both prescribing and resistance in England.

 

What can I do to help?

People can help cut antibiotic (or wider antimicrobial) resistance by recognising that many common infections, such as coughs, colds and stomach upsets, are often viral infections that will go away after a short period without treatment ("self-limiting" infections). These infections do not need an antibiotic prescription as they will have no effect.

If you are prescribed an antibiotic (or other antimicrobial), it is also important to make sure you take the full course as prescribed, even if you feel better before you finish the course.

This will reduce the chances of the organisms being exposed to the drug but then surviving, allowing them to develop resistance if they encounter it again.

It will also increase the chances of you getting better, as by not taking a full course you may find the infection comes back and requires further antibiotic prescriptions, which further increases the chances of resistant organisms developing.

 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Antibiotic resistance rise continues. BBC News, October 10 2014

Doctors urged to cut antibiotics prescriptions. The Guardian, October 10 2014

Out-of-hours GPs 'are fuelling a huge rise in drug-resistant bacteria': Number of antibiotics handed out at evenings and weekends up by a third since 2010. Daily Mail, October 10 2014

Hospitals and out of hours GPs are driving rise in antibiotics: report. The Daily Telegraph, October 10 2014

Doctors urged to become 'cleverer' in use of antibiotics. ITV News, October 10 2014

Health watchdog issues alert over needless antibiotic prescriptions. Daily Express, October 10 2014

Categories: NHS Choices

Could grapefruit juice protect against diabetes?

NHS Choices - Behind the Headlines - Thu, 09/10/2014 - 11:45

“Grapefruit juice 'could be the key to weight loss’,'' is the misleading headline in The Daily Telegraph.

It reports on a study in which mice fed a combination of a high-fat diet and grapefruit juice still put on weight – albeit at a lower rate than mice fed a sugary drink. Their blood sugar levels and insulin sensitivity were also better regulated than mice that did not drink grapefruit juice.

The mice were given either a high-fat diet or a low-fat diet in a range of experiments.

Mice fed a high-fat diet and grapefruit juice had an 18% reduced rate of weight gain compared with mice given sugary water with the same number of calories as the grapefruit juice. They also had 13% lower fasting blood sugar levels. There was no effect on weight gain in mice fed a low-fat diet.

Drinking grapefruit juice improved insulin sensitivity in mice, regardless of their diet (in people, reduced insulin sensitivity can be a sign of impending diabetes).

Grapefruit juice lowered blood sugar as effectively as metformin, a drug widely used to treat people with type 2 diabetes. However, none of the mice actually had diabetes, so this research has little immediate relevance to humans with the condition.

For the time being, people with diabetes should not swap their metformin for grapefruit juice on the basis of this study.

 

Where did the story come from?

The study was carried out by researchers from the University of California and was funded by the California Grapefruit Growers Cooperative, although it had no role in the study design, data collection, analysis or decision to publish.

The study was published in the peer-reviewed science journal PLOS ONE. This is an open-access journal, so the study is freely available to all.

Both the Mail Online and The Daily Telegraph’s headlines incorrectly state that grapefruit juice can help people lose weight. Leaving aside the fact that this study involved mice, rather than humans, none of the mice actually lost any weight – they just differed in the rate they put on weight.

The Daily Express’ headline was also irresponsible, as it suggests that grapefruits “tackle diabetes as well as a leading drug”, with an accompanying picture of a smiling woman (not a mouse) tucking into a grapefruit. None of the reports seemed to mention that the work was funded by the California Grapefruit Growers Cooperative. This doesn’t mean that the study results aren’t correct, but it's worth mentioning so people can make their own conclusions.

The Mail Online does, however, include a balancing comment from the British Dietetic Association, which said that until further trials are carried out in humans, it's too early for people to try grapefruit diets.

Links To The Headlines

Grapefruit juice 'could be the key to weight loss'. The Daily Telegraph, October 8 2014

How grapefruit really can help us lose weight: Drinking fruit's juice when eating fatty food can help reduce weight put on by a fifth. Mail Online, October 9 2014

Study shows grapefruits tackle diabetes as well as leading drug. Daily Express, October 9 2014

Links To Science

Chudnovskiy R, Thompson A, Tharp K, et al. Consumption of Clarified Grapefruit Juice Ameliorates High-Fat Diet Induced Insulin Resistance and Weight Gain in Mice. PLOS One. Published online October 8 2014

Categories: NHS Choices

'Healthy foods expensive' claim is unrealistic

NHS Choices - Behind the Headlines - Thu, 09/10/2014 - 10:54

“Healthy food now costs three times as much as junk, study shows,” The Independent reports. It also reports a sharper rise in the cost of fruit and veg over the past decade compared to other types of foods.

This news story is based on research which looked at changes in the price of 94 food items in the UK in the decade from 2002 to 2012. It found that in this period foods classified as healthier (such as fruit and vegetables) were more expensive per calorie than foods high in fat or sugar. The healthy foods increased more sharply in price over time, and in 2012 were three times more expensive on average per calorie than unhealthy foods.

Prices were assessed per 1,000 calories, as this is a standard way of assessing food poverty. However, as healthier foods tend to have a much lower energy density (fewer calories per gram) than less healthy foods, this measure may not always give a realistic comparison of different food choices you might buy. For example, you would need to buy and eat around 30 cucumbers to gain around 1,000 calories, compared to about one 200g packet of ginger nut biscuits (about 20 biscuits).

Given the recent economic climate and also concerns about diet-related health conditions, this is likely to be of interest to policy makers, as well as the public. This sort of information could contribute to discussions about whether changing food pricing could motivate people to eat more healthily. 

 

Where did the story come from?

This research was carried out by researchers at the University of Cambridge and the University of East Anglia. The study was funded by the British Heart Foundation, Cancer Research UK, Economic and Social Research Council, Medical Research Council, the National Institute for Health Research, and the Wellcome Trust, and took place in a UK Clinical Research Collaboration centre. One of the authors was funded by the Gates Cambridge Trust.

It was published in PLOS One, which is a peer-reviewedopen access science journal, so the study is freely available online.

The UK media generally covered this study accurately.

 

What kind of research was this?

This was a time trend study, looking at how the costs of more and less healthy foods changed over time in the UK. They used two sources of routinely available UK government data, as they hoped their method could be a way to routinely monitor how affordability of these foods is changing over time. They say that their study is the first to use UK data to assess price trends by nutrient composition of foods.

The researchers report that diet related ill health has been estimated to cost the NHS £5.8 billion per year – more than smoking, alcohol, or physical inactivity. Although consuming healthier foods is linked to better health outcomes, many people in the UK do not meet healthy eating recommendations. The researchers describe one survey which found that 39% of people rated price as the most important factor in their food choice compared to just 9% who considered a food’s healthiness to be most important.

So if healthier food is more expensive, this could be a significant barrier to people eating more healthily.

 

What did the researchers do?

The researchers selected 94 foods and drinks and classified them as “more healthy” or “less healthy” based on their calorie and nutrient contents. They identified their costs from 2002 to 2012, and compared the prices of the “more healthy” and “less healthy” foods over time to see how they differed.

Foods and drinks were chosen from UK Consumer Price Index (CPI), which the government uses to track the prices of commonly bought and used goods and services every quarter to measure inflation. The researchers used only those foods and drinks which remained in the survey between 2002 and 2012, and that did not include an element of service (for example a meal in a pub). They also excluded non-calorie containing foods such as tea bags, coffee and mineral water. This left them with 94 foods and drinks, and they obtained an average cost for each item for each year.

The researchers also obtained weight of the items where this was reported in CPI, or estimated the weight based on information on prices for similar items online, or for items with varying weights (such as individual fruit) by using the US Department of Agriculture’s National Nutrient Database standard reference weights.

The nutrient contents of the items was obtained using the UK Department of Health’s National Diet and Nutrition Survey. This survey includes detailed nutritional information on the foods eaten by 1,491 adults. The researchers identified the best match or matches to each of their 94 items from the survey. In some cases there were multiple similar items – for example, if the CPI item was a potato, the survey could contain nutritional information on boiled, baked, and fried potatoes. In these cases the researchers took the average nutritional values. The weight and nutritional information per weight data allowed researchers to calculate costs of each item per 1,000 kilocalories (kcal).

Foods were classified into categories in the Eatwell Plate:

  • bread, rice, potatoes and pasta
  • fruit and vegetables
  • milk and dairy foods
  • meat, fish, eggs, beans and other sources of protein
    food and drinks high in fat and /or sugar

The researchers also used a Department of Health tool which assigns an overall score to foods based on their level of nutrients per 100g, which allows classification of foods as “more healthy” or “less healthy” based on their score.

The researchers used statistical tests to see if the prices of the “more healthy” and “less healthy” foods, or different Eatwell categories differed over time.

 

What were the results of the study?

Average prices for both more and less healthy food rose by 35% between 2002 and 2012, from £3.87 per 1,000kcal to £5.21 per 1,000kcal.

Price per 1,000kcal was always highest for fruit and veg, lowest for starchy foods (bread, rice, potatoes and pasta), and second lowest for foods and drinks high in fat and/or sugar. The price of starchy foods per 1,000kcal stayed roughly the same between 2002 and 2012, while the other groups showed price rises. Each of the food categories, with the exception of fruit and veg, contained both foods classified as more healthy and some as less healthy.

Healthier foods increased in price per 1,000kcal more rapidly than less healthy foods. Healthier foods increased in price by an average of 17 pence per 1,000kcal per year while less healthy foods rose seven pence per 1,000kcal per year.

In 2012 the average price of more healthy foods was about three times higher – £7.49 for 1,000kcal compared to £2.50 for 1,000kcal of less healthy foods.

 

How did the researchers interpret the results?

The researchers concluded that “Since 2002, more healthy foods and beverages have been consistently more expensive than less healthy ones, with a growing gap between them.” They say that this trend may worsen social inequalities in health, and affect the population’s health as a whole. They also suggest that the findings support routinely monitoring food prices to inform possible economic policy responses.

 

Conclusion

The current study has found that the price of food per calorie in the UK between 2002 and 2012 was consistently higher for healthier food than for less healthy food. The suggestion is that this may affect people’s food choices, and therefore their long term health.

The method the researchers used took advantage of routinely available government data on food prices and nutritional content. This means it would not require collection of new data to keep track of healthy and unhealthy food prices per calorie.

There are some limitations to the findings, which the authors themselves discuss, including the small number of foods and drinks they assessed, as they were restricted to using those listed in the UK Consumer Price Index between 2002 and 2012. However, the index includes commonly bought items.

They assessed price per calorie, rather than price per unit weight, as this is the way international organisations assess food poverty. Also dietary recommendations are given in terms of calories rather than weight of food. However, one of the reasons for less healthy foods to be classed as less healthy is that they have high levels of calories per gram. So it is perhaps not surprising that less healthy food tends to costs less per calorie than more healthy foods such as fruit and veg, which tend to have fewer calories per gram. Building on this research to estimate the price of healthy and unhealthy diets as a whole, or also presenting prices per weight could help in giving an idea of the practical day to day impact of these differences.

This study has added another layer to the information available about food prices in the UK, linking it to nutritional value. Given the recent economic climate and also concerns about diet-related health conditions, this is likely to be of interest to both the public and policy makers.  

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Healthy food now costs three times as much as junk, study shows. The Independent, October 8 2014

How eating healthily can triple your shopping bill: Average price of eating 1,000 calories of healthy food reaches £7.49. Daily Mail, October 9 2014

Healthy diet costs three times that of junk food. The Daily Telegraph, October 9 2014

Links To Science

Jones NRV, Conklin AI, Suhrcke M, et al. The Growing Price Gap between More and Less Healthy Foods: Analysis of a Novel Longitudinal UK Dataset. PLOS One. Published online October 8 2014

Categories: NHS Choices

Questions about life after death remain unanswered

NHS Choices - Behind the Headlines - Wed, 08/10/2014 - 13:00

“Life after death is a real phenomenon,” Metro reports – but the headline is pure hype. Researchers were actually looking at “near-death experiences” – a very different thing. Indeed, the research involved people who did not die (even “technically”).

Near-death experiences are reported by people claiming to have had experiences when they were close to death, such as when their heart stops during a cardiac arrest.

Reported near-death experiences can range from the mystical (seeing a bright light) or having an out-of-body experience (feeling like you’re floating above your body), to the disturbing (a drowning sensation).

The study involved 140 people who had recovered from a cardiac arrest. Of these, 55 reported having a near-death experience during their cardiopulmonary resuscitation (CPR).

To assess the accuracy of claims of “out-of-body experiences”, researchers put shelves in hospital rooms where cardiac arrests were likely to occur, and placed one image on each shelf that could only be seen from above. One person recalled looking down from the top corner of the room. His descriptions appear to be accurate, but cannot be validated as his treatment occurred in an area without the shelves and pictures.

This study certainly does not provide proof of life after death. It suggests, but provides little evidence, that levels of awareness during CPR may be higher than expected.

 

Where did the story come from?

The study was carried out by researchers from the State University of New York at Stony Brook, the University of London, the University of Southampton and various other UK, US and Austrian Universities. It was funded by Resuscitation Council (UK), the Nour Foundation and the Bial Foundation.

The Bial Foundation says its mission is to “foster the scientific study of the human being from both the physical and spiritual perspectives”.

The Nour Foundation says that its “central goal” is to “stimulate an objective and intelligent discourse on existential questions from an unbiased and interdisciplinary perspective that is rooted not only in theories, but in shared commonality of personal experience as well.”

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

The media have all reported that these experiences occurred when the brain had “stopped” or “completely shut down”, when in fact all the people in the study were receiving CPR during the time of the experience, and so had oxygenated blood being pumped around their brain. Therefore, none of the claims around proof of an “afterlife” are strictly true.

A more accepted definition of death is when brain stem death occurs, which is when all neural activity in the deepest brain ceases. While it is possible to keep the heart functioning using life support systems, a person with brain stem death has permanently lost the potential for consciousness.

The existence of an “afterlife” remains a matter of belief, not scientific proof.

 

What kind of research was this?

This was an observational study that aimed to objectively assess reports of awareness and the broad range of mental experiences during CPR, including out-of-body experiences.

 

What did the research involve?

15 hospitals in the US, UK and Austria participated in the study between July 2008 and December 2012. To assess reports that people can look down on themselves from above, the hospitals installed shelves in places where cardiac arrests were likely to occur, such as the emergency department and acute medical wards, and placed one image on each shelf that could only be seen from above. These images included nationalistic and religious symbols, people, animals and major newspaper headlines. A triangle was placed on the underside of the shelf, so that they could assess whether patients looked up after recovery or had had their eyes open during cardiac arrest.

Participants were over 18 and had had a cardiac arrest – defined as no heartbeat or breathing, in or out of hospital with cardiopulmonary resuscitation (CPR) still occurring by the time they were in the emergency department. They had to be considered unconscious with a Glasgow Coma Scale Score of 3/15, meaning that they were unresponsive to pain. If they survived, and were well enough to be interviewed according to their doctor and family, then they were asked to participate.

A research nurse conducted a first general interview, preferably when the person was still in hospital, but some interviews were conducted over the phone. The second interview included the 16-point Greyson Near Death Experience (NDE) Scale, which asks questions including:

  • Did you have the impression that everything happened faster or slower than usual?
  • Did scenes from your past come back to you?
  • Did you see, or feel surrounded by, a brilliant light?
  • Did you see deceased or religious spirits?

An in-depth interview was conducted in those people who had detailed visual and sound experiences while they had a cardiac arrest.

 

What were the basic results?

There were 2,060 recorded cardiac events, and 330 people (16%) survived to hospital discharge. An interview was possible for 140 of them, and 101 completed two interviews. All of those who reported a near-death experience had at least two interviews, while nearly half of those who reported no such experience dropped out after the first interview.

The inpatient interviews took place between three days and four weeks after the event and the telephone interviews took place between three months and a year after the event.

There were 55 people (39%) who remembered something from the time that they were considered to be unconscious. There were no significant differences in age or sex between people who remembered something and those that didn’t.

Of the 101 people who completed the Greyson NDE Scale:

  • 27 had the impression that everything happened faster or slower than usual
  • 22 had a feeling of peace or pleasantness
  • 13 felt their senses were more vivid than usual
  • 13 felt separated from their body

Nine people experienced enough of the items on the scale strongly enough that they were classified as having a near-death experience.

Seven of these people had no auditory (sound) or visual recall, whilst the remaining two people described full visual and sound awareness. One was unable to complete an in-depth interview due to ill health, but the other male participant, aged 57, recalled looking down from the top corner of the room.

His descriptions of the people, sounds and the use of a defibrillator twice during his resuscitation appeared to be accurate, according to his medical records.

Unfortunately, his cardiac arrest occurred in an area without the pictures and the shelves (as did 78% of the cardiac arrests in the study), so the researchers were unable to determine whether he actually did have an out-of-body experience.

 

How did the researchers interpret the results?

The researchers concluded that people who survived cardiac arrest “commonly experience a broad range of cognitive themes, with 2% exhibiting full awareness. This supports other recent studies that have indicated consciousness may be present despite clinically undetectable consciousness. This together with fearful experiences may contribute to PTSD [post-traumatic stress disorder] and other cognitive deficits” following cardiac arrest."

 

Conclusion

This study set out to objectively test reports of awareness and the broad range of mental experiences during CPR, including people being able to look down at their body from above.

The study found that 39% of the survivors who agreed and were well enough to be interviewed remembered experiences while they appeared to be unconscious during CPR. This is probably due to the fact that although the participants had no heartbeat or spontaneous breathing, they were all receiving CPR, which means that their brains were still receiving oxygenated blood.

Only two people described full visual and sound awareness, and one of these was well enough to be interviewed, and described events in line with his medical records.

Other limitations of the study noted by the authors include:

  • potential recall bias due to the amount of time between the event and when the interviews were able to be conducted
  • the limited number of people who survived and had memories of the event
  • the small number of people meant that they were not able to adjust the results for other possible confounders, which could have impacted on the blood flow in the brain. These include the length of time the cardiac arrest continued, the quality of the resuscitation, whether it happened in or out of hospital, the heart rhythm and the use of hypothermia during the cardiac arrest

It is perfectly plausible that people would continue to have thoughts and experiences while there is still oxygenated blood flowing to the brain.

Overall, this study provides no evidence to support the existence of an afterlife, merely that people near death may still have memorable experiences.

Analysis by
Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Out of body experiences: Life after death is a real phenomenon, British scientists find. Metro, October 7 2014

Life after death? Largest-ever study provides evidence that 'out of body' and 'near-death' experiences may be real. The Independent, October 7 2014

First hint of 'life after death' in biggest ever scientific study. The Daily Telegraph, October 7 2014

Does astounding new evidence prove there's life after death? (For at least three minutes). Daily Mirror, October 7 2014

Have scientists proved there is life after death? Research into 'near-death' experiences reveals awareness may continue even after the brain has shut down. Mail Online, October 7 2014

Links To Science

Parnia S, Spearpoint K, de Vos G, et al. AWARE – AWAreness during REsuscitation – A prospective study. Resuscitation. Published online October 6 2014

Categories: NHS Choices

Vaginal orgasm 'doesn't exist', researchers argue

NHS Choices - Behind the Headlines - Wed, 08/10/2014 - 12:00

"There is no such thing as a vaginal orgasm," says the Mail Online, in a story that suggests some women have been diagnosed with sexual disorders based on the "myth" that they can orgasm through vaginal intercourse alone.

The news comes from a review of existing (not new) evidence, and its authors make some very bold assertions.

The researchers' main conclusion – that the vaginal orgasm does not exist – is based on their assertion that the vagina has no anatomical structure that can cause an orgasm.

In their opinion, this makes it impossible for a woman to achieve orgasm through penetrative sex alone.

However, they argue there are other effective methods for women to achieve orgasm, such as masturbation and oral sex.

If these arguments are true, it raises a couple of interesting related points. Foremost is the possibility that female sexual dysfunction, where a woman is unable to achieve an orgasm, may not be a "condition" at all if she is only experiencing the problem with penetrative sex.

Men who feel they have premature ejaculation problems because they are unable to "last" long enough to bring their partner to orgasm may in fact be unaware that their partner may not be able to orgasm through penetrative sex.

This is an interesting, if complex and unsupported, review of a subject of eternal fascination to the media – sexual arousal and orgasm in women.

Still, the main thrust of the researchers' argument – that penetrative sex is not the be all and end all of sexual activity – is a valid and reasonable one.

 

Where did the story come from?

The study was carried out by researchers from the Italian Centre of Sexology and the University of Florence. There is no information about any external funding.

It was published in the peer-reviewed journal Clinical Anatomy on an open-access basis, so it is free to read online.

The Mail Online went to town on the story, but its claim that, "for years women have often declared they can either orgasm through sex or foreplay" is not based on any evidence.

It also does not make it clear that this was an opinion piece summarising existing evidence and not research based on new evidence.

But, overall, the website made a fairly decent job of summarising some complex findings.

 

What kind of research was this?

This was a narrative review looking at the anatomical and physiological basis of female orgasm.

The authors say orgasm is a normal psychophysiological function and, in a statement of the rather obvious, women have the right to feel sexual pleasure.

For this reason, they say it is important that explanations of orgasm are based on female biology and not on hypotheses or personal opinion.

They also say some researchers have proposed a new "anatomical terminology" for the female sexual response, including an "inner clitoris" linked to the "G-spot". Their paper aims to clarify whether these new terms have a scientific basis.

A narrative review discusses and summarises the literature on a particular topic. As these reviews do not provide detailed information on the criteria for inclusion of the studies discussed, they are not considered as rigorous or reliable as systematic reviews.

With a narrative review, there is always the danger that "cherry-picking" of research may have taken place – where evidence that supports the authors' position is included, but contradictory evidence is ignored.

 

What does the review say?

The authors' main points were:

  • The "inner clitoris" suggested by some researchers does not exist. The entire clitoris is an external organ, composed of the glans, body and root (or crura).
  • There is no anatomical basis for a "clitoral-urethro-vaginal complex" (which others claim supports the idea of the "G-spot").
  • The vagina has no anatomical relationship with the clitoris.
  • There is no scientific basis for the existence of the G-spot, although it has become the centre of a "multimillion-dollar business" – for example, through surgical procedures that claim to help "enhance" the G-spot.
  • The vaginal orgasm does not exist.
  • The female erectile tissue responsible for orgasms is composed of the clitoris and its vestibular bulbs, the pars intermedia, labia minora and corpus spongiosum (of the female urethra). This, say the authors, corresponds to the penis in men and can be called the "female penis".
  • "Female orgasm" is the scientific term that should be used for all orgasms in women.

 

How did the researchers interpret the results?

The authors say that, worldwide, the majority of women do not orgasm during intercourse: "Female sexual dysfunctions are popular because they are based on something that does not exist; the vaginal orgasm."

Yet they say female orgasm is possible in all women if the female erectile organs – as they put it, the "female penis" – are stimulated.

This can happen during a variety of sexual activity, including masturbation, cunnilingus (oral sex) and intercourse (using the hands to stimulate the "female penis" during penetrative or anal sex).

The researchers say many men think long intercourse is the key to female orgasm, but this is not necessarily helpful to women, some of whom "may be grateful to get it over with quickly".

Male ejaculation does not automatically mean the end of sex for women, they say, and they romantically conclude that touching and kissing can be continued almost indefinitely.

 

Conclusion

This is an interesting, if complex, review of a subject of eternal fascination for the media – sexual arousal and orgasm in women. However, despite the authors' claim to the contrary, it is hardly likely to be the last word on the topic.

Some of the points it makes are in line with scientific opinion, which holds that no distinction should be made between "types" of female orgasm.

The "vaginal orgasm" theory – first posited by Freud as the sexual response of "mature" women, achievable through intercourse and separate from the "clitoral orgasm" (for adolescents only) – was criticised by feminists as long ago as the 1970s and is considered an outmoded theory by most experts in sexual medicine.

However, the relationship between the clitoris and the sensitivity of the vagina continues to be the subject of debate.

Many women worry about achieving – or failure to achieve – orgasm. There are many reasons for orgasm problems. Your GP may be able to refer you to a specialist doctor or therapist, who can check for any physical reasons and help with any psychological barriers. Use the NHS Choices search facility to find sexual health services near you.

And, as the authors point out, if penetrative sex is not particularly stimulating, there are other techniques your partner can explore, such as mutual masturbation and oral sex. For more information on good sex tips, see Talking about sex.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

The vaginal orgasm doesn't exist - it's the clitoris that holds the key to female pleasure, study claims. Mail Online, October 7 2014

'Final' word on female orgasm is an anti-climax. New Scientist, October 7 2014

There's no such thing as a vaginal orgasm! Salon, October 7 2014

Links To Science

Puppo V, Puppo G. Anatomy of sex: Revision of the new anatomical terms used for the clitoris and the female orgasm by sexologists. Clinical Anatomy. Published online October 6 2014

Categories: NHS Choices

Ebola could reach UK, but outbreak risk is low

NHS Choices - Behind the Headlines - Tue, 07/10/2014 - 12:12

“Global threat of Ebola: From the US to China, scientists plot spread of deadly disease across the world from its West African hotbed,” reports the Mail Online. This is a terrifyingly apocalyptic-sounding headline, yet the real story about Ebola is that, while still frightening and deadly, it is still a very low risk to people in the UK.

The Ebola virus causes a serious, usually fatal, disease, for which there are no licensed treatments or vaccines.

An ongoing outbreak of Ebola virus started in the West African country of Guinea, which was first reported in December 2013. This Ebola outbreak is the largest ever observed, both geographically and in terms of the number of people affected.

A study published on September 2 2014 has modelled how the virus may spread. It found that the short-term probability of international spread outside the African region was small, but not negligible. This short-term probability covered three and six weeks, which corresponded to September 1 and 22 2014. The study found that the country outside the African region with the highest risk of importation was the UK.

The original forecasts have since been revised and will have to be further updated after a Spanish nurse contracted Ebola. This happened after she treated two Spanish missionaries, who died of the disease after being flown back from Africa. This nurse is the first person known to have contracted Ebola outside of West Africa.

 

Where did the story come from?

The study was carried out by researchers from Northeastern University, the Fred Hutchinson Cancer Research Center, and the University of Florida, all in the US, and the Institute for Scientific Interchange in Italy. It was funded by the Defense Threat Reduction Agency and MIDAS-National Institute of General Medical Sciences.

The study was published in the peer-reviewed journal PLOS Current Outbreaks on September 2 2014. This is an open access journal, which is freely available to all.

The researchers state that the results of their model may change as more information becomes available and are publishing new data, projections and analysis online.

The media has reported the results of the updated projections published on the site above. It’s worth bearing in mind that, despite the very worrying headlines and the deadliness of Ebola, the risk to anyone in the UK is very low.

 

What kind of research was this?

This was a modelling study that aimed to forecast the local transmission of the Ebola virus in West Africa, and the probability of international spread if the containment measures are not successful at stopping the outbreak.

Like the weather forecast, modelling studies have to contain assumptions and approximations, and although they are useful tools to help predict what might happen, they are not always correct. The assumptions and approximations in this model are being updated by the researchers as new information becomes available.

 

What did the research involve?

The researchers used computer simulations to model the transmission of the Ebola virus.

 

What were the basic results?

The researchers estimate that each case of Ebola in West Africa will spread to 1.5 to 2 unaffected people.

In the short term (three and six weeks, which corresponded to until September 1 and September 22 2014), the probability of international spread outside the African region is small, but not negligible. The country outside the African region with the highest risk of importation in the short term is the UK.

The outbreak is more likely to spread to other African countries, which will increase the risk of international spread over a longer time period.

 

How did the researchers interpret the results?

The researchers conclude that their modelling has shown that, “the risk of international spread of the Ebola virus is still moderate for most countries. The current analysis, however, shows that if the outbreak is not contained, the probability of international spread is going to increase consistently, especially if other countries are affected and are not able to contain the epidemic”.

They go on to stress that the current model contains assumptions and approximations that may need to be modified as more information becomes available.

 

Conclusion

This modelling study found that the short-term probability of international spread outside the African region is small, but not negligible. The country outside the African region with the highest risk of importation is the UK.

The assumptions and approximations in this model are being updated by the researchers as new information becomes available, and these forecasts have since been revised.

If you are travelling abroad and are worried about infectious diseases, you may want to check out the country-by-country guide provided by the National Travel Health Network and Centre.

Health professionals should stay abreast of the latest Ebola advice from Public Health England.

 

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

Global threat of Ebola: From the US to China, scientists plot spread of deadly disease across the world from its West African hotbed. Mail Online, October 5 2014

Ebola outbreak: Virus could reach UK and France by the end of the month, scientists claim. The Independent, October 5 2014

Ebola outbreak: Britain has 50% chance of importing deadly virus with the next three weeks. Daily Mirror, October 5 2014

Deadly Ebola virus could reach Britain in THREE WEEKS say scientists. Daily Express, October 6 2014

Links To Science

Gomes MFC, et al. Assessing the International Spreading Risk Associated with the 2014 West African Ebola Outbreak. PLOS Current Outbreaks. September 2 2014.

Categories: NHS Choices

Cannabis labelled 'harmful and as addictive as heroin'

NHS Choices - Behind the Headlines - Tue, 07/10/2014 - 11:29

"Cannabis: the terrible truth," is today's Daily Mail front page splash story. The paper cites the risks posed by cannabis – including a doubling of the risk of schizophrenia – based on research the paper says has "demolished the argument that the drug is safe".

The "terrible truth" is we still don't know enough about the safety and harms of cannabis because it's legally and ethically a difficult area to research. However, we can be pretty certain you can't take a fatal overdose from recreational cannabis use.

The headlines in the Mail and several other papers were prompted by the publication of a narrative review of cannabis research by Professor Wayne Hall, an expert adviser on addiction to the World Health Organization.

Professor Hall concludes that cannabis research since 1993 has shown its use is associated with several adverse health effects, including a doubling of the risk of crashing if driving while "cannabis impaired". He also found that around one in 10 regular cannabis users develop dependence.

He also reports regular cannabis use in adolescence was strongly linked with using other illicit drugs, as well as increased risk of cognitive impairment and psychoses.

In addition, cannabis smoking probably increases cardiovascular risk in middle-aged adults with pre-existing heart disease, but its effects on respiratory function and respiratory cancer remain unclear as most cannabis smokers have smoked, or still smoke, tobacco.

But as this review was not systematic, it is impossible to tell if all relevant studies have been included. And all these conclusions were based on the results of observational studies, which means we can't tell if cannabis caused all the effects.

 

Where did the story come from?

The study was carried out by a single researcher from the University of Queensland Centre for Youth Substance Abuse Research, the University of Queensland Centre for Clinical Research, and the National Drug and Alcohol Research Centre in Australia, and the National Addiction Centre at King's College London.

It was funded by the National Health and Medical Research Council of Australia and was published in the peer-reviewed journal, Addiction.

Despite the somewhat hyped headlines, the media coverage of this study was generally accurate, but did not point out the limitations of the research. Indeed, the Mail's description of the study as "definitive" is rather at odds with the nature of the research.

 

What kind of research was this?

This was a narrative review that aimed to examine the changes in the available evidence on the adverse health effects of cannabis since 1993.

It was not clear how the author identified the studies used as a basis for the review. It may be the case there are other studies showing no effect or harm that have not been included in the review.

It is also not clear how the author compiled the results of the research to come up with strengths of effect.

A systematic review is required to assess the adverse health effects of cannabis use.

Also, although the author applied rules to the interpretation of the research, the conclusions are based on the results of observational studies.

It is difficult to conclude from these types of studies that cannabis causes the effects seen, as there are still potentially differences between people who use cannabis and people who don't that could explain the differences seen.

 

What did the research involve?

The author looked at studies published over a 20-year period since 1993 (when a previous review was conducted) to see if there was evidence that cannabis caused adverse health effects. To do this, Professor Hall looked at whether:

  • there were case control and cohort studies that showed an association between cannabis use and a health outcome
  • cannabis use preceded (started before) the outcome
  • the association remained after controlling for potential confounding variables
  • there was clinical and experimental evidence that supported the biological plausibility of a causal relationship

 

What were the basic results?

The author listed the conclusions that he believes can now reasonably be drawn in the light of evidence that has accrued over the past 20 years.

Adverse effects of acute use

Professor Hall concluded that:

  • The risk of a fatal overdose is considered to be extremely small. The estimated fatal dose in humans is between 15 and 70g, far greater than it is reported a heavy user could ever use in one day. There have also been no reports of fatal overdose in the literature.
  • Driving while cannabis impaired approximately doubles car crash risk.
  • Maternal cannabis use during pregnancy modestly reduces birthweight.
Adverse effects of chronic use

Professor Hall concluded that:

  • Around one in 10 regular cannabis users develop dependence, and this rises to one in six among people who start in adolescence.
  • Regular (daily or near daily) cannabis use in adolescence approximately doubles the risks of early school leaving and cognitive impairment and psychoses in adulthood.
  • Regular cannabis use in adolescence is also associated strongly with the use of other illicit drugs.
  • Cannabis smoking may increase the risk of cardiovascular events such as angina or heart attack in middle-aged and older adults with pre-existing cardiovascular disease. Some isolated reports suggest younger people not yet diagnosed with cardiovascular disease may also be at risk of cardiovascular events.
  • The effects of cannabis on respiratory function and respiratory cancer remain unclear because most cannabis smokers have smoked, or still smoke, tobacco.

 

How did the researcher interpret the results?

Professor Hall concluded that: "The epidemiological literature in the past 20 years shows that cannabis use increases the risk of accidents and can produce dependence, and that there are consistent associations between regular cannabis use and poor psychosocial outcomes and mental health in adulthood."

 

Conclusion

This narrative review has concluded that cannabis research in the past 20 years has shown that cannabis use is associated with a number of adverse health effects.

It also found driving while cannabis impaired approximately doubles car crash risk and around one in 10 regular cannabis users develop dependence.

Regular cannabis use in adolescence approximately doubles the risks of early school leaving and cognitive impairment and psychoses in adulthood, according to the review.

Regular cannabis use in adolescence is also associated strongly with the use of other illicit drugs.

In addition, cannabis use probably increases cardiovascular risk in middle-aged adults with pre-existing heart disease, but its effects on respiratory function and respiratory cancer remains unclear because most cannabis smokers have smoked, or still smoke, tobacco.

However, as this was not a systematic review it is impossible for readers to know whether all relevant studies have been included.

All the review's conclusions were based on the results of observational studies. So while it seems probable that cannabis use increases the risk of some adverse outcomes, it is also possible there are differences between cannabis smokers and non-smokers that explain some of the differences seen.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Cannabis as addictive as heroin, major new study finds. The Daily Telegraph, October 7 2014

Cannabis can damage you, warns study. The Times, October 7 2014

The terrible truth about cannabis: Expert's devastating 20-year study finally demolishes claims that smoking pot is harmless. Daily Mail, October 7 2014

Links To Science

Hall W. What has research over the past two decades revealed about the adverse health effects of recreational cannabis use? Addiction. Published online October 7 2014

Categories: NHS Choices

Eating with a fat friend 'makes you eat more'

NHS Choices - Behind the Headlines - Mon, 06/10/2014 - 13:00

“Sitting next to overweight people makes you more likely to gorge on unhealthy food,” the Daily Express reports.

The paper reports on a small-scale research experiment showing that the presence of an overweight woman (an actress in a fat suit) near a buffet made student volunteers choose and eat a larger amount of unhealthy food (spaghetti) than when she was a healthy weight (without the fat suit). This effect was not influenced by whether the actress chose to eat healthily or unhealthily herself, something the study also looked at.

The researchers’ explanation of this was, “that when eating with or near an overweight person, you may be less likely to adhere to your own health goals.”

The study was not wholly convincing and does not prove this phenomenon exists in the general population, where food and social interactions may be more complex and nuanced. Food choice was artificially restricted to just two foods: spaghetti and salad – not the best buffet going. The same results may not have been found if participants were given a more realistic range of food choices.

It is difficult to see what practical implications the study "brings to the table", other than to be conscious of your own food choices, regardless of the social situation.

This may be a poignant reminder to those looking to maintain a healthy weight that when it comes to “all-you-can-eat” situations, it’s probably best to regard it as a special offer, not a personal challenge.

 

Where did the story come from?

The study was carried out by researchers from Southern Illinois University and Cornell University (US). No funding source was mentioned in the publication. The study was published in the peer-reviewed science journal Appetite.

The Express generally covered the story accurately, though the headlines indulged in a bit of “fat shaming”, as eating a small extra amount of spaghetti was morphed into “greed”.

 

What kind of research was this?

This was a randomised, single blind, human study looking at the influence of an overweight eating companion on healthy and unhealthy eating behaviour.

The researchers indicated that many social factors influence food intake, such as the presence or absence of eating companions, as well as the body type of these companions.

This study aimed to investigate the effect of:

  • the presence of an overweight person on what other people chose to eat
  • whether this was influenced by what food (healthy vs. unhealthy) the overweight person served themselves

 

What did the research involve?

The research team recruited 82 undergraduate college students (average age 19.5 years; 40 women and 42 men) to eat a buffet meal restricted to spaghetti with meat sauce and or salad at lunch. They also enlisted an actress to wear a suit that added three-and-a-half stone (50 pounds) to her weight. Without the “fat suit” she was a healthy weight, but donning the fat suit put her at the border of overweight/obese categories (with a BMI of 29.3).

Each of the 82 participants was randomly assigned to one of four scenarios:

  • the actress served herself healthily (more salad and less pasta) while wearing the fat suit
  • she served herself the same healthy meal without the fat suit
  • she served herself less healthily (more pasta and less salad) while wearing the fat suit
  • she served herself the same less healthy meal without the fat suit

Participants in each scenario viewed the actress serving herself and then served themselves pasta and salad.

The actress was not known to the participants, but drew attention to what she was eating by asking out loud “do I need to use separate plates for pasta and salad?” and dropping her fork and asking for a new one. She also sat in full view of the buffet queue.

The first part of the study looked at the effect of the fat suit. The second part of the study looked at the influence on the participants’ food choice when the actress served herself either a small amount of pasta and a large amount of salad (described as the “healthy eating condition”), or a large amount of pasta and a small amount of salad (“unhealthy eating condition”).

Participants were asked to report the number of hours and minutes since they had last eaten, to control for their hunger prior to the experiment.

The participants knew that the study aimed to examine eating behaviour, including serving size and intake, but they were blinded to the scenario allocation of the actress. When asked, no participants revealed suspicion about the purpose of the study.

 

What were the basic results?

These were two main findings:

  • When the actress wore the fat suit, appearing overweight, the other participants served and ate more pasta regardless of whether she served herself mostly pasta or mostly salad, compared to when she was of normal weight.
  • When she wore the fat suit and served herself more salad, the other participants actually served and ate less salad.

This meant that, regardless of whether the actress served healthy or unhealthy food, participants served and ate a larger amount of pasta (unhealthy food) when she appeared overweight than when she appeared a healthy weight.

 

How did the researchers interpret the results?

The research team said their results “support the ‘lower health commitment’ hypothesis, which predicted that participants would serve and eat a larger amount of pasta when eating with an overweight person, probably because the health commitment goal was less activated.” They added that their, “results did not support the ‘avoiding stigma’ hypothesis, which predicted that participants would serve and eat a smaller amount of pasta when an overweight confederate served herself unhealthily, to avoid association with the stigmatised group”.

 

Conclusion

This small-scale research experiment found that the presence of an overweight woman (an actress in a fat suit) near a buffet made student volunteers choose a larger amount of unhealthy food than when she was a healthy weight (without the suit). This effect was not influenced by whether the actress chose to eat healthily or unhealthily herself.

These findings suggest that people may serve and eat larger portions of unhealthy foods and smaller portions of healthy foods when eating with or near an overweight person. The researchers did not test out any reasons for this, but speculated this might be, “because they are less in tune with their own health goals”. They said this phenomenon might be easy to avoid by “assessing your level of hunger before going to the restaurant and planning your meal accordingly”.

However, the study was not wholly convincing and doesn’t prove this phenomenon exists in the general population, where food and social interactions may be more complex. For example, the study was restricted to a relatively small amount of young American adults (average age of 19.5), which may not be representative of findings in older people, children or other countries and cultures.

Similarly, the study investigated a single eating scenario, a buffet, where food choice was artificially restricted to only two foods to help the study design. The same results may not have been found in other eating scenarios, or if participants were given a more realistic range of food choices at a buffet. In addition, they did not measure how much cheese or salad dressing was used, which could have a substantial impact on whether the meal was healthy or unhealthy.

The study participants were also aware that their serving and intake levels were being recorded, which may have influenced the results.

Anyone who has been to an all-you-can-eat buffet and over-indulged can probably recognise how the social context of a meal can influence the amount of food people eat. This study suggests a further influence, body type, may also be influential, but only tentatively. This phenomenon is likely to be the subject of future research. 

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

Having fat friends makes you greedy. Daily Express, October 4 2014

Fat friends DO make you eat more: Study finds we're more likely to ditch healthy eating when dining with overweight people. Mail Online, September 22 2014

Links To Science

Shimizu M, Johnson K, Wansink B. In good company. The effect of an eating companion's appearance on food intake. Appetite. Published online September 16 2014

Categories: NHS Choices

Green tea compound may improve cancer drugs

NHS Choices - Behind the Headlines - Mon, 06/10/2014 - 12:30

"Green tea could helps [sic] scientists develop new cancer fighting drugs," the Mail Online reports. But before you rush out to the shops, in no way does this study suggest green tea can fight cancer.

Instead, research has found a compound in green tea – the catchily named Epigallocatechin-3-O-gallate (EGCG) – may help improve the effectiveness of anti-cancer drugs such as Herceptin, used in the treatment of breast and stomach cancer.

This study used nanotechnology techniques to develop a new way of packaging and carrying protein drugs by combining them with EGCG.

Scientists formed a complex compound consisting of by-products of EGCG and the protein cancer drug Herceptin.

Tests in the laboratory and mice indicated the compound might have better anti-cancer properties than standard Herceptin treatment.

This is encouraging research and may lead to improvements in delivery mechanisms for protein drugs further down the line. However, it is at a very early stage of development, so new treatments are not guaranteed.

The results from the laboratory and mice studies need to be confirmed by other research groups before the team can consider testing potential treatments in humans.

Only then will they be able to assess whether such a drug delivery system could benefit people and in what circumstances. These studies will have to pay special attention to potential side effects of the drugs.

Overall, this new nanotechnology might prove useful in several years' time, but its immediate impact is minimal.

 

Where did the story come from?

The study was led by researchers from the Institute of Bioengineering and Nanotechnology, Singapore, and Beth Israel Deaconess Medical Center and Harvard Medical School in the US.

It was funded by the Institute of Bioengineering and Nanotechnology and the US National Institutes of Health.

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

The Mail Online's coverage was broadly accurate.

 

What kind of research was this?

This laboratory-based bioengineering study developed new drug carrier technology that was then tested in mice.

Most drugs require carrier substances to ensure the active drug ingredients reach the appropriate part of the body and are released at the appropriate time.

Carriers are usually inert and are broken down in the body over time. But high quantities of some carriers can produce toxicity in the body, leading to troublesome side effects.

This study aimed to improve current drug carriers by developing a carrier that was easily metabolised in the body, and may even do some good by itself.

The researchers said green tea extract was used because previous research indicated it had anti-cancer effects, as well as protective effects on the nervous system and DNA.

Many new technologies are tested in mice first as – despite the difference in size – they have a similar biology to humans. However, some things work differently in mice and men, so any positive findings in mice would not automatically apply to humans.

 

What did the research involve?

The research involved developing a new biological compound to carry cancer drugs based on derivatives (by-products) of one of the main ingredients in green tea, called Epigallocatechin-3-O-gallate (EGCG).

The research team joined EGCG derivatives with various anti-cancer proteins to form what are known as nanocomplexes – intricately engineered combinations of proteins.

One of the nanocomplexes comprised the anti-cancer protein Herceptin bundled with an EGCG derivative, forming a core, and a separate EGCG-derived shell around the outside.

They injected this into mice with cancer to see if the Herceptin-EGCG carrier nanocomplex was more or less effective at fighting tumour cells than "free" Herceptin alone.

 

What were the basic results?

The team found they were able to make stable nanocomplexes incorporating anti-cancer proteins with EGCG derivatives.

When the Herceptin-EGCG complex was injected into mice with cancer, it was better at targeting tumour cells (it had better "selectivity") and reducing their growth, and lasted longer in the blood than free Herceptin.

This complex also displayed better anti-cancer properties when tested on human breast cancer cells in the laboratory.

The researchers also coupled ECGC derivatives with another protein called interferon α-2a, which is used in combination with chemotherapy and radiation as a cancer treatment. This nanocomplex was better at limiting cancer cell growth than free interferon α-2a.

 

How did the researchers interpret the results?

The researchers stated they developed and characterised a new green tea-based mechanism for protein drug delivery where the carrier itself displays anti-cancer effects.

They said the nanocomplex effectively protected the protein drugs against many obstacles from the point of administration to the required delivery sites.

They concluded that, "The combined therapeutic effects of the green tea-based carrier and the protein drug showed greater anti-cancer effect than the free protein."

 

Conclusion

This study developed a new way of packaging and carrying protein drugs by combining them with a green tea extract called Epigallocatechin-3-O-gallate (EGCG), which itself may have anti-cancer properties.

They formed a complex between derivatives of EGCG and the protein cancer drug Herceptin. Tests in the laboratory and in mice indicated it might have better anti-cancer properties than non-complexed free Herceptin.

This is encouraging research and may lead to improvements in delivery mechanisms for protein drugs further down the line.

But this research remains at a very early stage of development. The results from the laboratory and mice studies need to be confirmed by other research groups before the team can consider testing potential treatments in humans.

Only then will they be able to assess whether such a drug delivery system could benefit people. These further studies will have to pay special attention to potential side effects of the drugs.

Green tea extracts are often the subject of news headlines, often in the very early stages of drug development.

Other claims made about green tea include how it can help prevent prostate cancer, reduce stroke riskboost the ability of the brain, and help ward off Alzheimer's disease.

Some people have even gone as far as claiming the beverage is a “"superfood". Many of these claims are not backed by robust evidence, however.

Overall, this new nanotechnology might prove useful in many years' time, but its immediate impact is minimal.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Green tea could helps scientists develop new cancer fighting drugs. Daily Mail, October 5 2014

Links To Science

Chung JE, Tan S, Gao SJ, et al. Self-assembled micellar nanocomplexes comprising green tea catechin derivatives and protein drugs for cancer therapy. Nature Nanotechnology. Published online October 5 2014

Categories: NHS Choices

Study finds clue to why colds trigger asthma

NHS Choices - Behind the Headlines - Fri, 03/10/2014 - 12:20

The Mail Online reports how "a simple cold can set off a deadly asthma attack: Scientists discover chemical can send the immune system into overdrive".

It is well known that in people with asthma, respiratory infections such as colds or flu can trigger asthma symptoms, and, in more serious cases, an asthma attack.

This study involved experiments in mice and humans to see exactly why this might be the case. In particular, the researchers wanted to find out how inflammatory processes might play a part.

They found in people with asthma, infection with the common cold virus (rhinovirus) causes an increase in levels of an inflammatory protein called IL-25 in the cells lining the airways.

This sets off a range of inflammatory processes, such as narrowing of the airways, which can cause asthma symptoms.

As the researchers suggest, the findings indicate using a drug to block IL-25 could prevent people with asthma getting worse symptoms if they catch a cold.

This research is in its early stages and further studies will now be needed to develop an IL-25-blocking drug for testing.

 

Where did the story come from?

The study was carried out by researchers from Imperial College London.

It was funded by the Medical Research Council, Asthma UK, the National Institute for Health Research, Imperial Biomedical Research Centre and the Novartis Institute for Biomedical Research.

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

The Mail Online's reporting of the study was accurate.

 

What kind of research was this?

This was laboratory, human and animal research that aimed to investigate the role a protein called interleukin-25 (IL-25) plays in triggering worsening symptoms in people with asthma when they catch a cold.

Viral infections such as the common cold (mostly caused by rhinoviruses) are known to be a trigger for worsening asthma symptoms or causing asthma attacks.

IL-25 is a protein involved in inflammatory and autoimmune processes (where the immune system attacks health tissue) in the body and has previously been identified as playing a role in asthma.

This study used laboratory experiments and studies in mice and humans. The results showed how people with asthma express more IL-25, and that infection with rhinovirus can increase levels of IL-25 and other inflammatory molecules.

 

What did the research involve?

The researchers first studied samples of the cells lining the airways in the lungs (the bronchi) obtained from 10 people with asthma and 10 people without asthma.

They looked at the levels of IL-25 and then looked at what happened when these cells were infected with rhinovirus.

They then followed up these laboratory results with studies in mice and humans. The researchers infected 39 people with rhinovirus – 28 people with asthma and 11 people without asthma – to see what effect this had on the levels of IL-25 in nasal secretions.

They then studied mice to look at the exact mechanisms by which rhinovirus may lead to increased IL-25 and so trigger asthma symptoms.

A mouse model of asthma was used in these experiments. In this model, the mice were sensitised with an allergen once daily for three days via the nose, while some were given a saline control.

The allergen used was RV-OVA, which causes allergic inflammation in the airways similar to that which occurs in people with asthma.

After this sensitisation, some were infected with rhinovirus, while some were not. The researchers then examined the levels of IL-25 and inflammatory cells in the airways. 

The researchers followed this up by investigating the effects of an IL-25-blocking antibody in mice.

 

What were the basic results?

In the first laboratory study, the researchers found the cells lining the airways in people with and without asthma were no different in how much IL-25 they produced when they were not infected with rhinovirus.

After eight hours of exposure to rhinovirus, infected cells showed tenfold greater levels of IL-25 than those not infected. Using allergy tests, the researchers found increased IL-25 expression was associated with increased sensitivity to various allergens.

Their next experiments in people both with and without asthma showed there was no significant difference in the level of IL-25 nasal secretions before rhinovirus infection.

Up to 10 days after infection with rhinovirus, 61% of those with asthma (17 of 28) demonstrated a significant increase in their IL-25 levels.

People without asthma also had a significant increase in IL-25 secretion, but peak levels during infection were higher in people with asthma.

The researchers found the "asthmatic mice" (whose airways had been sensitised by the allergen RV-OVA) had higher IL-25 levels, whether subsequently infected with rhinovirus or not, compared with the "non-asthmatic" mice.

When "allergic" mice were infected with rhinovirus, they had IL-25 levels 28 times higher than asthmatic mice who were not infected. Infection of non-asthmatic mice with rhinovirus also caused an increase in IL-25 levels compared with non-asthmatic, non-infected mice, but at much lower levels.

Further examination of lung tissue from the mice demonstrated the inflammatory response that was occurring in association with IL-25. Using an IL-25-blocking antibody blocked the inflammatory response in the mice's lungs that occurred after rhinovirus infection. 

 

How did the researchers interpret the results?

The researchers concluded that rhinovirus can induce IL-25 production in the lining of the airways, and that this is more pronounced in people with asthma than healthy controls.

In a mouse model of allergic asthma, rhinovirus infection induced IL-25 production, and blocking IL-25 could reduce rhinovirus-induced lung inflammation.

 

Conclusion

It is well known that respiratory infections such as colds or flu can trigger asthma symptoms in those who have the condition.

This study demonstrates how, in people with asthma, infection with the common cold virus (rhinovirus) causes an increase in levels of the inflammatory protein IL-25 in the cells lining the airways. This sets off an inflammatory process that could be causing the asthma symptoms.

As the researchers suggest, the findings indicate that using a drug to block IL-25 could be a promising way to try to prevent people with asthma getting worse symptoms if they catch a cold.

The research is in its early stages, and further studies will now be needed to develop an IL-25-blocking treatment that shows enough promise to be tested in human trials.

While there is no guaranteed way to prevent catching a cold, people can help prevent the spread of colds by always coughing or sneezing into a tissue, binning it and washing their hands.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

How a simple cold can set off a deadly asthma attack: Scientists discover chemical can send the immune system into overdrive. Mail Online, October 2 2014

Links To Science

Beale J, Jayaraman A, Jackson DJ, et al. Rhinovirus-induced IL-25 in asthma exacerbation drives type 2 immunity and allergic pulmonary inflammation. Science Translational Medicine. Published online October 1 2014

Categories: NHS Choices

Moderate regular drinking may 'damage sperm'

NHS Choices - Behind the Headlines - Fri, 03/10/2014 - 11:30

“Just five alcoholic drinks a week could reduce sperm quality,” The Guardian reports. A study involving Danish military recruits found that even moderate drinking, if done regularly, was associated with a drop in quality.

The study involved 1,200 young Danish military recruits (with an average age of 19), and assessed their semen quality, as well as questioning their alcohol intake in the week preceding the sample, or binge drinking in the past 30 days.

Overall, there was no clear association between semen quality and alcohol intake. However, in analyses restricted to the 45% of men who said this was a typical week for them, there was a dose-response relationship, with higher alcohol intakes associated with lower sperm quality.

Men who did not drink any alcohol at all also had impaired sperm quality. They could have had health issues that impacted on their sperm quality and also meant they needed to avoid drinking, although this is pure speculation.

As always, there are limitations. Importantly, as the study assessed alcohol intake and sperm quality at the same time, it cannot prove cause and effect. Various other factors could also influence the relationship.

There is also the possibility of inaccurate recall of alcohol units consumed, although we would suspect that young men tend to underestimate rather than overestimate how much they drink.

We also don’t know whether any of the measures of reduced sperm quality observed would actually have any effect on fertility.

Nevertheless, the detrimental effects of high alcohol intake in various areas of health are well known, so laying off the drink for a few days a week certainly wouldn’t hurt.

 

Where did the story come from?

The study was carried out by researchers from University of Southern Denmark, University of Copenhagen and Icahn School of Medicine at Mount Sinai, New York, and was funded by The Danish Council for Strategic Research, Rigshospitalet, European Union, DEER, The Danish Ministry of Health and The Danish Environmental Protection Agency, and Kirsten and Freddy Johansens Foundation.

The study was published in the peer-reviewed British Medical Journal Open, which is an open access journal, meaning the study is free to read online.

The UK media's reporting of the study is accurate and included some useful observations from independent fertility experts. However, the reporting doesn’t make clear that, overall, there was no clear association between semen quality and alcohol intake. An association was only seen in men who reported habitually drinking five units or more.

 

What kind of research was this?

This was a cross sectional study which aimed to look at the association between alcohol consumption, semen quality and reproductive hormones.

As the researchers say, several research studies have associated excessive alcohol consumption and binge drinking (defined in the paper as five units or more in a single day; roughly the same as two standard cans of UK premium 5% abv lager) with adverse health outcomes. Some studies have reported an association between alcohol consumption and semen quality, while others have not.

However, few studies have specifically examined the effect of binge drinking.

The main limitation with this type of study is that being cross sectional, it cannot show that alcohol consumption causes poor semen quality. It cannot show that the men previously had higher-quality semen and that they then developed these alcohol consumption patterns and had this effect. There could be other factors (confounders) that explain the association seen.

For example, the results of this study could also be used to suggest that men with poor semen quality are more likely to drink.

A more suitable study design would be a cohort study, where men are followed over many years, but these are both expensive and time-consuming to carry out.

 

What did the research involve?

This Danish study used a specific population of 1,221 men (average age of 19) recruited to compulsory military service between January 2008 and April 2012. At recruitment, they undergo a compulsory physical examination and were invited to have an assessment of semen quality. The semen samples were analysed for volume, sperm concentration, total sperm count and percentage mobile and morphologically normal. Blood samples were also tested for levels of sex hormones such as testosterone.

All the men completed a questionnaire which, as well as collecting medical information, also included assessment of alcohol intake. They completed a diary reporting their daily intake of red and white wine, beer, strong alcoholic drinks, alcopops and others during the week prior to the semen and blood samples. They were asked to give their intake in units, being told that one standard beer, one glass of wine or 40ml of spirits contained 1 unit of alcohol (≈12g of ethanol), one strong beer or one alcopop contained 1.5 units of alcohol, and one bottle of wine contained 6 units.

Alcohol intake was calculated as the sum of daily reported unit intakes within that week. They were asked whether the intake in that week was typical for them (habitual intake). They were also asked how many times during the past 30 days they had been drunk or had consumed more than five units of alcohol on one occasion, which was defined as binging.

In their analyses they considered alcohol intake in five unit intervals, with the intake of one to five units as the reference category to which all others were compared. They also categorised the number of binge episodes and the number of times a person was drunk in the past week.

 

What were the basic results?

The median (average) alcohol intake in the preceding week was 11 units, and beer was the most common drink (making up an average 5 units). In the past month 64% of the men had binge drunk and 59% had been drunk more than twice. Almost half of the men (45%) said the preceding week had been a typical intake week for them.

Semen quality generally decreased with increasing alcohol intake and binge drinking. Men with an intake of 30 units, or who frequently binged, tended to have higher caffeine intake, were more likely to be smokers, were more likely to report having had sexually transmitted infections and were younger. Overall, after adjusting for confounders, such as time since last ejaculation, smoking and body mass index (BMI), there was no clear association between semen quality and alcohol intake or binge drinking.

There was a dose-response association between increasing units per week (or increasing binge episodes or being drunk) and higher blood testosterone levels, and lower sex hormone-binding globulin (SHBG), indicating more testosterone is freely available to the body tissues. This dose-response association remained after controlling for confounders.

In analyses restricted to the 45% of men who said that this was a typical week for them, there was a dose-response association: as alcohol intake went up, sperm concentration, total sperm count and percentage morphologically normal sperm went down, even after adjustment. The trend was more pronounced among men with a typical weekly alcohol intake above 25 units.

No alcohol intake at all was also associated with reduced semen quality. It is unclear why this is the case.

 

How did the researchers interpret the results?

The researchers conclude that, “Our study suggests that even modest habitual alcohol consumption of more than 5 units per week had adverse effects on semen quality, although most pronounced associations were seen in men who consumed more than 25 units per week. Alcohol consumption was also linked to changes in testosterone and SHBG levels. Young men should be advised to avoid habitual alcohol intake.”

 

Conclusion

This study of more than 1,200 young Danish military recruits finds some associations between alcohol intake and measures of semen quality and sex hormones.

Overall, after adjustment for confounders, there was no clear association between alcohol intake in the past week or binge drinking in the past 30 days and semen quality. However, in analyses restricted to the 45% of men who said this was a typical week for them, there was a dose-response relationship, with higher alcohol intakes being associated with lower sperm concentration, total sperm count and percentage morphologically (structurally) normal sperm.

Increasing alcohol intake was also associated with increased levels of free testosterone in the body.

However, there are various points to consider when interpreting this study:

  • The main limitation with this study is that, being cross sectional, it cannot prove cause and effect. We do not know that the alcohol consumption has directly influenced the measures of sperm quality. Various other health and lifestyle factors could also be having an influence on the relationship (adjustment was only made for confounders of time since last ejaculation, smoking and BMI). For example, men who drink more may have poorer overall diet and activity and lifestyle habits, and these things may all be associated.
  • There is the possibility of inaccurate recall or inaccurate calculation of units of alcohol consumed in the previous week, or numbers of past binge drinking episodes.
  • Also, though the researchers asked whether this was a “typical week”, it cannot be known how representative it was of longer-term patterns. This is especially the case as this was a week in which they were due to be called up to military service which, depending on individual personality, may cause them to drink either more or less than usual.
  • Though this is a large sample of men, they were all young adult Danish men recruited to the military. Therefore, they may not be representative of all populations.
  • We don’t know that any of the measures of reduced sperm quality observed would actually have any effect on fertility.

Overall, this study is a valuable contribution to the body of literature assessing the relationship between alcohol intake and effects on semen quality, but it doesn’t provide conclusive answers on its own.

It is recommended, whether you are trying for a baby or not, to spend at least a few days per week without drinking alcohol.

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

Just five alcoholic drinks a week could reduce sperm quality. The Guardian, October 3 2014

Even moderate drinking reduces sperm count. The Daily Telegraph, October 3 2014

How just four pints of lager a week harms male fertility: More than 7.5 units over seven days found to affect sperm quality. Mail Online, October 2 2014

Links To Science

Jensen TK, Gottschau M, Madsen JOB, et al. Habitual alcohol consumption associated with reduced semen quality and changes in reproductive hormones; a cross-sectional study among 1221 young Danish men. BMJ Open. Published online October 2 2014

Categories: NHS Choices

Scientists look into regenerating retinal cells

NHS Choices - Behind the Headlines - Thu, 02/10/2014 - 13:00

“Scientists … have discovered stem cells in the human eye which can be transformed into light-sensitive cells and potentially reverse blindness,” The Daily Telegraph reports.

While this story is an accurate summary, the research is still at a very early stage, but does show potential.

The cells in question are called limbal neurosphere (LNS cells) and are located at the front of the eye. Unlike standard stem cells, these LNS cells have already started to become specialised eye cells. This new research has found that they may still have the ability to become different types of retinal cells.

Many common causes of blindness, such as macular degeneration, occur when retinal cells are damaged, so the ability to grow new retinal cells would be groundbreaking.

In the experiments, adult mouse LNS cells transplanted on to the retina of newborn mice were able to develop into mature light-detecting (photoreceptor) cells. However, they were not able to integrate into the retina. Human LNS cells showed some signs of developing into retinal cells in the laboratory, but they did not develop into mature cells. They survived when transplanted on to mice retina, but did not develop into retinal cells.

These rather significant hurdles need overcoming before any cure for human blindness becomes possible.

 

Where did the story come from?

The study was carried out by researchers from the University of Southampton, University Hospital Southampton NHS Foundation Trust and the University of Bristol. It was funded by the National Eye Research Centre, T.F.C. Frost Charity, Rosetrees Trust, the Gift of Sight Appeal and the Brian Mercer Charitable Trust.

The study was published in the peer-reviewed journal PLOS One. PLOS One is an open access journal, so the study is free to read online.

The UK media glossed over the preliminary nature of this study. They also didn't explain that the researchers were unable to get the human cells to grow into mature photoreceptor cells in either the laboratory or mouse settings.

 

What kind of research was this?

This study involved laboratory experiments using human and mouse eye tissues, and trials in mice. The researchers wanted to investigate progenitor cells (cells that can develop into one or more kinds of cells) called LNS cells. They aimed to see if mouse and human LNS would develop into retinal cells in the laboratory setting and in mice.

The light-sensory nerve cells (photoreceptors) in the retina cannot regenerate in humans once damaged. This means that currently the only option to fix this damage is to use a donor retina, and the availability of donations is limited. There is also the risk of an individual’s immune system rejecting the donation. Researchers wanted to find a way to take stem cells or cells at the next stage of development (progenitor cells) and use these to develop into any of the cells required to repair the retina – such as photoreceptors. Taking these cells and transplanting them back into the same person would prevent the rejection problems that are seen when a donor retina is used.

 

What did the research involve?

The researchers took limbal tissue (the border between the transparent cornea and opaque sclera) from donated human eyes from adults up to the age of 97, and mice. They extracted LNS cells from them and cultured (grew) them in the laboratory in different conditions, to encourage the cells to develop into mature retinal cells. This included growing them with retinal cells from newborn mice. They assessed whether the LNS cells started to look like retinal cells and express genes, and whether they produced proteins (“markers”) that are typically seen in mature light-sensing retinal cells.

The researchers then transplanted adult mouse LNS cells into the retina of newborn mice, and looked to see whether these cells developed into mature retinal cells. They then repeated this experiment, transplanting human LNS cells into the retinas of newborn mice.

 

What were the basic results?

At least some of the mouse LNS cells showed markers that indicated they appeared to have developed into mature light-sensing retinal cells in the laboratory. When transplanted into newborn mice, the cells produced markers that indicated they had developed into photoreceptor cells, but they did not integrate into – that is, become part of – the retina.

Human-donated LNS grown in the lab with retinal cells from newborn mice showed some signs of developing into retinal cells in the laboratory, but did not produce the mature photoreceptor cell markers. Human-donated LNS cultured with human-donated foetal retinal cells from week seven to eight did not show signs of developing into retinal tissue.

Human LNS transplanted into newborn mice’s retinas survived for up to 25 days, but did not develop into retinal-like cells, including photoreceptors.

 

How did the researchers interpret the results?

The researchers suggest that the human LNS cells were not able to develop into mature retinal cells because there may be a more complex regulatory mechanism in humans than mice. However, they concluded that “as a readily accessible progenitor cell resource that can be derived from individuals up to 97 years of age, LNS cells remain an attractive cell resource for the development of novel therapeutic approaches for degenerative retinal diseases”.

 

Conclusion

This early-stage research has found that LNS cells can be accessed from donated human eyes up to the age of 97. The mouse versions of these cells appear to retain the ability to develop into mature light-sensing retinal cells. However, the researchers have not yet worked out the conditions necessary for human LNS cells to fully develop into mature retinal cells or to integrate with the retina, which would repair it.

If they are able to achieve the necessary conditions for human LNS cells, then people with retinal damage could potentially have the cells taken from the front part of their eye and transplanted on to the retina to repair and regrow photoreceptors. This would remove the need to find a suitable donor, as well as preventing the problems seen with transplant rejections.

However, this is likely to require a lot more research, with the reality a long way off, even if the research proves successful.

Analysis by
Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

Hope for blind as scientists find stem cell reservoir in human eye. The Daily Telegraph, October 2 2014

How stem cells found on the front surface of the eye could lead to treatment for blindness. Mail Online, October 2 2014

UK scientists discover special stem cells that could cure blindness. Daily Express, October 2 2014

Links To Science

Chen X, Thomson H, Cooke J, et al. Adult Limbal Neurosphere Cells: A Potential Autologous Cell Resource for Retinal Cell Generation. PLOS One. Published online October 1 2014

Categories: NHS Choices

Does losing your sense of smell predict death risk?

NHS Choices - Behind the Headlines - Thu, 02/10/2014 - 11:29

"Sense of smell 'may predict lifespan'," BBC News reports. New research suggests people unable to smell distinctive scents, such as peppermint or fish, may have an increased risk of death within five years of losing their sense of smell.

The study found adults aged 57 or above who could not correctly identify five particular scents – peppermint, fish, orange, rose and leather – were more than three times as likely to die in the next five years.

The authors speculate loss of smell does not directly cause death, but it could be an early warning sign that something has gone wrong, such as exposure to toxic environmental elements or cell damage.

While this study is interesting, it does not prove that loss of sense of smell (anosmia) is a predictor of early death. Researchers used only five scents to identify people with anosmia and only tested people's sense of smell once, which makes the results less reliable. 

There are many reasons for temporary loss of sense of smell, including viral infections, nasal blockage and allergy, so you shouldn't panic if you suddenly stop "smelling the roses".  But you are advised to see your GP if there is no obvious reason for a sudden loss of smell.

 

Where did the story come from?

The study was carried out by researchers from the University of Chicago and was funded by the US National Institutes of Health, as well as other public bodies.

The study was published in the peer-reviewed journal, PLOS One. PLOS One is an open access journal, so the study is free to read online.

Many headlines were alarmist – for example, "Your nose knows death is imminent" in The Guardian and The Daily Telegraph's claim that, "A poor sense of smell could mean the end is nigh".

The Daily Mail took a more responsible approach by including comments from independent experts, who urged people with anosmia not to panic and said more research was needed on this topic.

 

What kind of research was this?

The research was part of a large US cohort study looking at health and social relationships in a large nationally representative sample of men and women aged 57 to 85. It is based on two surveys of about 3,000 participants – one carried out in 2005-06 and the second five years later.

The authors say sense of smell (olfactory function) plays an essential role in health and is also linked to key parts of the central nervous system. Normal olfactory function depends on cellular regeneration, which may be affected by the ageing process, they say.

They also say problems with sense of smell are already known as an early symptom of some major neurodegenerative diseases, including Alzheimer's and Parkinson's diseases.

Their hypothesis is olfactory dysfunction could be an early indicator of impending death. But because this was a cohort study, it is unable to prove cause and effect – in other words, that the loss of sense of smell led to death.

 

What did the research involve?

In 2005-06, researchers conducted interviews with 3,005 participants (1,454 men and 1,551 women) at home, assessing their ability to identify five common distinctive smells. These were, in order of increasing difficulty: peppermint, fish, orange, rose and leather.

Researchers used a validated odour identification test, presented using felt-tip pens. The five smells were selected and presented one at a time. Participants were asked to identify each by choosing from a set of four picture or word prompts.

The results were used to categorise olfactory function as:

  • anosmic (loss of sense of smell) by 4 to 5 errors
  • hyposmic (moderate loss of sense of smell) by 2 to 3 errors 
  • normosmic (normal sense of smell) by 0 to 1 error

In a second survey in 2010-11, researchers investigated which of the participants were still living. They did this either by speaking to the participants, family members or neighbours, or by examining public records or news sources.

They analysed their results using standard statistical methods and produced various models of their results, one of which adjusted for other factors that might affect mortality (confounders).

These included age, socioeconomic status, disease status, nutrition and body mass index. The researchers also controlled their results for frailty (measured by the inability to perform one or more of seven activities of daily living), cognitive function, smoking and drinking.

 

What were the basic results?

In 2010-11, 430 (12.5%) of the original 3,005 study subjects had died and 2,565 were still alive. In 10 cases it was unknown if the participant was alive or not, and these people were excluded from the analysis. A further 77 were excluded because of missing data.

Researchers found 39% of older adults with anosmia were dead at the time of the second survey, compared with 19% with hyposmia and 10% of those with a normal sense of smell. This pattern was seen in all age groups.

Once all other factors were taken into account, anosmic older adults had more than three times the odds of death at five years compared with those with a normal sense of smell (odds ratio 3.37, 95% confidence interval 2.04-5.57).

 

How did the researchers interpret the results?

The researchers say olfactory function is one of the strongest predictors of five-year mortality and may serve as a "bellwether" for slowed cellular regeneration, or as a marker for cumulative exposure to toxic environments.

They say loss of sense of smell was an independent risk factor stronger than several common causes of death, such as heart failure, lung disease and cancer.

Olfaction is "the canary in the coalmine of human health", they say, adding that "this evolutionarily ancient special sense may signal a key mechanism that affects human longevity".

A short olfactory test may be clinically useful in identifying patients at risk who might benefit from additional monitoring and follow-up.

 

Conclusion

This is an interesting study but it had limitations, including its use of only one short test and only five smells to identify people with anosmia. The diagnosis was not clinically verified and the test was performed in the person's home environment, rather than standardised across all participants in a clinic.

Although researchers tried to control for confounders, it is still possible that measured and unmeasured confounders played a role.

Even if the results of this study were robust, this study did not look at cause of death, so no preventative strategies were identified for people with anosmia.

Being told you have an increased risk of death is not particularly useful if there are no well-validated methods of reducing said risk. If anything, such news does more harm than good.

There are many reasons for temporary loss of sense of smell, including viral infections, nasal blockage and allergy. But anyone who suddenly loses their sense of smell is advised to see their GP as anosmia may be a sign of an underlying – and treatable – disorder.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Sense of smell 'may predict lifespan'. BBC News, October 1 2014

Your nose knows death is imminent. The Guardian, October 1 2014

People who can no longer smell peppermint, fish, rose or leather 'may have only five years left to live'. Daily Mail, October 2 2014

A poor sense of smell could mean the end is nigh. The Daily Telegraph, October 1 2014

Links To Science

Pinto JM, Wroblewski KE, Kern DW, et al. Olfactory Dysfunction Predicts 5-Year Mortality in Older Adults. PLOS One. Published online October 1 2014

Categories: NHS Choices

Minimum alcohol pricing would 'save 100s of lives'

NHS Choices - Behind the Headlines - Wed, 01/10/2014 - 13:30

“‘Hundreds of lives lost' over failure to bring in minimum alcohol pricing,” The Independent reports.

The news is based on research that modelled the effect of a minimum alcohol price per unit of around 40-50p. It suggested that this would be 50 times more effective than the current ban on "below-cost sales" (where alcohol is sold at a loss to attract sales of other goods).

The statistical analyses conducted in this study were based on a number of well-respected data sets, such Hospital Episodes Statistics from 2005 to 2006, showing alcohol-related admissions to hospital.

The model estimated that a minimum cost of 45p per unit of alcohol would affect 23.2% of alcohol units sold, compared to just 0.7% for the ban on below-cost selling. This would mean saving 624 alcohol-related deaths per year, compared to 14 for the ban on below-cost selling, as well as 23,700 fewer admissions to hospital per year, compared to 500 for the ban on below-cost selling.

It’s worth remembering the scientific truism that “all models are wrong, but some are useful”. Based on its methodology, this appears to be one of the useful ones.

We are unlikely to see a minimum alcohol price in 2014, but policymakers will be sure to consider this new study alongside other emerging evidence on how best to protect public health, while allowing people the freedom to enjoy their booze.

 

Where did the story come from?

The study was carried out by researchers from the University of Sheffield and was funded by the Medical Research Council and Economic and Social Research Council, in the UK.

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

Media reporting was accurate and provided comments from the chief executives of Alcohol Concern and Addaction regarding the importance of the findings.

 

What kind of research was this?

This was a modelling study that aimed to estimate the impact that different alcohol control measures might have on alcohol-related deaths, illnesses, admissions to hospital and quality-adjusted life years.

In May 2014, the government implemented a ban on "below-cost selling" of alcohol (selling at less than the cost of producing and selling the alcohol) in England and Wales. The researchers outline that as there is the alcohol beverage-specific duty tax and value added tax (VAT) of 20%, this ban affects drinks with higher duty rates such as spirits, and has less effect on drinks with lower duty rates, such as cider.

The government had previously considered alternative strategies, including having a minimum unit price for alcohol of between 40p and 50p. Minimum unit pricing would effectively target drinks that are high in alcohol content and sold relatively cheaply.

It is these types of drinks, such as extra-strength cider or lager, or cheap spirits, which many experts hold responsible for causing the increase in alcohol-related health problems that have occurred in recent years. For example, in some supermarket chains, cider with an alcohol content of 8% ABV is cheaper to buy than some brands of bottled water.

The researchers wanted to model the potential effects that different minimum unit prices would have on outcomes compared to the ban on below-cost selling of alcohol.

Modelling studies can provide a framework to look at the potential effects of different policies or procedures, but they cannot accurately predict the precise number that would be affected.

 

What did the research involve?

The researchers used data from the 2009 general lifestyle survey, which captured average daily and weekly alcohol intake for 11,385 people in England.

Estimates on the price paid for various different types of alcoholic drinks between 2001 and 2009 were acquired from annual two week purchasing diary surveys of around 6,500 UK households, which amounted to 227,933 transactions.

The researchers looked at 96 different subgroups from the sample, split by age, sex, mean consumption (moderate, hazardous and harmful) and income (below or above the poverty line), and compared the amount and cost of alcohol they purchased.

They then estimated the effect that different price changes would have on alcohol consumption in each of the subgroups. They looked at a ban on below-cost selling and minimum unit price policies with thresholds of 40p, 45p and 50p.

An example of the statistical model is that a 1% increase in the price of beer would be estimated to result in a 0.98% reduction in the amount purchased, but this might cause a slight increase in wine purchased of 0.096%. They performed different analyses according to the subgroups, accounting for:

  • younger men drinking more beer on nights out
  • middle-aged women drinking more wine at home
  • harmful drinkers spending less per unit of alcohol
  • people who drink cheaper cider being more affected by an increase in the minimum price per unit

Lastly, the researchers used this estimated change in alcohol consumption to model its effect on the mortality and disease prevalence of 47 conditions that are related to harmful alcohol use. These conditions include oesophageal cancer. The researchers used data from the Office for National Statistics and Hospital Episodes Statistics from 2005 to 2006.

 

What were the basic results?

A ban on below-cost selling is estimated to:

  • affect 0.7% of alcohol units sold
  • reduce harmful drinkers' mean annual consumption by 0.08% – around 3 units per year
  • save 14 deaths and 500 admissions to hospital per year

A minimum cost of 45p per unit of alcohol is estimated to:

  • affect 23.2% of alcohol units sold
  • reduce harmful drinkers’ mean annual consumption by 3.7% – around 137 units per year
  • save 624 deaths and 23,700 admissions to hospital per year

Interestingly, estimates of the impact on supermarkets and shops selling alcohol suggested minimum unit pricing would increase alcohol revenues by 5.6%, while banning below-cost selling would lead to a much smaller rise of 0.2%. The team expected this would translate into bigger profits for the retailers, but could not confirm this for sure because they weren’t able to access the commercially sensitive data needed to calculate this information.

 

How did the researchers interpret the results?

The researchers conclude that, “the UK government’s recently implemented ban on below-cost selling affects just 0.7% of alcohol units currently sold, and is estimated to have small effects on consumption and health harm. The previously considered policy of a minimum unit price, if set at expected levels between 40p and 50p per unit, is estimated to have an approximately 40 to 50 times greater effect”.

 

Conclusion

This modelling study provides a framework to look at the potential effects of two different alcohol control measures on alcohol-related illness and death across the UK. The policy background to this story is that the UK government originally announced plans to introduce minimum unit pricing, but later changed its view.

Instead, the government implemented a ban on below-cost selling. This modelling study suggested that minimum unit alcohol pricing originally announced (at between 40p and 50p) would have a 40 to 50 times greater beneficial impact on public health compared with a ban on selling alcohol below-cost price.

As it was based on a mathematical model, this study cannot accurately predict the precise number of deaths that could be avoided by changing alcohol use. However, it can provide an approximation, which is useful for policymakers.

Limitations for this particular model include its reliance on estimates from surveys, which could be open to recall bias regarding the amount of alcohol purchased or consumed. However, strengths of the model include the large number of people who were surveyed and that the survey was conducted without participants knowing that the information would be used in this way.

The researchers carried out a number of sensitivity analyses to test the reliability of their model using different inputs. The team said, “these effects suggest that the relative scale of impact between a ban on below cost selling and a minimum unit price are robust to a variety of assumptions and uncertainties”. This gives an added degree of confidence to the main findings.

If you are concerned that you may be drinking more than you should, then it may be useful to keep a “drink diary” in which you keep a note of the amount of units you drink over the course of a week. It could be a lot higher than you think. Download the drinks diary leaflet (PDF, 697kb) to work out your alcohol intake over a week. You can also download the NHS Choices drink tracker app, which is available for iOS devices.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

'Hundreds of lives lost' over failure to bring in minimum alcohol pricing, says study. The Independent, October 1 2014

Minimum unit price '50 times more effective' than alcohol floor price. BBC News, October 1 2014

Study backs minimum alcohol prices to cut drinking harm. The Daily Telegraph, September 30 2014

Minimum alcohol pricing 'more effective' than ban on bulk buying. ITV News, October 1 2014

Links To Science

Brennan A, Meng Y, Holmes J, et al. Potential benefits of minimum unit pricing for alcohol versus a ban on below cost selling in England 2014: modelling study. BMJ. Published online September 30 2014

Categories: NHS Choices

Viagra 'may cause visual disturbance' in some men

NHS Choices - Behind the Headlines - Wed, 01/10/2014 - 12:30

"Viagra may permanently damage vision in some men, study finds," reports The Guardian. But the news is, in fact, based on research in mice.

This research suggests the medication may not be suitable for men who carry a gene mutation associated with the inherited eye condition retinitis pigmentosa.

Researchers found Viagra (the brand name of the drug sildenafil) caused visual disturbance in mice genetically engineered to carry a single copy of the retinitis pigmentosa mutation.

It took two weeks for the mice's visual response to go back to normal.

The researchers say this has human implications as 1 in 50 men are believed to be retinitis pigmentosa carriers.

Retinitis pigmentosa is a hereditary condition that causes progressive loss of light reception and the outer fields of vision, leading to tunnel vision and blindness.

Despite The Guardian's headline, Viagra didn't cause permanent damage to the mice's eyes, and all of the mice in the study recovered. In addition, the doses used were between 5 and 50 times the equivalent recommended dose for men.

However, you should stop taking sildenafil citrate and seek immediate medical advice if you suddenly develop eye or eyesight problems.

 

Where did the story come from?

The study was carried out by researchers from the School of Optometry and Vision Science at the University of New South Wales, the Centre for Eye Health, Sydney, and the University of Melbourne in Australia, and the University of Auckland, New Zealand.

It was funded by the National Health and Medical Research Council of Australia.

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

The Guardian reported the study accurately, but its headline gave a stronger indication of permanent visual damage than was found in the study. It also implied the new research had been done on humans rather than mice.

 

What kind of research was this?

This was an animal study investigating the effects of sildenafil (more commonly known by the brand name Viagra) on the retina of mice. Temporary visual disturbance (blurred vision, increased light sensitivity and colour change) has been reported by some people after taking sildenafil.

Previous research in humans found 50% of healthy men who take at least double the maximum recommended dose of sildenafil will experience temporary visual disturbance (200mg rather than the recommended 25mg to 100mg).

The researchers wanted to see if the effect of sildenafil on sight was greater if there was a susceptibility to retinal damage, as it is estimated 1 in 50 men are carriers of a single copy of a gene for one of several degenerative retinal conditions, but have normal vision.

To test the theory, the researchers used mice genetically engineered to be carriers for the degenerative condition retinitis pigmentosa and checked if they were more susceptible to visual disturbance.

Retinitis pigmentosa is a hereditary condition that causes progressive loss of light reception and the outer fields of vision, leading to tunnel vision and blindness.

Most people with the condition have a defect in both genes. Some people with just one gene can be affected, though most have normal vision and are considered to have "carrier status".

 

What did the research involve?

The genetically engineered mice carriers for retinitis pigmentosa had normal retinal structure and function, as assessed by electroretinography (ERG). ERG uses electrodes to assess how the retina responds to certain types of visual stimulations, such as flashing lights.

However, there were molecular differences in the rod cells of the mice (rod cells detect light, shape and movement), which made them more sensitive to light than normal mice. The researchers suggest this also made their sight more susceptible to degeneration.

The researchers heavily anaesthetised normal mice and carrier mice using ketamine. They then measured their ability to detect flashes of light in a dark room by ERG.

The mice were also injected with doses of sildenafil (5 to 50 times higher than the equivalent recommended dose for humans) and the researchers repeated the ERG after an hour.

Some mice were given a dose 20 times higher, and the ERG was performed after a period of either one hour, two days or two weeks. They performed the same experiment using a saline (salty water) injection to act as a control.

The mice were then killed and their retinas were examined using several laboratory processes.

 

What were the basic results?

In normal mice, photoreceptor response decreased as sildenafil dose increased (this is termed a "dose-dependent" response). For the mice given 20 times the equivalent human dose, this decreased response resolved by day two, although at bright light levels a reduced ERG response was still apparent.

Although there was a decrease in photoreceptor response for the carrier mice after one hour, this was smaller than that seen in normal mice. Sildenafil also increased the response to light of the inner retinal neurons, especially in bright light.

For the mice given 20 times the equivalent human dose, this decreased response did not improve until two weeks later.

In the carrier mice, there were increased levels of cytochrome C, a molecule that indicates cell death, but there was no sign of cell loss or change in retinal thickness in any of the mice retina.

 

How did the researchers interpret the results?

The researchers concluded that in normal mice, sildenafil caused reduced electroretinogram (ERG) response that resolved within 48 hours.

In mice that were carriers for the degenerative condition retinitis pigmentosa but who had normal sight, the reduced ERG response took two weeks to return to normal, and they had an increase in a molecule that indicates cell death.

The researchers concluded this may mean sildenafil could cause retinal degeneration.

They say that, "The results of this study are significant considering approximately 1 in 50 people are likely to be carriers of recessive traits leading to retinal degeneration."

 

Conclusion

This study looked at the effects of sildenafil (Viagra) on the retinas of mice. It showed that genetically engineered mice with retinitis pigmentosa carrier status are more susceptible to the temporary side effect of visual disturbances than normal mice.

These carrier mice also had increased levels of the chemical cytochrome C, which is an indicator of cell death.

However, there was no sign of cell loss or change in retinal thickness in any of the mice retina. This research therefore did not prove sildenafil causes permanent retinal degeneration because the changes were reversible in all mice.

It should be emphasised the smallest amount of sildenafil used in these experiments was five times the equivalent recommended dose for men, so it is not clear whether similar results would be seen at normal dose levels.

The product information for sildenafil states its safety has not been determined for people with hereditary degenerative retinal disorders, so it is not recommended for this group.

However, this is only problematic for men who carry a single copy of the gene – although they might not be aware of this because it doesn't cause problems.

Studies conducted over a longer period of time would be useful to determine if sildenafil causes retinal degeneration or permanent visual changes, and whether these types of symptoms or changes are more likely in people with carrier status for a degenerative retinal condition.

If you do experience a sudden decrease or loss of vision, stop taking sildenafil and contact your doctor immediately. 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Viagra may permanently damage vision in some men, study finds. The Guardian, October 1 2014

Viagra 'may cause blindness': Ingredient in the drug can permanently affect sight, doctors warn. Mail Online, October 1 2014

Links To Science

Nivison-Smith L, Zhu Y, Whatham A, et al. Sildenafil alters retinal function in mouse carriers of Retinitis Pigmentosa. Experimental Eye Research. Published online September 17 2014

Categories: NHS Choices

High levels of tooth decay found in three-year-olds

NHS Choices - Behind the Headlines - Tue, 30/09/2014 - 12:20

"Tooth decay affects 12% of three-year-olds, says survey," BBC News reports. The survey, carried out by Public Health England, found big variations in different parts of the country. Experts believe sugary drinks are to blame for this trend.

The survey looked at the prevalence and severity of tooth decay in three-year-old children in 2013. This is the first time the dental health of this age group has been surveyed nationally. It found 12% of children surveyed had tooth decay – more than one in eight children.

Tooth decay (also known as dental decay or dental caries) occurs when a sticky acidic film called plaque builds up on the teeth and begins to break down the tooth's surface. A diet high in sugar can help stimulate the production of plaque.

As it progresses, tooth decay can cause an infection of underlying gum tissue. This type of infection is known as a dental abscess and can be extremely painful.

 

Who produced the children's dental health report?

The survey and subsequent report was produced by Public Health England (PHE), part of the Department of Health. PHE's role is to protect and improve the nation's health and wellbeing, and reduce health inequalities.

This survey of the prevalence and severity of tooth decay in three-year-olds was performed to help identify which age group interventions to improve tooth decay should be aimed at.

 

What data did the report look at?

The report looked at the prevalence and severity of dental decay in three-year-old children in 2013. At three years of age most children have all 20 milk teeth (also known as primary teeth).

PHE randomly sampled children attending private and state-funded nurseries, as well as nursery classes attached to schools and playgroups. The children's teeth were examined to see if they had missing teeth, filled teeth or obvious signs of tooth decay.

 

What were the main findings of the report?

Of the 53,814 children included in the survey, 12% had dental decay. Of the children with dental decay, on average these children had at least three teeth that were decayed, missing or filled.

Across all the children included in the survey, the average number of decayed, missing or filled teeth was 0.36 per child.

The report found a wide variation in the levels of decay experienced by three-year-old children living in different parts of the country. The four regions with the most dental decay were:

  • the East Midlands
  • the north west
  • London
  • Yorkshire and the Humber

 

What are the implications of the report?

Where there are high levels of tooth decay among three-year-olds, Public Health England wants earlier interventions to target this younger age group, rather than waiting until the age of five (when these interventions usually take place).

Where there are high levels of tooth decay found in the primary incisors (a condition known as early childhood caries), PHE wants local organisations to tackle problems related to infant feeding practices.

Early childhood caries are associated with young children being given sugar-sweetened drinks in a bottle – especially when these are given overnight or for long periods of the day.

Where tooth decay levels increase sharply between the ages of three and five, PHE wants local organisations to tackle this by helping parents reduce the amount and frequency of sugary food and drinks their children have, as well as increasing the availability of fluoride.

 

Conclusion

There are two important steps you can take to protect your children's teeth against tooth decay:

  • limit their consumption of sugar, especially sugary drinks
  • make sure they brush their teeth at least twice a day with fluoridated toothpaste
Sugar

Sugar causes tooth decay. Children who eat sweets every day have nearly twice as much decay as children who eat sweets less often.

This is caused not only by the amount of sugar in sweet food and drinks, but by how often the teeth are in contact with the sugar. This means sweet drinks in a bottle or feeder cup and lollipops are particularly damaging because they bathe the teeth in sugar for long periods of time. Acidic drinks such as fruit juice and squash can harm teeth, too.

Don't fall into the trap of thinking that a fruit juice advertised as "organic", "natural" or with "no added sugar" is inherently healthy. A standard 330ml carton of orange juice can contain almost as much sugar (30.4g) as a can of coke (around 39g).

As Dr Sandra White, director of dental public health at PHE, points out: "Posh sugar is no better than any other sugar … our key advice for [children] under three is to just have water and milk."

Tooth brushing

A regular teeth cleaning routine is essential for good dental health. Follow these tips and you can help keep your kids' teeth decay free:

  • Start brushing your baby's teeth with fluoride toothpaste as soon as the first milk tooth breaks through (usually at around six months, but it can be earlier or later). It's important to use a fluoride paste as this helps prevent and control tooth decay.
  • Children under the age of three can use a smear of family toothpaste containing at least 1,000ppm (parts per million) fluoride. Toothpaste with less fluoride is not as effective at preventing decay.
  • Children between the ages of three and six should use a pea-sized blob of toothpaste containing 1,350 to 1,500ppm fluoride. Check the toothpaste packet for this information or ask your dentist.
  • Make sure your child doesn't eat or lick the toothpaste from the tube.
  • Brush your child's teeth for at least two minutes twice a day, once just before bedtime and at least one other time during the day.
  • Encourage them to spit out excess toothpaste, but not to rinse with lots of water. Rinsing with water after tooth brushing will wash away the fluoride and reduce its benefits.
  • Supervise tooth brushing until your child is seven or eight years old, either by brushing their teeth yourself or, if they brush their own teeth, by watching how they do it. From the age of seven or eight they should be able to brush their own teeth, but it's still a good idea to watch them now and again to make sure they brush properly and for the whole two minutes. 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Tooth decay affects 12% of three-year-olds, says survey. BBC News, September 30 2014

One in 8 three-year-olds has rotting teeth... and fruit juice is to blame: Parents warned organic drinks and smoothies can contain as much sugar as a glass of coke. Daily Mail, September 30 2014

Sugary drinks in baby bottles triggering rise in tooth extractions. The Guardian, September 30 2014

Fruit drinks fuelling tooth decay among under 3s. The Daily Telegraph, September 30 2014

Three-Year-Old Children Suffering Tooth Decay. Sky News, September 30 2014

1 in 8 children suffering from tooth decay 'due to too much sugar'. ITV News, September 30 2014

Shock figures reveal 1 in 8 three-year-olds have tooth decay. Daily Mirror, September 30 2014

Rotten truth: Tooth decay in under-3s is on the rise. Daily Express, September 30 2014

Categories: NHS Choices

Deep-fried Mars bars: unhealthy, but no killer

NHS Choices - Behind the Headlines - Tue, 30/09/2014 - 11:50

“Eating a deep-fried Mars bar could give you a stroke in minutes,” reports the Metro.

However, the study that prompted this headline found no evidence that the Scottish snack can potentially trigger a fatal stroke within minutes. 

Fans of deep-fried Mars bars actually have little to worry about in this regard, aside from the obvious risks of regularly consuming a meal full of sugar and saturated fats.

The over-alarmist headlines are based on the results of a small study using 24 healthy participants, which looked at whether eating a deep-fried Mars bar could affect the body’s ability to respond to breath holding by increasing blood flow to the brain (termed “cerebrovascular reactivity”). Impaired cerebrovascular reactivity has been associated with stroke, but this latest study didn’t look at stroke as an outcome.

Importantly, it found no significant differences in cerebrovascular reactivity after eating either a deep-fried Mars bar or porridge.

When the researchers analysed men and women separately, they also found no significant differences in cerebrovascular reactivity after eating a deep-fried Mars bar or porridge in either men or women.

However, when the researchers compared men with women, they found a significant difference.

Common sense suggests that eating deep-fried Mars bars regularly is not good for your health. However, this study didn't find any evidence that a deep-fried Mars bar alone can trigger a stroke within minutes.

 

Where did the story come from?

The study was carried out by researchers from the University of Glasgow and the British Heart Foundation Cardiovascular Research Centre in Scotland, and was funded departmentally.

The study was published in the peer-reviewed Scottish Medical Journal.

The media coverage of this story was poor. The oft-repeated claim that the snack can trigger a stroke within minutes is entirely baseless. Obviously, if you are recovering from a stroke or told that you have risk factors for a stroke, then a deep-fried Mars bar would probably be bottom of the list of recommended foods. However, it seems unlikely that a single sugary snack would trigger a stroke.

Causes of stroke are usually a combination of interrelated risk factors, such as smoking, high blood pressure, high cholesterol, obesity and excessive alcohol consumption.

 

What kind of research was this?

This was a randomised crossover trial that aimed to determine whether eating deep-fried Mars bars impaired cerebrovascular reactivity in comparison to eating porridge.

Cerebrovascular reactivity is the change of blood flow in the brain in response to a stimulus. In this trial, the researchers looked at the change in blood flow after participants were asked to hold their breath for 30 seconds. Holding your breath should increase blood flow to the brain.

The researchers say that impaired change in brain blood flow following a stimulus is associated with an increased risk of ischaemic stroke (stroke caused by a lack of blood flow to the brain).

In this randomised crossover trial, all participants ate both a deep-fried Mars bar and porridge. Half the participants ate the Mars bar first, and half the participants ate the porridge first. Whether they ate the Mars bar first or the porridge first was randomised.

A randomised crossover trial is an appropriate study design to answer this sort of question.

 

What did the research involve?

The researchers studied 24 people, with an average age of around 21. Their body mass index (BMI) was within the healthy range (an average of 23.7).

After fasting for at least four hours, people were randomised to receive a deep-fried Mars bar or porridge.

The researchers looked at changes in blood flow in the brain after participants held their breath for 30 seconds, before and 90 minutes after, eating either a deep-fried Mars bar or porridge.

They looked at blood flow using ultrasound.

Participants returned to receive the other foodstuff on a second visit at least 24 hours after the first.

The researchers compared the changes in blood flow after participants ate the deep-fried Mars bar and porridge.

 

What were the basic results?

Eating a deep-fried Mars bar caused a non-statistically significant reduction in cerebrovascular reactivity compared to eating porridge.

The researchers then looked at men and women separately (14 of the 24 people in the study were male). Changes in cerebrovascular reactivity were not significant in either men or women after they ate a deep-fried Mars bar or porridge.

The researchers then compared men with women. They found there was a significant difference in cerebrovascular reactivity after eating a deep-fried Mars bar compared to eating porridge, with a modest decrease of cerebrovascular reactivity in males. 

 

How did the researchers interpret the results?

The researchers concluded that, “Ingestion of a bolus of sugar and fat caused no overall difference in cerebrovascular reactivity, but there was a modest decrease in males. Impaired cerebrovascular reactivity is associated with increased stroke risk, and therefore deep-fried Mars bar ingestion may acutely contribute to cerebral hypoperfusion [decreased blood flow] in men.”

 

Conclusion

This study found no significant differences in cerebrovascular reactivity (the body’s ability to respond to breath holding by increasing blood flow to the brain) after eating either a deep-fried Mars bar or porridge.

When the researchers analysed men and women separately, they found no significant differences in cerebrovascular reactivity after eating a deep-fried Mars bar or porridge. However, when the researchers compared men with women, they found a significant difference, although whether there is any clinical significance to this finding is unclear.

The researchers point out that there are limitations to their study, including the fact they studied young, healthy individuals. It may be that there are differences in cerebrovascular reactivity in older patients at risk of stroke.

Confirming whether the risk is significant in this sub-group would be challenging, not least due to ethical considerations. Assigning people a diet you suspect could harm them would be a serious breach of medical ethics.

Common sense suggests that eating deep-fried Mars bars regularly will not be good for your health, as a diet high in saturated fats and sugar can increase the risk of cardiovascular diseases (diseases that affect the heart and blood vessels).

However, the very occasional late night “guilty pleasure” is highly unlikely to trigger a stroke.

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Deep-fried Mars bar raises risk of having a stroke WITHIN MINUTES, experts claim. Daily Mirror, September 29 2014

Deep-fried Mars bars 'could trigger a stroke': Blood flow to the brain slows within minutes of eating the snack. Mail Online, September 29 2014

Eating a deep fried Mars bar could give you a stroke in minutes. Metro, September 29 2014

Links To Science

Dunn WG, Walters MR. A randomised crossover trial of the acute effects of a deep-fried Mars bar or porridge on the cerebral vasculature. Scottish Medical Journal. Published online September 22 2014

Categories: NHS Choices

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