Medical News

Social care reforms announced

Medical News - Tue, 01/19/2038 - 06:14

Most of the UK media is covering the announcement made in Parliament by Jeremy Hunt, Secretary of State for Health, about proposed changes to social care.

The two confirmed points to have garnered the most media attention in the run-up to the announcement are:

  • a ‘cost cap’ of £75,000 worth of care costs – after this point the state would step in to meet these care costs
  • raising the current means-testing threshold for people to be eligible for state-funded social care from £23,520 to £123,000

The government expects these changes will lead to fewer people having to sell their homes in order to pay for their long-term care needs.

Speaking in Parliament, Mr Hunt said that the current system was ‘desperately unfair’ as many older people face ‘limitless, often ruinous’ costs. The minister stated that he wants the country to be ‘one of the best places in the world to grow old’.


What is social care?

The term social care covers a range of services provided to help vulnerable people improve their quality of life and assist them with their day-to-day living.

People often requiring social care include:

  • people with chronic (long-term) diseases
  • people with disability
  • the elderly – particularly those with age-related conditions, such as dementia

Social care services can include:

  • healthcare
  • equipment
  • help in your home or in a care home
  • community support and activities
  • day centres


How does the current adult social care system work?

Currently, state funding for social care is based on two criteria:

  • means – people with assets of more than £23,520 do not qualify for funding
  • needs – most local authorities will only fund care for people assessed to have substantial or critical needs

The majority of people currently requiring social care pay for it privately. These are known as ‘self-funders’.


What prompted these reforms to adult social care?

Put simply, on average, the UK population is getting older.

When the welfare state was created in the early 20th century, it was not expected that people would someday routinely live into their 70s, 80s, and even 90s.

The increase in life expectancy is a good thing, however, it brings a new set of challenges.

While people are living longer, they are also spending more of their lives in ill health. Older people are more likely to have potentially complex care needs that can be expensive to manage.

Many people are currently ineligible for state-funded social care under the existing laws. To meet the costs of these care needs, these ‘self-funders’ have, in many cases, had to sell or remortgage their home, or sell other assets to pay for the costs of their care.

Without reforms, experts agree that the cost of social care for both the state (through taxes) and to ‘self-funders’ is likely to become increasingly problematic.

To try and find the best way to resolve some of the difficulties of fairly funding adult social care, the Department of Health set up a commission. This independent commission reported its findings to ministers in July 2011. The government considered these findings in its white paper on care and support published in July 2012, and in the drafting of the proposed new legislation.


What happens next?

The government has introduced a Social Care Bill which will need to be passed by the Houses of Parliament.

If the bill is successfully passed it is expected the amendments will come into force by 2017.


Edited by NHS Choices. Follow Behind the Headlines on twitter.

Links To The Headlines

Social care: Jeremy Hunt hails 'fully-funded solution'. BBC News, February 11 2013

Social care reforms: Almost 2 million pensioners will be denied state help. The Daily Telegraph, February 11 2013

Social care reform: how your family may be affected. The Daily Telegraph, February 11 2013

Dilnot 'regrets' decision to set social care cap at £75,000. The Guardian, February 11 2013

Hunt statement on adult social care cap: Politics live blog. The Guardian, February 11 2013

Categories: Medical News

Too soon to say being tall increases cancer risk

Medical News - Fri, 10/02/2015 - 17:00

"Higher risk of cancer if you are tall," says the Daily Mirror. Most media outlets provided a similar spin on the seemingly big news that the risk of developing cancer increases with every 10cm of height.

Tall people shouldn't lose any sleep over this news: let's face it, there's nothing you can do about your height (although there are plenty of things you can do to reduce your risk of cancer). What's more, the research these stories are based on does not provide proof being tall means you will get cancer.

Currently, only preliminary results have been presented in the form of a conference abstract, and the research hasn't had the kind of independent rigorous scrutiny you'd hope for in published science.

That's not to say this was bad research: the study was large, involving 5.5 million adults, which is usually a good thing. However, it did not take into account many known risk factors for cancer, such as smoking. 

Neither the study nor any of the papers covering the story suggested adult height directly causes cancer. Theories presented in the media about why being taller would increase cancer risk are simply speculation – no matter how well informed they are.

Where did the story come from?

The study was carried out by researchers from Karolinska Institute in Stockholm and was funded by HKH Kronprinsessan Lovisas förening för Barnasjukvård and Stiftelsen Samariten.

It was summarised briefly ahead of the European Society for Paediatric Endocrinology conference in a very short article called a conference abstract. This means there is little detail on the methods and results presented, and its strengths and weaknesses can't be appraised in any depth.

It has not yet been published in a peer reviewed journal, so the research hasn't been scrutinised by experts for scientific accuracy or rigour.

Generally, the media reported the story accurately. It was made clear that no-one was saying being tall causes cancer directly. However, because the actual science was not presented in great detail, most padded out their copy with speculation about what could cause the link between being tall and cancer. Fortunately, the media outlets that did this tended to use independent and informed commentators. 

What kind of research was this?

This was a cohort study of a very large group of mostly Swedish adults over several decades. The researchers were looking for a link between height and risk of cancer.

Previous studies have linked being taller with a higher risk of developing cancer overall – breast cancer and skin cancer in particular – and this was also the focus of the new study.

According to media reports, the research team don't believe increased height directly causes cancer. Instead, height is thought to be a marker of other factors that raise the risk of cancer.

One theory presented in the media is that taller people have more cells in their body growing and dividing, with more potential to undergo cancerous change. The higher food intake needed to maintain a larger body size may also play a part.

For this particular study, the researchers were less interested in explaining exactly how height might be linked to cancer risk – they first wanted to establish whether height was linked to cancer.

Apparently, the topic hadn't been studied on a large scale before. Using a large group of people, as they did, increases the chances of finding a true link if one exists, and also increases the accuracy of any calculations of the risk.  

What did the research involve?

The researchers tracked 5.5 million Swedish adults aged over 20 over several decades, although the average time was not reported in the brief summary available.

Sweden has very complete information on its residents. This meant it was relatively simple for the researchers to get height measurements from a combination of military conscription records and passports. These heights ranged from 3 feet 3 inches (100cm) to 7 feet 5 inches (225cm).

The researchers were also able to easily link the height data to medical records showing when a person was diagnosed with cancer and the cancer type.

The team then calculated the risk of people getting cancer for every 10cm increase in height. They worked this out for men and women separately, working out the risk for cancer overall and separately for breast cancer and skin cancer.

Adjustments were made for education level and income, which are known to influence both height and cancer risk. There was no adjustment for smoking, alcohol intake, sun exposure or other factors known to affect cancer risk. 

What were the basic results?

The results presented showed that:

  • Both taller men and taller women had a higher risk of developing cancer overall. For every extra 10cm of height as an adult, the risk of cancer rose by 11% in men and 18% in women.
  • For breast cancer, a 10cm increase in height raised the risk of breast cancer in women by 20%. As breast cancer is much rarer in men, their risk was not calculated.
  • A 10cm increase in height raised the risk of skin cancer by 32% in men and 27% in women.  
How did the researchers interpret the results?

Dr Emelie Benyi, who led the study, said the results could help identify risk factors that could lead to the development of treatments.

She added: "As the cause of cancer is multi-factorial, it is difficult to predict what impact our results have on cancer risk at the individual level." 


This large, long-term cohort study was able to give precise estimates of the risk increase of cancer for taller adults.

Currently, this information has only been presented as a conference abstract and accompanying press release. It is not possible to fully assess the study's methods, strengths and limitations from this, but some potential limitations are apparent.

While the study clearly showed a link between height and cancer, it did not take into account a range of confounding factors known to affect cancer risk – things like smoking, alcohol intake and sun exposure.

The problem is cancer risk may be influenced by these factors – and potentially others – and may explain some or all of the risk increases linked to height here. This study really doesn't provide much in the way of an explanation of how height might be linked to cancer, although media reports mentioned a number of theories.

These theories were largely speculative. The study did not look at whether taller people were more likely to die of cancer, but this is something they plan to do in the future.

Tall people shouldn't be worried by this study. There is not much you can do as an adult to change your height. But the good news is there are many simple things you can do that may help reduce your risk of cancer – for example, eating a balanced, healthy diet, taking regular exercise, not smoking, and drinking alcohol in moderation.

Read more about how a healthy lifestyle can help reduce your chances of developing cancer.

Links To The Headlines

Being tall can increase your risk of cancer, say researchers. The Guardian, October 2 2015

The taller you are, the higher your risk of getting cancer. The Times, October 2 2015

The taller you stand the higher your risk of cancer, scientists calculate. The Daily Telegraph, October 2 2015

Tall people exposed to greater risk of many forms of cancer, say scientists. The Independent, October 1 2015

If you're tall, your risk of cancer could be up to 30% higher. Daily Mail, October 1 2015

Higher risk of cancer if you are tall. Daily Mirror, October 1 2015

Cancer risk linked to your height. Daily Express, October 2 2015

Study supports cancer link with height. BBC News, October 2 2015

Taller people are more likely to develop cancer, says study. Metro Online, October 2 2015


Links To Science

Conference abstract

Benyi E. et al. Positive Association between Height and Cancer in the Swedish Population. ESPE Abstracts. 2015. 84 FC4.6

Categories: Medical News

High blood pressure: does it lead to diabetes?

Medical News - Thu, 10/01/2015 - 16:30

"Study gives strongest link yet between blood pressure and diabetes," says The Guardian. At first glance these might be considered two unconnected conditions, but research over the years has led to diabetes being classified as a risk factor for cardiovascular disease.

Researchers looked at data on more than 4 million people in the UK who were free of any vascular disease or diabetes. They then analysed these people's medical records for around seven years and recorded new cases of diabetes and changes in blood pressure.

People with high blood pressure were found to have around a 50% increased risk of developing type 2 diabetes. The researchers then backed up their findings by looking at previous research and found a risk of more than 70%.

While these types of studies can't prove increased blood pressure causes diabetes, they lend weight to the advice to take steps to lower your blood pressure if it's high to reduce your risk of diabetes.

Read our advice on how to look after your heart and circulation

Where did the story come from?

The study was carried out by researchers from the University of Oxford and was funded by the UK National Institute for Health Research.

It was published in the peer-reviewed Journal of the American College of Cardiology.

This story has been reported widely in the media. Both The Guardian and The Independent have responsibly provided quotes from one of the researchers, who explained the findings tell us a link exists, but we don't know whether high blood pressure is a cause of diabetes or whether it's a risk factor. 

What kind of research was this?

This was a large cohort study and systematic review with meta-analysis to determine whether there is an association between blood pressure and type 2 diabetes.

While the cohort study cannot prove causation, it does provide a link to be investigated further. Combined with a meta-analysis of previously reported studies, we can see if the findings are in agreement. 

What did the research involve?

Researchers collected data from the UK Clinical Practice Research Datalink (CPRD) of 4.1 million people who had a blood pressure measurement recorded in the previous year.

The researchers included people who were aged between 30 and 90 years and were free of any form of vascular disease or diabetes.

Baseline measurements were recorded for:

  • body mass index (BMI)
  • cholesterol (total and high-density lipoprotein)
  • smoking status

The main outcome measures were a diagnosis of diabetes or the prescription of diabetic medication.

A meta-analysis was carried out using prospective observational studies assessing the link between blood pressure and risk of diabetes. The medical database Medline was searched to identify relevant reports.

Studies were only included if they had:

  • at last one year of follow-up
  • looked at the risk associated with a higher systolic blood pressure of 20mmHg 
  • adjusted the findings for sex, age and BMI

Data was combined to assess the risk of diabetes, with separate analyses performed to investigate differences because of gender, BMI and age. 

What were the basic results?

The cohort study included 4.1 million adults (median age 46) who were free of diabetes and cardiovascular disease at the start of the study.

These adults were an average of 46 years old (median), had a BMI slightly above the healthy range (median 25.7), and were followed up for around seven years. There were 186,698 new cases of diabetes during the study period.

Analysis of the data found raised systolic blood pressure of 20mmHg increased the risk of diabetes by 58% (hazard ratio (HR) 1.58; 95% confidence interval (CI) 1.56 to 1.59) and a higher diastolic blood pressure of 10mmHg was associated with a 52% higher risk of diabetes (HR 1.52; 95% CI 1.51 to 1.54). There was a weaker association between blood pressure and diabetes observed with increased age and BMI.

The literature search identified 30 relevant studies, including 285,664 participants and 17,388 new cases of diabetes. Pooling and analysis of the data found a 77% increased risk of diabetes for a 20mmHg higher usual systolic blood pressure (relative risk (RR) 1.77, 95% CI 1.53 to 2.05). 

How did the researchers interpret the results?

The researchers concluded that, "People with elevated [blood pressure] are at increased risk of diabetes. The strength of the association declined with increasing body mass index and age. Further research should determine if the observed risk is modifiable." 


A large-scale cohort study and meta-analysis has assessed the link between increased blood pressure and risk of type 2 diabetes, and found an increase of 20mmHg systolic blood pressure raised the risk of type 2 diabetes by 58%. It also found a higher diastolic blood pressure of 10mmHg was associated with a 52% increased risk of type 2 diabetes.

These findings were confirmed by the results of the meta-analysis, which found a 77% increased risk of diabetes for a 20mmHg higher than usual systolic blood pressure. This study was very large and followed the patients for a fairly long period of time, so we can be more certain of the links it makes.

However, as the authors say, there is a risk the electronic health records misclassified people's blood pressure. An interesting addition to the study would have been to analyse risk according to ethnic group.

Reducing your risk of diabetes and increased blood pressure can be done in similar ways, such as by:

  • maintaining a healthy weight
  • taking regular exercise
  • stopping smoking 
  • eating a healthy diet

Links To The Headlines

Study gives strongest link yet between blood pressure and diabetes. The Guardian, September 29 2015

High blood pressure is linked to greater risk of developing diabetes. The Times, September 29 2015

People with high blood pressure 'more likely to suffer diabetes' - new study finds. Mirror, September 29 2015

High blood pressure 'increases risk of diabetes by 60%'. The Independent, September 29 2015

Links To Science

Emdin CA, et al. Usual Blood Pressure and Risk of New-Onset Diabetes: Evidence From 4.1 Million Adults and a Meta-Analysis of Prospective Studies. Journal of the American College of Cardiology. 2015. 66:1552-62

Categories: Medical News

Probiotic friendly bacteria may play role in stopping asthma

Medical News - Thu, 10/01/2015 - 13:23

"'Good bacteria' key to stopping asthma," says BBC News.

Before you go out and buy a year's supply of probiotic yoghurt drinks, it's worth noting a few points that burst the hype bubble.

The news is based on research that found that the lack of some types of bacteria in babies' guts affected their later chances of asthma. However, this was only the case for three-month-olds so the effect, if it exists, is likely to be time-limited.

The researchers did an experiment to demonstrate the concept – by feeding poo from these babies with the relevant bacteria added in to mice that had an asthma-like condition. The offspring of these mice were less likely to have the disease, but this is not the same as a real-life (and potentially unpalatable) experiment in humans.

Asthma has been linked to the "hygiene hypothesis", a theory that says asthma happens when the immune system does not develop properly. Some believe this can happen if a growing baby is not exposed to enough varied bacteria, with antibiotics and caesarean births implicated.

While this new study has provided evidence in support of this theory, it is too early to say the case is proven. We don't know for sure that the levels of these bacteria directly affect risk of asthma in the way suggested.


Where did the story come from?

The study was carried out by researchers in Canada, from the University of British Columbia, the Child Research Institute and British Columbia Children’s Hospital, McMaster University, the University of Toronto, Hospital for Sick Children Toronto, University of Alberta and University of Manitoba. It was funded by the Canadian Institutes of Health Research. The study was published in the peer-reviewed journal Science Translational Medicine.

The story was not widely covered in the media. BBC News published an accurate account of the research, although the headline that these bacteria are "key to stopping asthma" probably overstates the results.


What kind of research was this?

This research included two separate studies. The first was a nested case-control study of children, who were taking part in the bigger, ongoing Canadian Healthy Infant Longitudinal Development study, a prospective cohort study. The second study was a laboratory experiment using mice.

Case-control and longitudinal studies can highlight links between two factors – in this case between the type of bacteria in the gut and the chances of having asthma – but cannot prove by itself that one causes the other. The mouse study shows what happens when you do something to mice, and although it does provide support for the hypothesis, we don't know for certain if the results are directly applicable to humans.


What did the research involve?

For the study in children, researchers selected groups of children at different levels of asthma risk, and analysed samples of their poo (stools), which had been taken at three months and one year of age. They looked for differences between the composition of the gut bacteria in the children at different asthma risk levels.

They later carried out tests to see whether they could find differences in how the children's digestion worked, and whether these could be linked to specific bacteria.

Researchers selected 319 children with relevant samples. They chose all those who fitted the criteria at age one of having both allergic reactions (tested by skin-prick tests) and wheezing, wheeze only or allergic reactions only. They also looked at a sample of children with neither allergy or wheeze, to act as a comparison group. Children with allergic reactions and wheeze have a much higher chance than those without these conditions of being diagnosed with asthma by age five.

The researchers used DNA analysis to identify bacteria in the stool samples and looked for differences in the bacteria present between the groups at highest and lowest risk of asthma. After analysing the bacteria in the gut, researchers looked for differences in products of digestion, including certain short-chain fatty acids. They wanted to see whether the differences in bacteria were linked to differences in the way the children's digestion worked.

In a separate experiment, researchers took mice bred to be free from bacteria and introduced either a stool sample from a child at high risk of asthma, or the same sample with additional bacteria. They allowed these mice to breed, and showed that their offspring carried the bacteria their parents had been given in their guts. The researchers then provoked an asthma-like condition in these offspring, and later provoked an immune response in the lungs of these animals and looked at the resulting levels of inflammation.


What were the basic results?

The 22 children who had both allergic reactions and wheeze at age one, had similar overall amounts and range of different types of bacteria in their stool samples, compared with other children. However, the researchers found that their levels of four particular types of bacteria were much lower, compared to children at the lowest asthma risk.

These bacteria were Faecalibacterium, Lachnospira, Rothia and Veillonella. Babies who had both allergic reactions and wheeze at age one were also more likely by the age of three to either have been diagnosed with asthma or meet criteria for being at high risk, including having had recurrent wheezing episodes.

Importantly, the researchers only found differences between the groups' stool samples when the children were three months old. By one year, the differences had gone.

The researchers also found that children at higher asthma risk had some differences in the way their body digested food, shown by the fact that they had lower levels of a type of short-chain fatty acid called acetate in their stool.

In the mouse experiment, the offspring of mice given the stool sample with additional samples of the four missing bacteria had a lower level of inflammation in the lung, compared to those mice that did not get the additional bacteria. The stool sample with no added bacteria did not have this effect.


How did the researchers interpret the results?

The researchers say their research shows that changes in the gut bacteria in the first few months of life may be "an important factor influencing asthma development", and that the four bacteria they identify may have a "protective role" against the disease.

They went on to say that the findings "enhance the potential for using rationally designed microbe-based therapies to prevent the development of asthma and other allergic diseases that begin in childhood". By this they mean scientists may be able to design a "friendly bacteria" cocktail to be given to children at high risk of asthma, which could reduce their chances of getting allergies and asthma.



This complicated and interesting study sheds light on one potential cause of asthma in children, and points towards areas where research might lead to a treatment to prevent it or reduce its severity. However, this exciting prospect depends on much more work to confirm the results of this study and find out whether what seems to work in laboratory mice can also work in people.

The idea that reduced exposure to bacteria in childhood might increase the chances of getting allergies and asthma has been around for some time. This theory suggests that, for a child's immune system to develop well, it needs to be exposed to a wide variety of bacteria and viruses. If this doesn't happen, the immune system might become oversensitive and react to things that it shouldn't, like certain types of food, or pollen in the atmosphere.

This study suggests that particular types of gut bacteria in the first few months of life might be important for the development of a healthy immune system. However, the study has limitations. While 319 babies were studied, only 22 had wheeze and allergic reactions at age one, and only 19 of these were in the group classified as having, or being at highest risk of, asthma at age three. 

We need to see these results replicated in bigger studies to be sure that all or most babies at risk of asthma have low levels of these specific bacteria. Also, this type of study alone cannot prove that the differences in gut bacteria actually cause asthma. There may be other factors that are important but have not been considered in this study.

We should also be wary of animal studies. While there are a lot of biological similarities between different species, there are differences. In this study, the mice had an asthma-like condition, but the authors acknowledge that this is not exactly the same as human asthma. Also, the bacteria in the guts of the mice in this study and humans are likely to be different. The effect of adding certain bacteria to a mouse gut may be very different if tried in a human. We need to see carefully controlled studies in humans to know whether this treatment could work.

However, the study suggests lots of future research pathways that could increase our understanding of how asthma develops and how it might best be treated, or eventually prevented. For now, we still don't fully understand what causes asthma. 

Links To The Headlines

'Good bacteria' key to stopping asthma. BBC News, October 1 2015

Links To Science

Arrieta M-C, et al. Early infancy microbial and metabolic alterations affect risk of childhood asthma. Science Translational Medicine. September 30 2015

Categories: Medical News

Are calcium pills any good at preventing bone fractures?

Medical News - Wed, 09/30/2015 - 13:28

"Calcium supplements don't work, say experts," The Daily Telegraph reports.

While this headline is not strictly true, new research has shown that for most healthy people, calcium supplements will make little difference to your bone health or risk of breaking a bone.

The researchers looked at the best studies they could find that had looked at the relationship between calcium and bone fracture. 

For many years, older people have been advised to increase their dietary calcium intake or take a calcium supplement, as calcium is a building block of strong bones. Vitamin D is often recommended alongside calcium, as the body can't absorb calcium without vitamin D.

However, the researchers found that increasing calcium to the high levels recommended in some countries (although not the UK) did not make much difference to the chances of breaking a bone, even when taken alongside vitamin D. 

Calcium pills did increase bone strength by about one to two per cent, but the researchers say this is unlikely to make a difference to fracture risk.

Previous studies have shown that calcium supplements may cause side effects, including constipation. 

However, there's no need to stop taking calcium and vitamin D supplements if you've been advised to take them by your doctor, as there is little doubt they can help people who are deficient in these nutrients. As for everyone else, it seems that taking these pills is an unnecessary expense. 


Where did the story come from?

Both studies were carried out in New Zealand by researchers from the University of Auckland and the University of Otago – plus researchers from the Starship Hospital involved in the bone density study. They were funded by the Health Research Council of New Zealand.

The studies were published in the peer-reviewed British Medical Journal (BMJ) on an open-access basis, so are free to view online.

The main messages of the studies came across in the media reports, although they did not go into detail about the different findings for supplements and dietary calcium, or the problems with some of the studies. 

The Mail Online focused on the potential harms of calcium supplements, such as stomach upsets and heart problems, which were not included in this research.


What kind of research was this?

The researchers carried out two systematic reviews. The first looked at the effect of increased calcium on people's bone strength, the second looked at the effect of increased calcium on people's risk of having a fracture.

Systematic reviews are the best way of summarising the evidence on a topic at any one time. However, the results are only as good as the trials done so far.


What did the research involve?

Researchers searched for all the good quality studies they could find that looked at calcium intake and subsequent fracture or bone strength in people over 50. 

Where possible, the researchers pooled the results to get an overall answer to the question of whether increasing calcium intake, from pills or food, had an effect on either fracture or bone strength.

The researchers began by looking at randomised controlled trials (RCTs) of increased dietary calcium or calcium supplements (including studies with calcium plus vitamin D). They did not find enough RCTs looking at the effects of dietary calcium on fracture to answer the question, so they also included cohort studies exploring this relationship.

The researchers pooled all the results from RCTs to give an overall figure for the effect of calcium on bone strength, measured as bone mineral density (BMD) and the chances of having any fracture, or a specific fracture of the wrist, hip or spine. They then looked at the range of results to see whether they showed the sort of spread you would expect to see by random chance.

For the cohort studies, the researchers found that the studies didn't report their results in a consistent way. This meant they could not combine the figures in one pooled analysis. Instead, they looked at how many studies reported any effect of increased calcium intake on fracture risk.


What were the basic results?

The researchers found 59 RCTs looking at the effect of calcium on bone mineral density, including 13,790 people. The effect of increased calcium after one year was a 0.6% to 1% increase in BMD.

When they looked at the effects of eating more calcium in the diet, the researchers found 14 out of 22 cohort studies (covering 291,273 people) did not show that calcium had any effect on the chances of breaking any bone. Of those studies that found people with a higher intake of calcium were less likely to have had a fracture, most showed only a small effect.

The 26 RCTs of calcium supplements, which covered 69,107 people, showed a small effect. They appeared to reduce the risk of fractures by 11% (relative risk 0.89, 95% confidence interval 0.81 to 0.96).

However, when they looked at the overall range of results, the researchers said there were more positive results from small studies than you would expect to see by chance. They say this shows evidence of "publication bias", where only positive studies are published and studies with negative outcomes aren't. 

They looked at the results again, including only the bigger, more reliable studies. This analysis did not show an overall protective effect from calcium supplements.

Only in one big study of frail elderly women living in nursing homes, who had very low levels of calcium and vitamin D at the outset, did supplements make a difference to the risk of hip fracture.


How did the researchers interpret the results?

The researchers say their results show that increasing calcium in the diet is not likely to decrease risk of broken bones, on current evidence. 

They say the benefits found from calcium supplements are small and inconsistent, and "probably have an unfavourable risk benefit profile" given the known side effects of taking calcium.

Talking about the one study that showed a significant reduction in hip fracture, the researchers say this group of elderly women were known to have been deficient in vitamin D, and therefore to have been at higher risk of breaking bones. 

They said this study should not be included in the same analyses as other studies of generally healthy people living in the community, nor should it be used to come up with calcium recommendations for the general population.



These two studies pour cold water on the idea that most healthy people aged over 50 need to eat more calcium than they currently do, or that they need to take calcium supplements. They found that, for most people, increased calcium has little effect on bone strength or chances of breaking a bone.

However, the research is based on available studies, of which there were only two small randomised controlled trials with a combined total of 262 people that looked at calcium intake and risk of fracture. 

The cohort studies found are not able to show cause and effect as they are subject to confounding, so the combination of these limitations reduces the strength of the results found in this systematic review.

The UK government currently recommends getting 700mg of calcium daily – and says a healthy, varied diet is likely to provide this for most people. 

Good sources of dietary calcium include dairy products such as milk, cheese and yoghurt; oily fish such as sardines and anchovies; or nuts and seeds such as almonds and sesame seeds. To get higher levels of calcium, recommended by some organisations, calcium supplements may be needed.

The results of this study suggest most people are unlikely to benefit from taking additional calcium.

We know from previous studies that calcium supplements can have side effects in some people, including constipation and kidney stones. Calcium supplements have also been linked to an increased chance of having a heart attack. You are unlikely to get these side effects from eating a normal amount of calcium as part of a healthy diet.

It's important to remember that most of these studies were looking at generally healthy older people, not people who had a medical reason for taking calcium supplements. 

If you've been advised by your doctor to take calcium and vitamin D supplements because you have weak bones (osteoporosis), or because you are deficient in these nutrients, you should continue to take them. 

Links To The Headlines

How calcium tablets can do more harm than good: Pills can increase risk of stomach upsets and heart problems while not cutting the risk of broken bones. Mail Online, September 29 2015

Calcium supplements don't work, say experts. The Daily Telegraph, September 29 2015

Links To Science

Bolland MJ, et al. Calcium intake and risk of fracture: systematic review. BMJ. Published September 29 2015

Tai V, et al. Calcium intake and bone mineral density: systematic review and meta-analysis. BMJ. Published September 29 2015

Categories: Medical News

Olive oil and wholegrains 'lower heart disease risk'

Medical News - Tue, 09/29/2015 - 15:00

"Butter isn't better than margarine after all," declares the Mail Online, after a new study found eating less saturated fat does indeed lower the risk of heart disease.

The study, which followed the dietary habits of nearly 130,000 people over almost 30 years, found those who had a diet high in unsaturated fats, such as olive oil, and wholegrains had a lower risk of heart disease.

The findings, published in the Journal of the American College of Cardiology, showed replacing 5% of saturated fats in the diet with unsaturated fats reduced the risk of coronary heart disease (CHD) by 25%.

Recent studies have cast doubt on the link between saturated fat intake and the risk of developing CHD. Researchers did not find a link between eating less saturated fat and a lower death rate.

The authors of the study claim this is because many people who cut down on saturated fats replace it with added sugar and refined carbohydrates, such as white bread, which are also linked with CHD.

Overall, the study suggests consuming higher amounts of unsaturated fats and wholegrains was associated with a lower risk of developing heart disease.

While the study included a large sample size and long follow-up period, it cannot prove causality. There is the possibility people didn't accurately recall their diet, and other health and lifestyle factors could be influencing any observed link.

And the results of this study cannot apply to the whole population – it only included health professionals, who may have distinct health and lifestyle characteristics.

Nevertheless, it is advisable to follow a healthy lifestyle, taking regular exercise and eating a balanced diet that includes complex carbohydrates like wholegrains, and is low in saturated fat, salt and sugar.

While the study does not show saturated fats should be avoided altogether, it perhaps supports the well-known adage "everything in moderation". 

Where did the story come from?

The study was carried out by researchers from Harvard Medical School and the Wellness Institute at Cleveland Clinic, and was funded by the US National Institutes of Health.

It was published in the peer-reviewed Journal of the American College of Cardiology.

The UK media reported the findings of the study accurately, but some of the strengths and weaknesses were not explicitly mentioned.

The Mail reports a quote from one of the lead authors of the study, Professor Frank Hu, who said: "Our research does not exonerate saturated fat. In terms of heart disease risk, saturated fat and refined carbohydrates appear to be similarly unhealthy."

He adds: "Our findings suggest that when patients are making lifestyle changes to their diets, cardiologists should encourage the consumption of unsaturated fats like vegetable oils, nuts, and seeds, as well as healthy carbohydrates such as wholegrains". 

What kind of research was this?

This was an observational study that investigated the associations between saturated fat (such as butter, cheese and whipped cream) compared with the intake of unsaturated fat (such as vegetable oil, sunflower oil and walnuts) and different sources of carbohydrates, and the risk of developing heart disease.

Recent studies have cast doubt on the link between saturated fat intake and the risk of developing CHD. But researchers say these studies did not consider that when cutting down on saturated fat, people tended to replace it with carbohydrates from added sugars and refined starches, such as potatoes, white bread and pasta, which did not reduce their CHD risk.

This type of study, involving many people over many years, can show an association between eating less saturated fat and a reduced CHD risk. But it cannot show causality, as many other factors may be involved, including the participants' ability to accurately remember their diet.

What did the research involve?

This study included 84,628 women from the Nurses' Health Study (aged 30 to 55 at enrolment) and 42,908 men from the Health Professionals Follow-up Study (aged 40 to 75 at enrolment). These individuals were free from diabetes, cardiovascular disease and cancer at the start of the study.

Participants completed a food frequency questionnaire once every four years throughout the study period. They were asked what type of fat oil they used for frying and baking, and if they used any margarine during the past year. The questionnaire had nine possible responses, ranging from "never" to "less than once per month", to "more than six times per day".

Daily fat intake by type was calculated by multiplying the frequency of the food consumption with its nutrient content using US Department of Agriculture food composition data.

In the study, carbohydrates were classed as either wholegrains or refined starches, added sugars, refined grains, and sugary foods and drinks.

The outcomes of interest were non-fatal heart attack, heart disease overall, and deaths as a result of heart disease, which were identified through a review of medical records.

What were the basic results?

Over a follow-up period of 24 to 30 years, there were 7,667 cases of heart disease (4,931 non-fatal heart attacks and 2,736 deaths from heart disease).

Some of the main findings of the study are listed below:

  • Highest intake of unsaturated fats was associated with a 20% significantly lower risk of heart disease compared with individuals with the lowest unsaturated fats intake (hazard ratio [HR]: 0.80, 95% confidence interval [CI]: 0.73 to 0.88).
  • Highest intake of carbohydrates from wholegrains was associated with a 10% significantly lower risk of heart disease compared with individuals with the lowest wholegrain intake (HR 0.90, 95% CI 0.83 to 0.98).
  • There was a borderline significant trend for high intake of carbohydrates from refined or added sugars to be associated with increased risk of heart disease (HR 1.10, 95% CI 1.00 to 1.21).
  • Replacing 5% of energy intake from saturated fats with equivalent energy intake from unsaturated fats, monounsaturated fatty acids, or carbohydrates from wholegrains was calculated to reduce the risk of heart disease by 25%, 15% and 9% respectively. 
How did the researchers interpret the results?

The researchers concluded unsaturated fats and high-quality carbohydrates, such as wholegrains, can be used to replace saturated fats to reduce CHD risk.

They said: "Unsaturated fats, such as those from vegetable oils, nuts, and seeds, should have an expanded role as a replacement for [saturated fats].

"However, our data from national surveys suggest that, when decreasing [saturated fats] intake, most people appear to increase the intake of low-quality carbohydrates, such as refined starches and/or added sugars, rather than increase the intake of unsaturated fats." 


This observational study looked for an association between saturated fat intake compared with unsaturated fat intake and complex carbohydrate intake, and the risk of developing heart diseases.

Overall, the study suggested consuming higher amounts of unsaturated fats and complex carbohydrates such as wholegrains was associated with a lower risk of developing heart disease.

This study has several strengths, such as the inclusion of a large sample size of both men and women, and a long follow-up period. But because of the observational study design, it cannot prove causality.

The researchers have adjusted their analyses for various health and lifestyle factors that could be influencing the link, such as body mass index (BMI), smoking status, physical activity and alcohol intake.

However, it is difficult to fully account for the influence of all of these factors – or others that were unmeasured – that could be involved in the diet and heart disease link.

Another important limitation is the possibility of recall bias. People were asked to specify by quantity the types of fat they used in baking and frying in the previous year, and the amount and types of carbohydrates they had eaten. It's possible some of this information may have been inaccurate, and some people could have been put into the wrong intake groups.

As the participants were all health professionals, they may have distinct health and lifestyle characteristics, meaning their results cannot be applied to the population as a whole.

Links To The Headlines

Now butter ISN'T better than marg: Advice U-turn after scientists find reducing saturated fat DOES slash the risk of heart disease. Daily Mail, September 28 2015

Links To Science

Yanping L, Hruby A, Bernstein AM et al. Saturated Fats Compared With Unsaturated Fats and Sources of Carbohydrates in Relation to Risk of Coronary Heart Disease: A Prospective Cohort Study. Journal of the American College of Cardiology. Published online September 28 2015

Categories: Medical News

Too soon for 'aspirin doubles cancer survival' claim

Medical News - Mon, 09/28/2015 - 16:30

"Aspirin could almost double your chance of surviving cancer," the Daily Mail reports, with most of the newspapers featuring similar claims.

According to the Mail: "Three quarters of people with bowel, stomach or throat cancer were still alive five years later, and aspirin is the 'magic bullet' that should be prescribed as soon as someone is diagnosed."

Unfortunately, the claims appearing in the media are based solely on a press release and abstract of research being presented at a scientific conference. This means the results and conclusions won’t have been verified by independent experts and we don’t have all the information to appraise such research. For these reasons, we need to be cautious about this finding.

Compounding our scepticism over these reports are apparent inconsistencies between the sources used to compile the stories, including survival figures we cannot verify from the information available.

It’s also worth noting that the type of study means we can’t prove aspirin itself was improving people’s chances of surviving gastrointestinal cancer.

With those notes of caution in mind, and as further information comes to light, it may be the case that this is a cheap, readily-available drug that can be used to help people diagnosed with cancer to survive longer.

However, it should be noted that the researchers have not found that taking aspirin can stop you getting cancer. Also, taking aspirin regularly carries a risk of side effects, such as internal bleeding. It would need to be ensured that the benefits of the drug in terms of cancer survival outweighed these risks.


Where did the story come from?

The stories follow a conference abstract and accompanying press release related to a study due to be presented at The European Cancer Congress 2015. 

This congress is described as the largest European platform for presenting groundbreaking cancer research to a global audience, renowned for presenting practice-changing information.

The study being presented was conducted by researchers from Leiden University Medical Centre, and other oncology research centres in The Netherlands. The researchers report no conflicts of interest.

The media coverage would benefit from highlighting the limited information available so far, and that this is not a published study.


What kind of research was this?

The study in question is a retrospective cohort study that looked back at a cancer registry of people with cancers of the gastrointestinal tract (the mouth, oesophagus and so on, out to the rectum) and looked at how taking aspirin after diagnosis and was linked to survival.

Previous research has suggested a relationship between aspirin and possible preventative and therapeutic effects for cancer. However, the biological mechanism by which aspirin could be having these effects is controversial. A previous study also focused solely on bowel cancer, while this study looked at all gastrointestinal tract cancers.

As this is a retrospective observational study rather than a prospective trial randomising people to aspirin use or not, it cannot prove aspirin as being the cause in difference in survival.

However, as information on this trial is so far only available as a conference abstract, without full publication of the study in a peer-reviewed journal it is not possible to give a full critique of the design, methods and implications. 


What did the research involve?

The researchers say they used the population-based Eindhoven Cancer Registry to identify all people with a cancer of the gastrointestinal tract diagnosed between 1998 and 2011. These people were then linked to drug dispensing data from the PHARMO Database Network (the Institute for Drug Outcomes Research) to identify whether they had used aspirin after their cancer diagnosis.

Researchers noted whether each person used or did not use aspirin in particular time periods. Overall survival for people in the cohort was compared with expected survival in the general population.


What were the basic results?

The study featured 13,715 people with a gastrointestinal tract cancer. Just under a third of them had used aspirin before cancer diagnosis, just under two-thirds were non-users, and just under 1 in 10 had solely used aspirin after cancer diagnosis.

The analysis focused on comparing the non-users with the post-diagnosis users only. The majority of all of these people had bowel or rectal cancer, and the remaining 10% had oesophageal cancer.

The abstract says that average follow-up time for all patients was just over two years. The researchers reported that five-year survival was 56%, but did not report how this differed between people who used or did not use aspirin. The researchers say they are providing more information on comparative survival rates at the congress.

The accompanying press release provides more specific data, but it appears inconsistent with that presented in the abstract.

In the press release, the researchers say: "[Average] follow-up time for all patients was 48.6 months, with 28% of patients surviving for at least five years. Patients using aspirin after their diagnosis had a chance of survival twice as high than that of those who did not use it in the same circumstances.

"The beneficial effect of aspirin use on survival was seen in patients with [gastrointestinal] tumours after adjusting for potential confounding factors such as sex, age, stage of cancer, surgery, radiotherapy, chemotherapy and other medical conditions or disorders."


How did the researchers interpret the results?

The researchers conclude: "Aspirin use initiated after diagnosis of gastrointestinal malignancies is associated with higher overall and relative survival rates."



This large observational study, which is being presented at The European Cancer Congress 2015, used official data to look at whether using aspirin after being diagnosed with gastrointestinal cancer influenced survival in a population.

Because the results are only available as a brief conference abstract and press release, and given the apparent discrepancies between the sources, it is difficult to give further appraisal or interpretation of the results. Publication of the study in a peer-reviewed journal is needed to be able to understand the strengths and limitations of this study.

The main limitation was that it is only an observational study. However, it is apparently large and – according to the abstract – is likely to have accounted for potential confounders. Despite this, it may still be difficult to pin any effect on survival directly on the action of aspirin, rather than other factors associated with aspirin use.

A randomised controlled trial, where people with a new cancer diagnosis are randomly told to take (or not take) aspirin, would better balance out any differences between the study population and would be more reliable for looking at the direct effects of aspirin.

The researchers say there is a new trial currently in action in the Netherlands that has randomised elderly people with bowel cancer to take daily aspirin or placebo. This may provide more convincing evidence of a benefit from aspirin treatment.

If these combined studies are positive, as lead researcher Dr Frouws says: "Given that aspirin is a cheap drug with relatively few side-effects, this will have a great impact on healthcare systems, as well as patients".

The scientific co-chair of ECCO, Professor Peter Naredi, who was not involved in the research, says in the press release: "We have good evidence that the frequent use of aspirin in the population can prevent some cases of [bowel] cancer ... With more and more data to support the beneficial role of aspirin, we must consider whether we should recommend it to a wider public."

The evidence for aspirin in cancer seems to be going in a promising direction, but given the unpublished status of all this evidence, it is too early to suggest aspirin as a "magic bullet" for improving gastrointestinal cancer survival.

Links To The Headlines

Aspirin could double cancer survival rates. The Times, September 28 2015

Aspirin can double life expectancy of those with common cancers. The Telegraph, September 28 2015

Miracle drug? An aspirin a day could double survival chances of cancer sufferers. Daily Express, September 28 2015

Aspirin could almost double your chance of surviving cancer. Daily Mail, September 27 2015

Aspirin 'may double life expectancy of cancer patients'. The Guardian, September 2 2015

Links To Science

Frouws M et al. Aspirin and gastro intestinal malignancies; improved survival not only in colorectal cancer? Conference abstract. European Cancer Congress 2015

Categories: Medical News

Doctors should 'wait longer' before diagnosing miscarriage

Medical News - Fri, 09/25/2015 - 13:35

"Doctors are being advised to wait longer before they diagnose a miscarriage," The Guardian reports. 

A new study has found evidence to suggest that women should be given a second ultrasound scan, two weeks after the first, to confirm the diagnosis.

Researchers looked at the specific transvaginal ultrasound scan findings that are used to diagnose miscarriage in early pregnancy. The study aimed to investigate whether the current measurements used, and the delay period between a first and repeat scan, are suitable to diagnose a miscarriage.

The study included almost 3,000 pregnant women who had an early pregnancy scan because of pain, bleeding, severe morning sickness or had previously experienced miscarriage or an ectopic pregnancy

It found that measurements of the developing embryo currently used for diagnosis are appropriate. When all measures are taken into account, no healthy, continuing pregnancies would be wrongly diagnosed as a miscarriage.

However, the study did find that if a repeat scan is needed to confirm miscarriage, there are timing issues to consider. Current protocols run a small risk of coming up with a false-positive result – stating a miscarriage has occurred when the pregnancy is actually viable.

It should be noted that most women are able to have a healthy pregnancy after a miscarriage, even in cases of recurrent miscarriages.

It is likely that the results of the study will be looked at by the bodies that set clinical guidelines regarding pregnancy care, such as the National Institute for Health and Care Excellence and the Royal College of Midwives.

Where did the story come from?

The study was carried out by researchers from a number of hospitals, including Queen Charlotte’s & Chelsea, St Thomas’ and St Mary’s Hospitals. The study was funded by the National Institute for Health Research Biomedical Research Centre, based at Imperial College Healthcare NHS Trust, and Imperial College London.

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

The media coverage primarily relates to the finding of a need for better guidance on when repeat ultrasounds should be performed, so they are not performed too soon after the initial scan.


What kind of research was this?

This was a prospective multicentre cohort study looking at the specific transvaginal ultrasound scan findings used to diagnose miscarriage in early pregnancy.

There has been debate over which are the best measurement cut-offs to use to distinguish between a viable pregnancy (a healthy, developing embryo) and a non-viable one. This includes measuring the diameter of the gestational sac (the fluid sac that surrounds the developing embryo in early pregnancy), or the embryo’s "crown-to-rump" length. Previously, different guideline groups had been using different cut-offs. In 2011, new guidance was issued to update the recommended cut-offs to use.

This study aimed to look at the reliability of changes to guidance on cut-off measurement values for diagnosing a miscarriage.

Its observational design is appropriate for such an investigation, as it does not interfere with the pregnancy in any way or cause unnecessary risk to the baby or mother. 


What did the research involve?

The study included 2,845 pregnant women, mainly from hospital units within London. They attended an early pregnancy ultrasound scan because they had pain, bleeding or severe morning sickness, or to give reassurance following a previous miscarriage or an ectopic pregnancy. 

During early pregnancy (the first 12 weeks) transvaginal ultrasound is usually used, because this is much more reliable for viewing the developing baby in the early stages than the standard abdominal ultrasound used in later stages of pregnancy.

Demographic information was recorded, including:

  • reason for scanning
  • maternal age
  • ethnicity
  • gestational age at first scan (calculated from last menstrual period or embryo transfer date after infertility treatment)

Measurements were taken for:

  • gestational sac diameter
  • presence of a yolk sac (present within the gestational sac and which provides key nutrients to the early developing embryo)
  • embryo crown-to-rump length
  • presence or absence of a heartbeat

All scans were carried out by experienced nurse practitioners, ultrasonographers, and doctors with an interest in the use of ultrasound in early pregnancy.


What were the basic results?

Researchers found that women who eventually had a non-viable pregnancy (i.e. who miscarried) generally presented at a later pregnancy stage and had a higher average gestational sac diameter and crown-to-rump length than viable pregnancies.

The study presents extensive data for different cut-off measures and by different pregnancy outcome, which is too in-depth to go into here. A summary of the main findings is given.

At initial scan, the following factors were 100% reliable for indicating miscarriage:

  • empty gestational sac with average diameter of 25mm or greater
  • embryo with crown-to-rump length of 7mm or more without visible heart activity
  • after 70 days of pregnancy, gestational sac with average diameter of 18mm or greater and without an embryo
  • after 70 days of pregnancy, embryo with crown-to-rump length of 3mm or more without visible heart activity

At repeat scan, the following were 100% reliable for indicating miscarriage:

  • both initial scan and repeat scan at seven days or more showing an embryo without visible heart activity
  • pregnancies without an embryo and average gestational sac diameter of less than 12mm where the mean diameter has not doubled after 14 days or more
  • pregnancies without an embryo and average gestational sac diameter of 12mm or more showing no embryo heartbeat after seven days or more

No embryo heart activity and empty gestational sacs at both initial and repeat scans were very high indicators of a non-viable pregnancy.

The researchers noted that gestational sac size at initial scan should be used to guide timing of the repeat scan. An average gestational sac diameter of less than 10mm at initial scan should have a repeat scan more than two weeks later. Current thinking is that the second scan should be carried out around 7-10 days after the first.


How did the researchers interpret the results?

Researchers conclude that, "Recently changed cut-off values of gestational sac and embryo size defining miscarriage are appropriate and not too conservative, but do not take into account gestational age". 

They go on to recommend that guidance on timing between scans and expected findings on repeat scans continue to be too liberal and that protocols for diagnosis should be reviewed to avoid the risk of terminating viable pregnancies.



This observational study reviewed the reliability of different measurements taken at a transvaginal ultrasound scan to diagnose miscarriage during early pregnancy. 

The recommended cut-off values for gestational sac diameter and embryo crown-to-rump length were changed in 2011 based on a number of reports, with mixed findings suggesting previous ones may have been unreliable.

This study looked at the performance of currently used cut-off values, and found that the current cut-offs used to diagnose miscarriage are reliable. No healthy, continuing pregnancies would be wrongly diagnosed as miscarriage using these values.

However, a finding of note was that if a repeat scan is needed to confirm miscarriage, there are some issues around timing. If there is a gestational sac only, with no embryo present, reliable diagnosis can be harder, and researchers say there should be a wait of two weeks rather than one before carrying out a repeat scan. This reduces the chance of incorrect diagnosis from 2% to 0%. If an embryo is identified at the first scan, then interpretation of miscarriage is more straightforward and timing between scans is less of an issue.

This study has a number of strengths, namely a prospective design and large sample size, with measurements taken by experienced professionals, thereby increasing the certainty of the findings. However, there was no available data for 337 women and this may have influenced results.

Miscarriages are common, can happen for many reasons, and most of the time cannot be prevented. If a woman has experienced previous miscarriages, then she may receive closer care and observation during pregnancy.

Lifestyle factors that are linked to miscarriage and that may help to reduce the risk of miscarriage include not smoking or using illegal drugs, not binge drinking, and, if possible, not drinking alcohol altogether, particularly during the first 12 weeks.

If you have been emotionally affected by a miscarriage, either yours or your partner's, your hospital can offer advice on bereavement counselling and coping with the aftermath.

Links To The Headlines

Doctors advised to wait longer before diagnosing miscarriages. The Guardian, September 24 2015

Doctors diagnosing miscarriage 'too early'. The Daily Telegraph, September 23 2015

Doctors told to delay miscarriage diagnosis to avoid risk of terminating healthy babies. Daily Mirror, September 24 2015

Links To Science

Presler J, Kopeika J, Ismail L, et al. Defining safe criteria to diagnose miscarriage: prospective observational multicentre study. BMJ. Published online September 23 2015

Categories: Medical News

'No significant link' between breastfeeding and higher IQ

Medical News - Thu, 09/24/2015 - 15:30

"Breastfeeding has no benefit over bottle feeding when it comes to a child's IQ," the Daily Mail says, reporting on the results of a study that found no significant link between breastfeeding and increased intelligence.

Researchers assessed the intelligence of children involved in the Twins Early Development Study between the ages of two to and 16, testing them 9 times over the course of the study.

They found a small increase in the average IQ of breastfed girls compared with bottle-fed girls at the age of two, but this did not affect boys. They found no differences in average IQ between those fed by breast or bottle in later years.

The idea that breastfeeding might improve IQ is based on the idea certain proteins only found in human breast milk could be important for developing nerve cells.

Previous studies have reported that breastfeeding improves children's intelligence. However, it is possible that these older studies were not sufficiently rigorous to get a reliable result.

While breastfeeding may not be a brain booster, it does bring physical health benefits, such as improved immune protection against infection.

Read more about the physical health benefits of breastfeeding.

Still, the results of the study should reassure women who are unable to breastfeed for health reasons. As the lead author puts it, "Being bottle-fed as an infant won't cost your child a chance at a university degree later in life." 

Where did the story come from?

The study was carried out by researchers from the University of London and King's College London. We currently do not have information about who funded the study. 

It was published in the peer-reviewed journal PLOS One.

The study was covered accurately by the UK media, and most news stories included reminders that breastfeeding is likely to have other important health benefits. 

What kind of research was this?

This research used information from an ongoing prospective cohort study of twins from the age of two to 16 years called the Twins Early Development Study.

Cohort studies allow researchers to collect a lot of data about a large group of people, which they can then use to look for links between different factors – in this case, whether breastfeeding has any effect on children's IQs over time. But this type of study cannot prove one factor directly causes another. 

What did the research involve?

The researchers used data from the study to construct a model of the children's IQs over time, based on nine assessments of their intelligence carried out from ages 2 to 16.

The researchers looked at whether there were differences between the IQs of children who had been breastfed and those who had not. They looked for differences at the start of the study and at how the children's IQs changed as the study progressed.

Based on previous studies, the researchers thought they might find that breastfed children had a higher IQ at two years old, and the difference between the IQs of breastfed and bottle-fed children would stay the same over time, but not increase.

If the IQ differences started mainly in later childhood or the gap increased, it would suggest that other factors – such as the children's education – were more important than breastfeeding.

Breastfeeding is more common among better-off families, so breastfed children might have gone to better schools and had access to private tuition.

Additional factors taken into account in the model were the parents' educational achievement and type of employment, the mothers' ages when the children were born, and the children's gestational age (how many months after conception they were born). 

What were the basic results?

The researchers found a small but statistically significant difference in the IQs of girls who had been breastfed and girls who had not at the age of two.

However, the link was quite weak. There was no difference in IQ between boys who had or had not been breastfed.

After that initial stage, there was no statistically significant difference in average IQ between children who had or had not been breastfed once other factors had been taken into account.

Of the children in the study, 62% were breastfed for an average of four months.

How did the researchers interpret the results?

The researchers were cautious about the small increase in IQ they found in breastfed girls at the age of two.

"Because our observed effects were weak and at best modest, we interpret the findings as evidence for the lack of benefits of breastfeeding on cognitive development," they said.

In a press statement, they added: "Comparatively small events like breastfeeding are very unlikely to be at the core of something as big and complex as children's differences in IQ."

They said that children's family background and schooling were more likely to explain any differences.  


This study suggests that if breastfeeding has any effect on children's intelligence, the effect is small and does not last beyond early childhood. While the study does not rule out any effect, it seems likely that other factors, such as family background, are much more important.

This study has a number of strengths, including the fact that a lot of children (11,582) from a range of backgrounds, representative of the UK population as a whole, were used.

The children were tested nine times during their childhood, using a range of tests previously shown to be a good way of assessing IQ. The researchers constructed their model in a way that took into account factors such as family background before they looked for the effect of breastfeeding.

However, there were a couple of limitations, although the results of this large, well-conducted study appear to be robust and reliable. The number of additional factors included that might have affected children's IQs was relatively small. We don't know anything, for example, about the children's diet after weaning, or their education.

Although they have previously been judged as reliable, the tests used to measure IQ were carried out by the children at home, supervised by the parents. Some early tests relied on the parent's observations about the child, rather than an objective test of ability.

It's possible that these tests were less reliable than if they'd been given by a trained, impartial researcher. All the children involved in the study were twins, so the results may not be directly applicable to single births.

However, breastfeeding has many beneficial effects on children's health, including the development of a healthy immune system. Public Health England recommends that babies should only be fed breast milk for the first six months of life, where possible.

Other ways you can help your child's cognitive development include reading to them and involving them in creative play, such as drawing or playing pretend games. Read more about play ideas and reading with your child.

Links To The Headlines

Breast is NOT best - when it comes to IQ: Children who are breastfed 'are no more intelligent than those who are bottle fed'. Daily Mail, September 23 2015

Breastfeeding does not improve IQ, study finds. The Daily Telegraph, September 23 2015

Breast-fed babies are no more clever than bottle-fed. Daily Express, September 23 2015

Links To Science

Von Strumm S, Plomin R. Breastfeeding and IQ growth from toddlerhood through adolescence. PLOS One. Not yet online

Categories: Medical News

Fidgeting probably not a useful alternative to proper exercise

Medical News - Thu, 09/24/2015 - 13:28

"Fidgeting 'offsets unhealthy effects of sitting for long periods and may help you live longer'," the Daily Mirror reports.

A new study reported fidgeting may help make up for the harmful effects of most people's sedentary lifestyles. Sitting down for most of the day has been linked to an increased risk of diabetes and heart disease.

A study following more than 10,000 women for 12 years found an association between high levels of self-reported fidgeting and reduced risk of death. This was despite them spending several hours a day sitting. 

But while the media reports fidgeting is therefore good for you, this study had major limitations and the results were mixed.

The women were asked to rate how much they fidget on a scale of 1 (none) to 10 (constantly) in a single questionnaire. Other details, such as activity level, amount of time sitting, occupation and diet, were also only collected at a single point in time. 

These estimates may be inaccurate, and each factor may have changed over the study period. This means we cannot be confident fidgeting reduces the negative effects associated with a sedentary lifestyle.

Going for a brisk walk, jog, or swim is almost certainly better for you than tapping your feet. Read more about the benefits of regular exercise

Where did the story come from?

The study was carried out by researchers from University College London, Heriot-Watt University, the University of Edinburgh, and the University of Leeds.

It was funded by the World Cancer Research Fund, the Biotechnology and Biological Sciences Research Council, and the Medical Research Council. No potential conflicts of interest were reported.

The study was published in the peer-reviewed American Journal of Preventive Medicine.

In general the UK media reported the findings of the study at face value, not mentioning any of the study's limitations.

The Guardian incorrectly described fidgeters as people whose "limbs tapped, wobbled and gently vibrated" or "colleagues who are constantly tapping their feet", but this was not how the questionnaire asked women to rate their level of fidgeting.  

What kind of research was this?

This cohort study followed more than 10,000 women over a period of 12 years to see if there was a link between fidgeting, the amount of time spent sitting, and risk of death.

Cohort studies like this are a good way of finding associations between environmental and lifestyle factors and outcomes because they can involve large numbers of participants and are done over a long period of time to capture the long-term effects of an exposure.

However, they cannot prove cause and effect, which would require a randomised controlled trial. Such a trial would be tricky to organise, however. 

What did the research involve?

The researchers analysed data on a sample of 10,937 women who participated in the United Kingdom Women's Cohort Study (UKWCS).

These women completed a sociodemographic and food frequency questionnaire at some point between 1995 and 1998. At that time they were aged between 35 and 69.

They completed a second questionnaire between 1999 and 2002, which included information on health behaviours, illness, 24-hour activity, physical activity and fidgeting.

Fidgeting was assessed on a scale from 1 to 10 using the question, "How much of your time do you spend fidgeting?". A score of 1 would mean "no fidgeting at all", with 10 indicating "constant fidgeting".

The women were followed up until December 2013. The results were analysed to look for an association between the level of self-reported fidgeting and risk of death.

The researchers adjusted the results to take into account the following possible confounding factors:

  • age
  • chronic disease
  • physical activity level
  • sitting time
  • level of education
  • occupational social class
  • retirement status
  • smoking status (current versus former or never)
  • alcohol use
  • fruit and vegetable consumption
  • hours of sleep

The researchers performed additional analyses to see if body mass index (BMI) could account for the results seen. 

What were the basic results?

Women who reported the lowest fidgeting rate had a 30% increased risk of death from any cause if they sat for seven or more hours a day compared with less than five hours (hazard ratio [HR] 1.30, 95% confidence interval [CI] 1.02 to 1.66).

For women in the highest self-reported fidgeting group, sitting for five or six hours a day was associated with a 37% reduction in risk of death compared with sitting for less than five hours a day (HR 0.63, 95% CI 0.43 to 0.91).

Sitting for longer than six hours a day was not associated with an increased or decreased risk of death in this group.

The length of sitting time was not associated with risk of death in women classed as being in the middle group of fidgets. BMI did not alter the results. 

How did the researchers interpret the results?

The authors concluded that, "Fidgeting may reduce the risk of all-cause mortality associated with excessive sitting time." They called for "more detailed measures of fidgeting … to replicate these findings". 


This cohort study found fidgeting may reduce the risk of death associated with sitting for long periods of time. 

The study's strengths include the large number of participants, long follow-up period and attempts to account for a number of potential confounding factors.

However, the study is purely based on one self-reported estimate of most of these factors, which reduces confidence in the strength of the results. Fidgeting is largely an unconscious activity, so many people could have no accurate recall of how much or how little they fidget.

Not only could the estimates be unreliable, but many of these variables may have changed over the course of the 12 years of follow-up, such as activity level, diet, smoking and employment status.

The analyses did not consider whether the sitting was related to occupation, leisure time or watching TV, which may have influenced the results.

A further major limitation is in the assessment of the amount of fidgeting. Again, this was only assessed on one occasion through the women guessing how much they fidget on a scale of 1 to 10. This was not validated through any objective measurement or asking family, friends or colleagues to see if they agree. 

The researchers suggested future studies could try to address this limitation through combining the self-report with tri-axial accelerometers (movement sensing devices that people wear).

In conclusion, though interesting, the results of this study do not lead to a call for people to fidget more. Instead, the advice remains the same: stop smoking, drink alcohol within safe limits, eat a balanced diet that includes plenty of fresh fruit and vegetables, and keep physically active

Links To The Headlines

Fidgeting 'offsets unhealthy effects of sitting for long periods and may help you live longer'. Daily Mirror, September 23 2015

Always fidgeting? Well, you just might be doing yourself a world of good. The Guardian, September 23 2015

Fidgeting may help you live longer say researchers. ITV News, September 23 2015

Want to boost your health? Fidget! Restless movements 'undo the damage caused by sitting for a long time'. Mail Online, September 23 2015

Links To Science

Hagger-Johnson G, Gow AJ, Burley V, et al. Sitting Time, Fidgeting, and All-Cause Mortality in the UK Women's Cohort Study. American Journal of Preventive Medicine. Published online September 23 2015

Categories: Medical News

UK women's life expectancy 'second worst' in Western Europe

Medical News - Wed, 09/23/2015 - 14:10

"British women have second worst life expectancy in Europe," The Guardian reports. This is one of the findings of a Europe-wide health report carried out by the World Health Organization (WHO). The report also warned that European levels of alcohol consumption, smoking and obesity are alarmingly high, which could result in the following possibility: "Young Europeans may die at an earlier age than their grandparents".

In the interests of accuracy, we should point out that the claim British women have the second worst life expectancy in Europe is incorrect. This figure is based on an analysis of countries traditionally regarded as being part of Western Europe. Life expectancy figures in other parts of Europe, such as Russia and the Balkan states, are significantly lower than in the UK.


What is the basis of these reports?

The WHO has published its European Health Report, which measures progress against health targets for Europe, looking at how individual countries compare, and commenting on possible future threats to the health of the region. It publishes this regional report every three years.


What data did they look at?

The WHO looked at progress towards six targets for Europe. These were:

  • to reduce premature mortality (early death)
  • to increase life expectancy (how long people born now can expect to live)
  • to reduce inequalities in the health of people across the European region
  • to enhance wellbeing
  • to move towards everyone in Europe having access to healthcare
  • to establish individual targets for European countries

They reviewed statistics on death from:

  • heart disease, strokecancers and respiratory diseases, such as chronic obstructive pulmonary disease (COPD)
  • estimates of the life expectancy of male and female children today
  • comparisons between different states of health outcomes
  • measures of wellbeing
  • lifestyle factors, such as tobacco smoking, alcohol consumption and obesity
  • health policies in different countries

Many figures were based on estimates. For example, figures on tobacco and alcohol use are estimates by the WHO researchers, who applied trends in tobacco reduction from the period 2000-08 to national figures collected in 2010. The report authors say more up-to-date information had not been submitted by individual countries.


What are the main findings?

Despite the tone of the news coverage, the report is generally positive, showing that Europe is on track to achieving targets to reduce premature death from cardiovascular diseases, cancer, diabetes and lung diseases.

However, it says that most of the recent progress has been seen in the countries that had the worst health records, rather than countries like the UK, which were already doing relatively well.

The report warns that Europe has the highest rates of alcohol consumption and tobacco smoking in the world, with obesity rates second only to North America. The report authors warn that these lifestyle factors "are among the major public health problems" in Europe and that Europe is likely to miss a target to reduce tobacco use by 30% by 2025.

Looking at country-specific figures, the report says that people in the UK are much less likely to smoke (estimates are around 20%, compared to a European average of 30%). People in the UK drink, on average, 9-12 litres of pure alcohol a year (equivalent to around 100-130 bottles of wine), in line with the European average of 11 litres.

Rates of obesity and overweight are among the highest in Europe, with only Turkey and Andorra reporting more obese people.

The report showed life expectancy at birth has been rising in Europe since the 1990s and stood at 76.8 years in 2011 (the most recent date for which figures were available). Women live longer than men, with an average life expectancy of 73 for men and 80 for women. In the UK, the figures are 78.8 for men and 82.7 for women. While this is better than the European average, it puts life expectancy for UK women low on a WHO list of 15 benchmark Western European countries. Most of the figures for life expectancy for women on this list cluster around the 83- to 84-year mark, ranging from 82.1 in Denmark to 85.5 in Spain.

The media reports of British women's life expectancy being the "second lowest in Europe" does not reflect that this is based on a list of just 15 countries – not the whole of Europe. By contrast, life expectancy for women in Russia (which is not on the list) is just 75.


What does this mean for me?

If you compared this data to data from 100 years ago, a trend would become immediately obvious. In 1915, many Europeans would die of infection. Today, the biggest killers are what are known as non-communicable diseases (NCDs). These are non-infectious diseases such as lung cancer, heart disease and stroke, which are usually associated with lifestyle factors including obesity, smoking and alcohol consumption.

The report warns that NCDs are now the biggest threats to future health in Europe.

The good news is, while there is no room for complacency, UK rates of tobacco smoking are below the European average and continue to fall.

Alcohol consumption in the UK is in line with the rest of Europe – and Europeans are the biggest consumers of alcohol in the world. However, perhaps what is most worrying are the statistics on obesity and overweight, where the UK is among the worst in Europe.

The report says the figures on alcohol, tobacco and obesity are "alarmingly high" and acknowledges that individual countries have made progress in tackling them. Commenting on the report, the WHO warns that, while Europeans are living longer, these lifestyle factors "could mean that the life expectancy of future generations will fall". 

Ways you can reduce your risk of developing one or more NCDs include stopping smoking, drinking alcohol in moderation and maintaining a healthy weight through diet and exercise. These steps should also help keep your cholesterol and blood pressure at a healthy rate.

Links To The Headlines

Young Europeans may die at earlier age than their grandparents, says WHO. The Guardian, September 23 2015

British women have second worst life expectancy in Europe. The Guardian, September 23 2015

UK women dying two-and-a-half years 'too early': Lifestyle and diet leave us lagging behind rest of Europe in life expectancy league. Daily Mail, September 23 2015

Life-expectancy for British women is the second lowest in western Europe. The Daily Telegraph, September 23 2015

Girls born in the UK have SECOND lowest life expectancy in Europe. Daily Mirror, September 23 2015

Categories: Medical News

Could an arthritis drug also help treat Alzheimer's disease?

Medical News - Tue, 09/22/2015 - 16:30

"Arthritis drug could soon reverse Alzheimer's symptoms after successful tests on mice," The Independent reports. The drug – salsalate – may help regulate levels of the abnormal tau protein associated with Alzheimer's disease, which could improve memory skills.

Salsalate, which belongs to the non-steroidal anti-inflammatory drug (NSAIDs) class of medicines, has been used for many years. And as The Daily Telegraph points out, it was even mentioned by the 5th century BC physician Hippocrates.

This study was conducted in mice with clumps of tau in their brains. Salsalate was given to the mice and was found to block the process that can lead to a further protein build up. Treated mice also performed better in tests designed to assess memory skills.

While these findings show promise, the studies were conducted in mice and were only conducted for a couple of months. 

Further human studies will be required to determine how effective the drug is and over what timescale. But because this drug has already been approved for use in humans, these tests may come sooner rather than later.

To reduce your risk of Alzheimer's disease, a healthy and active lifestyle is recommended. This includes stopping smoking, reducing your alcohol consumption, having a good diet and taking regular exercise

Where did the story come from?

The study was carried out by researchers from several Gladstone Institutes in San Francisco, the University of California, Stanford University School of Medicine, and the Buck Institute for Research on Aging.

Funding was provided by Tau Consortium and the US National Institutes of Health.

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

This story has been reported in a number of media sources, but it is misleading to say the drug could "soon reverse Alzheimer's," as The Independent put it. These findings were in mice, and trials also need to be conducted in humans. 

The Daily Telegraph correctly informed readers that, "While there is potential that drugs used to treat other diseases could be of benefit in dementia, nobody should be taking such drugs until clinical trials have shown them to be safe and effective for the treatment of dementia."

Salsalate can be dangerous for certain groups of people, such as those recovering from heart surgery. You should never take salsalate unless it's been prescribed for you by a qualified doctor.  

What kind of research was this?

This animal study in mice investigated the changes occurring in the brain in a mice model of the early stages of Alzheimer's disease.

This condition is characterised by the accumulation of tau proteins and a reduction in brain volume, especially in an area called the hippocampus, which is important for forming memory. 

Further investigation was carried out to assess the effect of the prescription drug, salsalate, on the accumulation of tau proteins and brain volume.

While this is a good method to investigate effects, any findings would have to be confirmed in humans.  

What did the research involve?

Researchers used human brain samples to investigate how the tau protein builds up in the brain in Alzheimer's disease.

They identified how greater levels of tau acetylation – a chemical process that alters the tau protein, causing it to build up and induce cognitive defects – was associated with progression of disease.

The study then involved laboratory mice with dementia to firstly confirm a similar mechanism of tau acetylation and disease, and then test the effect of salsalate on disease progression.

Mice with dementia and normal mice were assigned to receive salsalate or a placebo daily. Female mice aged eight to nine months were treated for a total of 60 days, and male mice aged seven to eight months were treated for 84 days. Brain volume was assessed at the end of the trial.

Behavioural tests for spatial learning and memory retention were conducted on the 35th day for female mice and about the 60th day for the male mice. Investigators who performed the dosing and behavioural tests were blinded to the type of mice or treatment received to reduce the risk of bias.  

What were the basic results?

The study identified a chemical change called tau acetylation as an early change in Alzheimer's disease brains in mice. The altered tau protein is slow to break down, causing an accumulation and leading to cognitive decline.

Researchers found salsalate prevented the chemical change occurring, allowing the tau protein to break down as normal and reducing its build up.

At eight months, the brain volume in the hippocampus was the same in both groups of female mice. After treatment at 10 months of age, the volume had reduced in mice with dementia that had been given a placebo. 

In mice with dementia given salsalate, there was no reduction in brain volume compared with normal mice, showing it had halted this part of the disease process. Similar results were found for the male mice.  

How did the researchers interpret the results?

The researchers concluded salsalate lowers levels of tau protein with protective effects.

Targeting tau acetylation could be a new therapeutic strategy against neurodegenerative disease, they say. 


Salsalate was found to inhibit the tau acetylation process and prevent an accumulation of the tau protein in the brains of mice. It was also found to improve memory retention and prevent the loss of hippocampal brain volume.

However, we do not know whether salsalate would replicate the effects observed in mice when used in humans. But these findings do provide a route for further research in a drug already prescribed to people with arthritis. 

Although we are aware of the potential side effects at doses suitable to help arthritis, we don't know what dose may be required to be effective against dementia. This could alter the side effect profile if the dosage needs to be higher.

It is unclear whether this drug is actually prescribed in the UK, as it is unlicensed for use in this country. Salsalate is also currently being used in a clinical trial for another brain disease. 

Other ways to reduce your risk of Alzheimer's disease include stopping smoking, lowering your alcohol intake, eating a good diet and taking regular exercise.

Links To The Headlines

Arthritis drug could soon reverse Alzheimer's symptoms after successful tests on mice, say scientists. The Independent, September 21 2015

Arthritis drug 'can help beat dementia': Disease's impact on memory could be reversed. Mail Online, September 22 2015

Drug hope for Alzheimer's as scientists find old arthritis treatment can reverse disease. Daily Mirror, September 21 2015

Drug mentioned by Hippocrates may reverse Alzheimer's memory loss. The Daily Telegraph, September 21 2015

Links To Science

Min Sm Chen X, Tracy TE, et al. Critical role of acetylation in tau-mediated neurodegeneration and cognitive deficits. Nature Medicine. Published online September 21 2015

Categories: Medical News

'Dementia could strike 1 in 3 born this year', claims report

Medical News - Mon, 09/21/2015 - 13:28

"One in three people born in the UK this year will suffer from some form of dementia in their lifetime," Sky News reports. This is the stark finding of a report commissioned by Alzheimer's Research UK and carried out by the private research institute the Office of Health Economics.

The report can be read here (PDF, 604kb).
What evidence did the report look at?

The report’s findings are based on the combination of two data sets. The first, by the Office of National Statistics, is a 2010 estimation of the likely life expectancy of children born during this decade.

The second, by the Cognitive Function and Ageing Studies, is an on-going study looking at the prevalence of dementia in an increasingly ageing population.


What were the findings of the report?

The report estimated that for all children born in this year:

  • 27% of males will develop dementia
  • 37% of females will develop dementia
  • in total, 32% of all people will develop dementia



The NHS has helped increase life expectancy by reducing the burden of chronic diseases such as lung cancer and heart disease through public health initiatives. However, this has led to an increase in age-related diseases, including dementia.

The findings of the report do make for sobering reading, though the estimates are based on the assumption that effective treatments, or even a cure, will not be discovered at some point in the future.

The field of dementia research is fast-moving, so there are cautious reasons for optimism.

While there are currently no guaranteed methods of preventing dementia, there are measures you can take to ensure you live as healthy a life as possible. These include doing regular exercise, eating a healthy diet, stopping smoking if you smoke, cutting your alcohol consumption and maintaining a healthy weight.

Read more about dementia prevention

Links To The Headlines

'One In Three' Born This Year Will Get Dementia. Sky News, September 21 2015

One-third of British people born in 2015 'will develop dementia'. The Guardian, September 21 2015

One in three born this year could be hit by dementia: Experts warn of 'looming national health crisis'. Mail Online, September 21 2015

'One in three' Brits born this year will develop dementia as experts warn of national health crisis. ITV News, September 21 2015

One in three will suffer dementia, study warns. The Times, September 21 2015

Categories: Medical News

Tai chi 'may help people cope better with diseases of ageing'

Medical News - Mon, 09/21/2015 - 13:23

"Tai chi can help older patients with disabling conditions," The Guardian reports after an analysis of old data found the martial art may help relieve some symptoms of four age-related diseases: cancer, heart failureosteoarthritis and chronic obstructive pulmonary disease (COPD).

Notable significant effects were seen, with improvements in walking for those who had heart failure, improved strength of the big quadriceps muscles for those with heart failure and COPD, and pain and stiffness for people with osteoarthritis. There were also trends for effects on depression and quality of life for those with heart failure and COPD.

However, this review can't prove tai chi will definitely have a positive effect for people who have these conditions. The trials were highly variable in their study population, the type of tai chi practised, the type of comparison intervention, and the outcomes examined. Despite the large collective number of studies, most of the individual results were based on only one or a few studies. 

Nevertheless, remaining active and exercising within your limits is positive in all stages of life, even for those who have a chronic disease. If you find tai chi enjoyable and it boosts your physical or mental wellbeing, that can only be a good thing.

If tai chi is not your cup of oolong, you could always try the Strength and Flex exercise plan

Where did the story come from?

The study was carried out by researchers from the University of British Columbia and the University of Toronto, and was funded by the University of British Columbia and the British Columbia Lung Association.

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

The UK media provide a generally accurate picture of the evidence. However, it would have been helpful to note that this study was limited by the highly variable studies the researchers looked at, which makes it difficult to form any definite conclusions.   

What kind of research was this?

This systematic review aimed to identify trials looking at the effectiveness of tai chi for four common chronic conditions: cancer, heart failure, COPD and osteoarthritis. The results of the identified trials were then pooled in a meta-analysis to give an overall effect.

Tai chi involves gentle flowing movements to improve strength, posture and balance, and has become an increasingly popular form of exercise, particularly among the middle-aged and elderly.

It has also been tried as a complementary healthcare approach for many different conditions, with some studies suggesting it has both physical and psychosocial benefits.

This review aimed to gather the evidence surrounding the martial art to get an overall conclusive summary of its effects. However, the results of a systematic review are only ever as good as the studies included, so there may be inherent limitations in the quality of the various studies and the methods used.   

What did the research involve?

The researchers searched four literature databases up to the end of December 2014 for randomised controlled trials published in English that compared tai chi with any other control group in people with four chronic conditions: cancer, heart failure, COPD and osteoarthritis. The studies were assessed for quality, and the outcomes were pooled for different disease-specific symptoms and outcomes.

33 studies met the inclusion criteria, but several reported data in two or more publications, giving a total of 24 individual trials. There were five studies available each for cancer, heart failure and COPD, and nine for osteoarthritis. The results of all the osteoarthritis studies, and four of the studies for each of the other conditions, were pooled in the meta-analysis.

The trials were of average quality, with most having a score of five out of 10 on the quality scale used (the PEDro scale). The sample size of the trials included ranged from 11 to 206. The average age of the participants varied, but they tended to be in their 60s and 70s. 

What were the basic results?

The studies examined different physical and psychological outcomes. The main effects were as follows.

Physical symptoms
  • Walking – tai chi gave significant improvements on the six-minute walk test in people with heart failure and COPD. One study each for cancer and osteoarthritis found no effects on walking.
  • Muscle strength – one COPD and one heart failure study found significant improvement in knee extensor strength, but there was no effect in the osteoarthritis studies.
  • Getting up and moving – the osteoarthritis studies found tai chi improved the timed get up and go test result, as well as sit to stand times. One heart failure study found no effect.
  • Chronic disease symptoms – tai chi significantly improved pain, stiffness and physical function in osteoarthritis. In COPD, there was a trend towards tai chi improving shortness of breath compared with control, but this was non-significant. No two cancer studies reported the same outcome. There was a trend for reduced fatigue in one study, but this had an extremely small sample size.
  • Other physiological effects – heart failure studies found no effect on blood pressure or respiratory function.
Psychological outcomes
  • Quality of life – tai chi had significant effects on osteoarthritis, but there were no significant effects in COPD, cancer or heart failure studies.
  • Depression – tai chi was associated with significant improvements in depression symptoms in heart failure studies, but there were non-significant trends in osteoarthritis and COPD studies. In cancer, it was the control intervention (stress management) that improved symptoms rather than tai chi.  
How did the researchers interpret the results?

The researchers concluded that, "The results demonstrated a favourable effect or tendency of tai chi to improve physical performance, and showed that this type of exercise could be performed by individuals with different chronic conditions, including COPD, heart failure and osteoarthritis." 


This review searched the literature to summarise the effects of tai chi on four common chronic conditions. It identified a large number of trials collectively examining many different physical and psychological outcomes in a predominantly middle-aged to elderly population. 

The notable significant effects seemed to be for improvements in walking for those with heart failure, knee extensor strength for those with heart failure and COPD, and pain and stiffness for those with osteoarthritis. There were also trends for effects on depression and quality of life for people with heart failure and COPD.

The researchers concluded that tai chi could be performed by individuals for many different chronic conditions. However, this review can't demonstrate that tai chi will definitely have a positive effect if it's tried out by someone who has one of these chronic conditions.

Overall, the systematic review is a high-quality study design. However, the evidence is only as good as the studies included. The 24 individual studies in this review were widely different, and most results are based on one to a few studies.

Variations across the studies included:

  • The type of tai chi, the overall duration of the intervention, and the frequency and duration of individual sessions.  
  • The type of disease and severity, even within the same chronic disease category – for example, most cancer studies were in breast cancer, but even these varied in their stages, while another was just in "unknown cancer survivors".
  • Osteoarthritis varied between spine, hip and knee, and the severity of pain and disability.
  • The comparison groups varied – for example, some were just usual care or waiting list, others self-help education, some spiritual or psychological-related, and others varied physical activities such as walking, aerobics or stretching programmes. 
  • As demonstrated by the results, the outcomes examined varied widely, and individual outcomes were only examined by one to four studies per condition.
  • Sample sizes varied, and some were extremely small – for example, only 11 people in one study. Sometimes within these small studies, the dropout rate from the trial was also high – for instance, 10 people dropping out from a starting size of just 31 participants.

This makes it very difficult to say whether a certain type of tai chi will help individuals with chronic conditions.

Nevertheless, the benefits of exercising within our limits are well known – even when a person has a chronic disease. If you find tai chi enjoyable, this can only be a good thing.

The Tai Chi Union for Great Britain website has information about classes available in your area. 

Links To The Headlines

Tai chi can help older patients with disabling conditions – study. The Guardian, September 17 2015

Tai Chi 'could be prescribed' for illnesses. BBC News, September 18 2015

Tai Chi could help older people with cancer, heart disease and osteoarthritis. Daily Mirror, September 18 2015

Links To Science

Chen Y, Hunt MA, Campbell KL, et al. The effect of Tai Chi on four chronic conditions—cancer, osteoarthritis, heart failure and chronic obstructive pulmonary disease: a systematic review and meta-analyses. British Journal of Sports Medicine. Published online September 17 2015

Categories: Medical News

Smoking linked to raised diabetes risk – including passive smoking

Medical News - Fri, 09/18/2015 - 16:30

"Passive smoking raises risk of type 2 diabetes," The Guardian reports. A major new analysis of previous studies found a significant association between exposure to tobacco smoke – including secondhand smoke – and type 2 diabetes.

People who had never smoked, but were exposed to secondhand smoke, were at a 22% higher risk of developing type 2 diabetes than people who had never smoked, but had been exposed to secondhand smoke.

The study crunched data on almost 6 million people – an impressive feat – meaning it had lots of statistical power to pick out links accurately. It also having took account of many known contributory risk factors for diabetes, including diet and physical activity. The data for passive smokers came from around 150,000 people. 

The diabetes risk increase varied in line with smoking intensity and length of time a person had quit – suggesting that a direct cause and effect link is possible. A randomised controlled trial would be needed to know for sure; however, it would be unethical to allocate people to something that is known to harm.

It is unclear why smoking would increase diabetes risk. Speculations offered in the paper include the fact that smoking can increase inflammation levels and cause cell damage. Interestingly, a study earlier this week found an association between cannabis smoking and diabetes.

Giving up smoking, if you smoke, is one of the biggest steps you can take to improve your health.  

Where did the story come from?

The study was carried out by researchers from universities based in China, Singapore and the US. It was funded by the Chinese National Thousand Talents Program for Distinguished Young Scholars, US National Institutes of Health, the Chinese National 111 Project, and the Program for Changjiang Scholars and Innovative Research Team in University, from the Chinese Ministry of Education.

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

Generally, the UK media reported the story accurately, with most headlines focusing on the 22% risk increase attributed to secondhand smoke exposure – otherwise known as passive smoking.


What kind of research was this?

This was a systematic review and meta-analysis of different smoking behaviours and type 2 diabetes.

Smoking remains the biggest cause of self-inflicted death and disease in the world, killing 6 million people each year and causing a higher proportion of a smoker’s life to be lived in poor health than non-smokers.

Many studies have suggested links between different smoking behaviours – active smoking, passive smoking, and being an ex-smoker – with a higher risk of developing type 2 diabetes. This systematic review pooled all the studies it could find on the issue in an effort to better understand the link.

A systematic review and meta-analysis is one of the best ways to summarise the results of many different studies. Pooling results of similar studies creates more reliable and accurate estimates of any links. However, the pooled results are only ever as good as the studies that feed into them. If you put rubbish in, you get rubbish out.


What did the research involve?

The researchers identified 88 prospective studies containing 5,898,795 people, 295,446 of whom developed type 2 diabetes during the study periods. Where possible, they pooled the study findings into summary estimates of how different smoking behaviour was linked to the risk of developing type 2 diabetes.

The team systematically searched electronic databases to identify relevant studies with a prospective design. This means that smoking behaviour was known before people developed type 2 diabetes. This eliminates the risk of reverse causation – where people with diabetes may be more likely to smoke.

Each study was rated for quality, and this took into account whether the studies adjusted for lifestyle variables – such as diet, alcohol intake and physical activity – that could influence diabetes risk independently of smoking behaviour. Studies with substantial loss to follow-up (>50%) were excluded – this is a way of selecting only the more reliable studies.

The main analysis estimated links between current smoking, former smoking and passive smoking, and the risk of developing type 2 diabetes. The study sample was very large, so the researchers were able to analyse the effects of many subgroups. This includes, for example, the effect of smoking intensity, time since someone quit smoking, ethnicity, blood pressure, diet, physical activity, alcohol, and study location, among others.


What were the basic results?

Follow-up times varied between studies and about a third of participants had long-term follow-up, lasting over 10 years.

Current smoking, former smoking and passive smoke exposure in people who had never smoked themselves were all consistently linked with a higher risk of developing type 2 diabetes.

The following results were found:

  • Current smokers were 27% more likely to develop type 2 diabetes than current non-smokers (relative risk [RR] 1.37, 95% confidence interval [CI] 1.33 to 1.42) based on 84 studies, totalling 5,853,952 people)
  • Former smokers were 14% more likely to develop type 2 diabetes than those who had never smoked (1.14 95% CI 1.10 to 1.18), based on 47 studies with 2,930,391 people)
  • Those who had never smoked, but had been exposed to passive smoke, were 22% more likely to develop type 2 diabetes than those who had never smoked (RR 1.22, 95% CI 1.10 to 1.35, based on seven studies with 156,439 people)

The risk of diabetes increased in proportion to the amount smoked, adding weight to a possible causal link. Compared with those who had never smoked, the relative risks were 21% higher (1.21, 95% CI 1.10 to 1.33) for light smokers, 34% higher (1.34, 95% CI 1.27 to 1.41) for moderate smokers, and 57% higher (1.57% 95% CI 1.47 to 1.66) for heavy smokers.

The risk also started to decrease in proportion to the time since a person kicked the habit – another signal that the link may be causal. Compared with those who had never smoked, new quitters (less than five years since they quit smoking) were at a 54% raised risk of type 2 diabetes (RR 1.54, 95% CI 1.36 to 1.74), 18% for middle-term quitters (5-9 years, RR 1.18 95% CI 1.07 to 1.29) and 11% for long-term quitters (10 years or more, RR 1.11, 95% CI 1.02 to 1.20). These results came from 10 studies with 1,086,608 participants.

Based on the assumption that the association between smoking and diabetes risk was 100% causal – that is, that all the diabetes risk increase was due to smoking – they estimated that 11.7% of type 2 diabetes cases in men and 2.4% in women were attributable to active smoking. This amounts to around 28 million cases worldwide.


How did the researchers interpret the results?

The study group concluded that: "Active and passive smoking are associated with significantly increased risks of type 2 diabetes. The risk of diabetes is increased in new quitters, but decreases substantially as the time since quitting increases. If the association between smoking and risk of type 2 diabetes is causal, public health efforts to reduce smoking could have a substantial effect on the worldwide burden of type 2 diabetes".



This large, robust systematic review and meta-analysis of prospective studies shows a consistent and dose-responsive link between smoking and a higher risk of developing type 2 diabetes. This is suggestive of a causal link. This included exposure to secondhand smoke through passive smoking – a link that grabbed the media’s attention.

The study crunched data on almost 6 million people, meaning it had lots of statistical power to pick out links, having taken account of many known confounders.

The results were consistent and the increases in diabetes risk linked to smoking varied in line with smoking intensity and length of time a person had quit. While prospective studies cannot prove cause and effect, these findings do hint at one. A randomised control trial would be needed to know for sure, but is not feasible, as it would be unethical to allocate people to smoke, due to its known health effects.

A comment article published alongside the Lancet study says "smokers tend to have lower average educational attainment, worse diets, lower physical activity levels, and greater alcohol consumption than non-smokers". This signals that smokers are generally less healthy than non-smokers. This underlying unhealthiness could account for some of the diabetes risk increase – an example of residual confounding. How much of the risk increase is due to this underlying unhealthiness and how much is due to smoking is not easy to define.

The article also reminded us: "we cannot say definitively, based on the existing evidence, that smoking directly increases diabetes risk". 

Though the link appears clear for passive smoke exposure, it is also worth noting that self-reported passive smoke exposure could have covered various intensities of smoke exposure. This result was based on seven studies – three from the US, two from Europe, one from Korea and one from Japan. The specific questioning to establish passive smoking status is not reported. For example, some people could have meant they have been extensively exposed to smoke in their homes throughout their lives, while others could just have been referring to being exposed to passive smoke in public places occasionally. Therefore, although the link seems clear, the 22% increased risk estimate may be imprecise and could not easily be applied to particular individuals with passive smoke exposure.

Overall, while there is not a conclusive proof that passive smoking can increase diabetes risk, the harms of exposure to smoke, such as increased cancer risk, are well established.

Links To The Headlines

Passive smokers have 20% higher risk of diabetes, new study finds. The Independent, September 18 2015

Passive smoking raises risk of type 2 diabetes. The Guardian, September 17 2015

Passive smokers in diabetes alert: Risk of developing Type 2 increases by 22% compared to non-smokers. Mail Online, September 18 2015

Links To Science

Pan A, Wang Y, Talaei M, et al. Relation of active, passive, and quitting smoking with incident type 2 diabetes: a systematic review and meta-analysis. The Lancet – Diabetes and Endocrinology. Published online September 17 2015

Categories: Medical News

Antidepressant paroxetine study 'under-reported data on harms'

Medical News - Thu, 09/17/2015 - 13:28

"Seroxat [paroxetine] study under-reported harmful effects on young people, say scientists," The Guardian reports. Researchers have reanalysed data about the antidepressant paroxetine – no longer prescribed to young people – and claim important details were not made public.

Researchers who looked at data from the now infamous 1990s "study 329" trial of the antidepressant paroxetine, found reports of suicide attempts that were not included in the original research paper.

The makers of paroxetine, GlaxoSmithKline (GSK), marketed paroxetine as a safe and effective antidepressant for children, despite the evidence of harms. The US Department of Justice sued GSK for a record $3 billion for making false claims.

The new analysis of thousands of pages of data contradicted the original claims that paroxetine was "generally well-tolerated and effective" for treating adolescents with depression. By contrast, the new analysis found "no advantage" from paroxetine and an "increase in harms", compared to placebo.

This new analysis found that the original study paper over-reported the effectiveness of paroxetine and under-estimated potential harms. It raises questions about how much we can rely on the reported results of medical trials, without independent access to review the raw trial data.  

Where did the story come from?

The study was carried out by researchers from Bangor University in Wales, Emory University in Atlanta, US, the University of Adelaide in Australia and the University of Toronto in Canada. The researchers say they had no specific funding source for their work.

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

The story was, in the main, accurately reported in The Independent, The Guardian and the Mail Online.


What kind of research was this?

This was an unusual study, in that it was a re-analysis of a previously reported placebo-controlled double-blind randomised controlled trial

This type of trial is seen as very high-quality, because researchers can directly compare what happens to people taking one type of drug compared to another type, or to a placebo.

However, there have been concerns about how accurately adverse effects are reported in randomised controlled trials, especially those funded by drug manufacturers.


What did the research involve?

The independent researchers asked the manufacturer of paroxetine, GSK for access to the original trial data. They re-analysed the data according to the original trial protocol (the document setting out how the trial should be run). They then compared their findings to the research paper that reported the trial results, which was published in 2001.

The original study reported on 275 young people aged 12 to 18 with major depression, who were randomly allocated to either paroxetine, an older antidepressant drug called imipramine, or placebo, for eight weeks.

The documents studied by the researchers included the clinical study report showing the researchers’ raw data, and one third of the original case reports on the young people who took part in the trial. 

They checked this sample of 93 patients for reports of adverse events, recorded these, and compared them to the events recorded in the clinical study report and the 2001 published research paper.

Because research practices have changed since the 1990s, they analysed the research in different ways, to give comparisons between how the results would have been reported under current best practice, compared to best practice at the time.


What were the basic results?

The researchers found that neither paroxetine or imipramine was more effective than placebo, using the outcome measures specified in the original research protocol. However, the 2001 research paper picked a different set of outcome measures, which they said showed that paroxetine worked better than placebo. This is suspicious, because it suggests that the new outcome measures were chosen specifically to show a positive result, after the original outcome measures failed.

The researchers also found that the 2001 paper seriously under-reported cases of suicidal or self-harming behaviour. The 2001 paper reported five cases of suicidal behaviour for people taking paroxetine, three taking imipramine and one taking placebo. Yet the clinical study report on which the paper should have been based reported seven events for people taking paroxetine.

When the researchers included new cases identified from the case reports of 93 of the 275 patients in the study, they found 11 reports that could be classed as suicidal behaviour. They also found that many hundreds of pages of data were missing from the reports they looked at, without clear reason.

They said the 2001 paper reported 265 adverse events for people taking paroxetine, while the clinical study report showed 338. They said their analysis of the clinical study report identified 481 adverse events, and their scrutiny of case records found that another 23 not been previously reported.


How did the researchers interpret the results?

The researchers said their findings showed "evidence of protocol violations" with the addition of new outcome measures after the results were known, and "unreliable" coding of adverse events, such as suicidal behaviour.

They said the extent of the serious adverse events associated with paroxetine were only apparent when they looked at the individual case reports – a huge task, which involved trawling through 77,000 pages of data made available by GSK.



This study stands as a warning about how supposedly neutral scientific research papers may mislead readers by presenting findings in a certain way.

The differences between the independent analysis published in the BMJ and the 2001 research paper are stark. They cannot both be right. The "authors" of the 2001 paper appear to have picked outcome measures to suit their results, in the way they present evidence of effectiveness. 

It has subsequently come to light that the first draft paper was not actually written by the 22 academics named on the paper, but by a "ghostwriter" paid by GSK.

The study also seems to have under-reported adverse events, even those that were included in the researchers’ clinical study report.

The re-analysis does have some potential flaws. The researchers admit to some uncertainty about how to classify adverse events that happened after the end of the main eight-week phase of the trial, which could be seen as either withdrawal effects or effects of the drug. Because the numbers of young people reported as having suicidal behaviour is relatively small, the re-coding of adverse effects has a large impact.

It is possible that an alternative coding of adverse effects would change the results again. However, re-coding does not explain why adverse effects from the researchers’ clinical study report did not make it into the 2001 paper. The researchers were also able to look at only 93 of the 275 case reports, because they had insufficient time or resources. It is possible that a full re-analysis might change the overall message.

We don’t know how many young people may have been prescribed paroxetine for depression as a result of the 2001 paper. It was prescribed to 8,000 under-18s in the UK in 2001, before the regulatory authorities in the UK banned it for under-18s. However, paroxetine was used much more widely in the US.

The National Institute for Health and Care Excellence (NICE) recommends that only one antidepressant, fluoxetine, should be used for under-18s with moderate to severe depression, and only alongside psychological therapy. Three antidepressants (fluoxetine, sertraline and citalopram) are recommended as additional options for children who have not responded to treatment or who have recurrent depression.

This new analysis seems to show that paroxetine was not effective or safe for the young people in the trial. The fact that the 2001 paper reported it to be both effective and safe raises serious questions about the reliability of industry-funded clinical trials.

Links To The Headlines

Seroxat study under-reported harmful effects on young people, say scientists. The Guardian, September 16 2015

Anti-depressant was given to millions of young people 'after trials showed it was dangerous'. The Independent, September 16 2015

Bad medicine: Drug companies cannot be trusted to tell the truth about the efficacy of their products – outside scrutiny is crucial. The Independent, September 17 2015

Global drug giant GSK 'published a flawed study which led to millions of children being wrongly prescribed dangerous antidepressants'. Mail Online, September 17 2015

Links To Science

Noury JL, Nardo JM, Healy D, et al. Restoring Study 329: efficacy and harms of paroxetine and imipramine in treatment of major depression in adolescence. BMJ. Published online September 16 2015

Categories: Medical News

Decreasing portion sizes could cut obesity levels

Medical News - Wed, 09/16/2015 - 18:35

"Reducing the portion sizes … would help reverse the obesity epidemic, say researchers," BBC News reports. 

The researchers, who pooled the results of more than 70 previous studies, found a link between portion size and overeating.

Researchers found that increased portion size, packaging and the size of a plate led to people choosing larger amounts of food and eating more. It may be that the old saying "you have eyes bigger than your belly" rings true for some people. They eat what they are given, not what they need.

People also drank more when non-alcoholic drinks were provided in shorter, wider glasses and bottles than tall, thin ones. The researchers say that although the results were not surprising, they lend weight to the argument for portion sizes to be decreased to help reduce the UK's obesity epidemic.

It should be noted that the quality of the individual studies was rated as poor by the researchers, and most of the studies were conducted in the US, where portion sizes are infamously large.

The studies also did not look at whether people were able to reduce their intake over the long term through smaller portion sizes.

These limitations aside, it would seem a sensible option to choose a smaller portion if you are trying to achieve or maintain a healthy weight. Making sure you get your five portions of fruit and vegetables a day and increasing physical activity levels will also help.


Where did the story come from?

The study was carried out by researchers from the University of Cambridge, the University of Oxford, MRC Human Nutrition Research, the University of Plymouth and the University of Bristol. It was funded by the UK Department of Health Policy Research Programme.

The study was published in the peer-reviewed online medical resource The Cochrane Database of Systematic Reviews. As with all Cochrane studies, the research has been made available on an open-access basis, so it is free to read online.

The UK media reported the findings accurately and supported the notion that portion sizes have been increasing, which may be contributing to increasing obesity levels.

The Independent provided helpful expert commentary from one of the lead authors, Dr Gareth Hollands, that "helping people to avoid 'overserving' themselves or others with larger portions of food or drink by reducing their size, availability and appeal in shops, restaurants and in the home, is likely to be a good way of helping lots of people to reduce their risk of overeating". 


What kind of research was this?

This was a systematic review of studies that have looked at the effect of different portion sizes on the consumption of food, alcohol or tobacco. The researchers pooled the results together in a meta-analysis

Although this type of research brings together all of the evidence available for a topic, the results are reliant on the quality of the individual trials.

In this case, only randomised controlled trials were included, either comparing consumption between two groups or in individuals in crossover studies. However, despite this type of study design being the "gold standard", the researchers judged the studies to be at high or unclear risk of bias, so they say the overall evidence is of moderate to very low quality.


What did the research involve?

The study searched 12 medical databases and trial registries for relevant studies up to July 2013. Randomised controlled trials were included in the analysis if they compared the amount of food, alcohol or tobacco consumed or chosen, according to different portion:

  • size
  • shape
  • package
  • crockery dimensions

Standard Cochrane techniques were used for the search strategy in applying inclusion and exclusion criteria consistently across the identified search results, and when performing the statistical analyses.


What were the basic results?

There were 72 studies that met the inclusion criteria; 69 assessed food portion size and three looked at cigarette size. No studies were identified that assessed alcohol portion size.

Exposure to larger food portions, packaging or crockery size was associated with moderately increased food consumption for adults and children (standardised mean difference (SMD) 0.38, 95% confidence interval (CI) 0.29 to 0.46). 

The researchers estimated that if smaller portion sizes were used consistently across meals, the average daily calorie consumption could reduce by 144 to 228 calories per day. This would be equivalent to 4,032 to 6,384 less calories per month, which would equal a weight loss of one to two pounds (0.45kg to 0.9kg) if everything else stayed the same.

A meta-analyses of 13 studies found that increased portion or crockery size led to adults selecting a greater amount of food (SMD 0.55, 95% CI 0.35 to 0.75). This was not found in studies on children.

There was low-quality evidence from three studies that shorter, wider glasses or bottles compared to thin, tall glasses increased the amount of non-alcoholic drinks selection (SMD 1.47, 95% CI 0.52 to 2.43). 

Only one study looked at consumption of non-alcoholic drinks, which found that young adults drank more water if using shorter, wider bottles, but this was judged as very low-quality evidence (SMD 1.17, 95% CI 0.57 to 1.78).

Meta-analyses of the three studies on cigarette size found low-quality evidence that the length of cigarette did not influence the amount consumed. No studies were identified that looked at the effect of differently sized packs, such as packs of 10 cigarettes compared to packs of 20.


How did the researchers interpret the results?

The researchers concluded that, "people consistently consume more food and drink when offered larger-sized portions, packages or tableware than when offered smaller-sized versions". 

They say this "suggests that policies and practices that successfully reduce the size, availability and appeal of larger-sized portions, packages, individual units and tableware can contribute to meaningful reductions in the quantities of food (including non-alcoholic beverages) people select and consume in the immediate and short term". 

There was insufficient evidence for them to make recommendations for tobacco or alcohol portion sizes.



This systematic review and meta-analysis suggests that increased portion sizes, packaging and crockery influences the amount people choose to eat and actually consume. 

The methods used to produce this review are robust; however, all 72 identified studies were assessed as being at high risk of bias or of unclear risk. This reduces confidence in the results. Other limitations include:

  • the majority of studies were conducted in the US, so the results may not be directly applicable to the UK, because of the potential differences in portion sizes
  • most studies were not conducted on people who were trying to lose weight, so it is not clear how effective this strategy would be for weight loss
  • the studies included only assessed food consumption or selection at one time point, or over short time periods. This means that the studies did not look at whether eating more at one meal was compensated for at subsequent meals that day
  • the studies were performed in controlled environments such as a laboratory, so it remains unclear what effect portion size may have in "normal" environments over the long term

Overall, common sense tells us that people are likely to eat more if the portion size is bigger for a variety of potential reasons, such as:

  • social norms – someone has decided the portion size is appropriate, which may challenge internal perceptions.
  • there is a delay in the time it takes to feel full (satiety) than the time it takes to consume the food in front of you
  • people may not want to waste food and are taught from an early age to "finish your plate"

Reducing portion size or the size of the plate the food is presented on is not a new concept for weight loss – it is a strategy employed by many diet regimes. Other strategies to help maintain a healthy diet can be found in the healthy eating pages

Links To The Headlines

Portion size key in tackling obesity, says study. BBC News, September 15 2015

Serving food on a larger plate 'makes people eat more'. The Independent, September 15 2015

End to supersizing could reverse obesity trend. The Daily Telegraph, September 15 2015

Links To Science

Hollands GJ, Shemilt I, Marteau TM, et al. Portion, package or tableware size for changing selection and consumption of food, alcohol and tobacco. Cochrane Database of Systematic Reviews. Published online September 14 2015

Categories: Medical News

UK ban on trans fats 'would save thousands of lives'

Medical News - Wed, 09/16/2015 - 15:00

"Trans fat ban could save 7,200 lives by 2020, says study," The Guardian reports. This is the conclusion of a new modelling study looking at whether banning trans fatty acids – associated with "bad" cholesterol and heart disease – would improve public health outcomes.

Trans fats make up around 0.8% of the estimated energy consumption of the average UK diet. There are two types of trans fat: naturally occurring trans fatty acids found at low levels in meat and dairy products, and artificially made trans fatty acids labelled as hydrogenated fats or oils in some processed foods.

The artificial type became a popular ingredient for the food industry as they help prolong shelf-life while also improving taste. But research has shown a link between trans fats and heart disease. This led to several countries banning the use of artificial trans fats in food products.

In the UK there is no ban, but in 2012 most supermarkets and the bigger fast food chains agreed to sign up to a voluntary agreement not to use artificial trans fats. It is unclear how many products still contain trans fats.

The researchers calculated how many deaths they think could be avoided if a total ban was imposed, and what savings could be made in health and other costs.

While the figures are interesting, they are all based on assumptions fed into a mathematical model. It's hard to know how accurate these predictions are.  

Where did the story come from?

The study was carried out by researchers from the University of Lancaster, the University of Liverpool and the University of Oxford, and was funded by the National Institute for Health Research. 

It was published in the peer-reviewed BMJ and has been made available on an open access basis, which means anyone can read it free online

Most of the UK media covered the study accurately, although few questions were asked about how the figure of 7,200 prevented deaths had been reached.

Oddly, the Daily Mirror claimed a ban on trans fats "could prevent at least 10,000 deaths". They appear to have added a calculated 3,000 reduction in unequal deaths to the total 7,200 deaths prevented, when actually the 3,000 figure is part of the 7,200. 

What kind of research was this?

This was an epidemiological modelling study, which means it used data gathered about populations to create mathematical models to estimate the effect of possible changes in policy.

This type of study is a useful way to calculate the possible future effect of change, but it cannot be seen as a precise prediction of exactly what will happen. 

What did the research involve?

Researchers used several big data sets and the results of previous studies to construct mathematical models about the possible effects of three policies over the next five years:

  • banning trans fats
  • improving labelling of food containing trans fats
  • banning trans fats only from restaurant and fast food outlets

They then calculated the effects in terms of deaths avoided or delayed, healthcare costs, costs to the economy, and the effect on health inequalities.

The researchers used the findings of a 2006 meta-analysis, which estimated the effect of how many trans fats we eat as a proportion of total energy intake. The meta-analysis found there are 23% more new cases of heart disease for every 2% of total energy that comes from trans fats.

The researchers then combined this figure with information from questionnaires from the National Diet and Nutrition Survey (an ongoing government project to monitor dietary trends) to find out what proportion of people's diets consisted of trans fats.

They also used data about the socioeconomic status of people in England, which assigned people into five groups depending on their wealth and levels of deprivation.

They used a mathematical model to calculate the different effect various policies might have on these groups – for example, people in the lowest socioeconomic group eat the most trans fats as percentage of diet, so any policy that affected this group more would have a bigger effect on health overall.

The researchers made assumptions for their models. For example, they assumed changing labelling would have a bigger effect on people in higher socioeconomic groups than on lower groups, and people from lower socioeconomic groups were more likely to eat at fast food outlets and less likely to eat at restaurants.

They did multiple calculations using this data to work out the possible reduction in deaths from heart disease, the savings to the taxpayer, the effect on health inequalities, and the savings to the economy overall. 

What were the basic results?

The researchers calculated an outright ban on the use of trans fats in food products would cut the amount of trans fats eaten by half, from 0.8% to 0.4% of total energy – the remainder would be the amount still consumed from naturally occurring trans fats in meat and dairy.

Their models found improved labelling or bans in restaurants and fast food outlets would, at best, achieve half that reduction, lowering trans fat consumption to around 0.6% of total energy.

They say most of the benefit from improved labelling or restaurant bans in terms of trans fat reduction would be seen among higher socioeconomic groups, so the policies would widen health inequalities.

In contrast, they say a total ban would affect lower socioeconomic groups more because they eat more trans fats, so it would narrow health inequalities. The researchers suggest the "gap" between the numbers of people from upper and lower groups who died of heart disease would narrow by about 3,000 people with a total ban.

They used the figures from the previous analysis to calculate the effect of this reduction in trans fat in the diet. They assumed deaths from heart disease would fall at the same rate as numbers of new cases of heart disease, giving a total figure of 7,200 deaths delayed or avoided over five years from a total ban (95% confidence interval [CI] 3,200 to 12,500).

They said improved labelling or restaurant bans might delay or avoid 1,800 to 3,500 deaths, depending on the model used. They claim a total ban would save £297 million (95% CI £131 to £466 million). These savings mainly represent savings in "informal care" – the care given to people with heart disease by friends and family.

They also included productivity at work and healthcare costs. Estimated direct healthcare savings are relatively small, at around £42 million, while estimated informal care savings are £196 million. 

How did the researchers interpret the results?

The researchers say their findings show that, "elimination of trans fatty acids from processed foods is an achievable target" and "would lead to health benefits at least twice as large as other policy options".

They warn trans fats "could creep back into processed foods" if action is not taken now to ban them completely. 


Trans fats are already at low levels in the UK diet compared with 10 or 20 years ago. However, this study suggests lowering them even further could reduce the number of people getting and dying from heart disease over the next five years.

This study does have limitations, however, which means we cannot rely on the findings to be precise. Any study that uses a mathematical model relies on the researchers making correct assumptions when they feed in the data.

The researchers say they have had to make assumptions based on little data in some cases. For example, there is no information about what proportion of the diet is made up of trans fats for those in the top socioeconomic class. We also don't know what proportion of trans fats are consumed in restaurants or fast food outlets.

More importantly, it is possible reducing consumption of trans fats will not have the effect on heart disease the researchers think it will. They used a study from 2006 that combined the results of previous trials to come up with their figure. But this study's finding that trans fats are linked to an increased chance of heart disease does not automatically mean reducing trans fats will reduce the chance of heart disease by the same amount.

However, it does seem likely reducing trans fats will reduce the numbers of people getting heart disease and dying from it. Whether or not banning trans fats will have exactly the effect the researchers predict is less certain. 

Links To The Headlines

Trans fat ban could save 7,200 lives by 2020, says study. The Guardian, September 15 2015

Ban on trans fats in processed food could save 7,000 lives over the next five years. Daily Mail, September 16 2015

Banning trans fats in Britain would save lives, research suggests. The Daily Telegraph, September 16 2015

Banning trans fats could prevent 7,000 deaths from heart disease over next five years, claim experts. The Independent, September 15 2015

Banning trans fats could prevent at least 10,000 deaths in the UK over 5 years. Daily Mirror, September 16 2015

Links To Science

Allen K, Pearson-Stuttard J, Hooton W, et al. Potential of trans fats policies to reduce socioeconomic inequalities in mortality from coronary heart disease in England: cost effectiveness modelling study. BMJ. Published online September 15 2015

Categories: Medical News

Study finds North-South divide in UK life expectancy

Medical News - Tue, 09/15/2015 - 14:50

"England's richest people 'live eight years longer than the country's poorest'," The Independent reports. 

A major new study has found a significant difference in life expectancy of the richer South East England compared to the poorer North.

The researchers found that overall life expectancy increased by more than five years from 1990 to 2013, from 75.9 to 81.3 years. The gap in mortality between men and women has also decreased, which is encouraging. 

However, more deprived areas have failed to catch up with less deprived areas, with a difference of more than eight years. Areas of deprivation were mainly located in the North, the Midlands and some areas of London.

There is also evidence that, while there has been an overall decline in mortality, there has been less of a reduction in the length of time people are living in poor health with chronic illness or disability. 

The study has shown where improvements have been made and areas that would benefit from more attention. Many of the leading causes of death are preventable through an active and healthy lifestyle and a good diet.

Where did the story come from?

The study was carried out by researchers from a number of institutions, including Public Health England and the London School of Hygiene and Tropical Medicine. 

Funding was primarily provided by the Bill & Melinda Gates Foundation. Additional funding for the study was provided by Public Health England.

The study was published in the peer-reviewed medical journal The Lancet on an open-access basis, so it is free to read online or download as a PDF.

The study has been widely reported in the UK media. Reporting of the study was accurate for all sources.


What kind of research was this?

This study used data from the Global Burden of Disease (GBD) 2013 study to analyse the burden of diseases and injuries in England, by region and within each region by level of deprivation. GBD is an ongoing global collaboration looking at trends in diseases that can cause death or disability.

Researchers compared this data with earlier years, going back to 1990. This method is able to look at large amounts of data for a long period to draw overall patterns and conclusions. However, it cannot provide definite answers as to why mortality or illness rates are as they currently stand, or why they have changed.


What did the research involve?

This study used data from the GBD 2013 study on causes of death, disease, and injury incidence and prevalence, as well as years lived with disability (YLDs) and disability-adjusted life-years (DALYs). DALYs is a term used by epidemiologists to measure the number of "healthy years" lost due to ill health, disability or early death.

Researchers looked at the following countries:

  • England
  • UK
  • The first 15 EU members (excluding the UK)
  • Australia
  • Canada
  • Norway
  • US

The GBD 2013 study also provides independent and overlapping attributable risk for five tiers of risk factors:

  1. All GBD risks combined.
  2. Three large categories of metabolic, behavioural, and environmental and occupational risks.
  3. Single risks, such as high blood pressure, and risk clusters, such as child and maternal under-nutrition or air pollution.
  4. Single risks within such clusters, such as vitamin A deficiency or household air pollution.
  5. Individual occupational exposure to cancer-causing substances or the division of childhood underweight into stunting, underweight and wasting.

The Index of Multiple Deprivation (IMD-2010) was used to measure deprivation. This is a government study that aimed to assess levels of deprivation in areas of the UK. 

Mortality data for the period 1990 to 2012 was obtained from the Office for National Statistics and split into regional and deprivations groups based on postcode.


What were the basic results?

The study found that from 1990 to 2013, life expectancy from birth in England increased by 5.4 years (95% confidence interval [CI] 5.0 to 5.8) from 75.9 years (95% CI 75.9 to 76.0) to 81.3 years (95% CI 80.9 to 81.7). A greater improvement in life expectancy gains was seen for men than for women.

Rates of age-standardised years of life lost (YLLs) reduced by 41.1%, which indicates a greater reduction in premature mortality compared with overall mortality. A small decrease was seen for age-standardised YLDs. DALYs were reduced by 23.8%.

The range in life expectancy across deprivation areas has stayed the same for men since 1990 – an 8.2 year difference between the least and most deprived areas. However, for women, the deprivation differences decreased from 7.2 years in 1990 to 6.9 years in 2013. In 2013, the leading cause of YLLs was heart disease, and the leading cause of DALYs was low back and neck pain. Leading behavioural risk factors were suboptimal diet and tobacco.

Overall, England ranked better than the other UK countries and was found to be the EU country with one of the largest gains in life expectancy among men (6.4 years). This is less than Luxembourg, but the same as Finland. 

All English regions except for South West England, gained at least six years, which is equal to or greater than all comparator countries except Austria, Finland, Ireland, Germany and Luxembourg. 

Among women, the increase in life expectancy in England overall was 4.4 years, which is equal to or in excess of all countries except Finland, Germany, Ireland, Luxembourg and Portugal.


How did the researchers interpret the results?

The researchers conclude that, "Health in England is improving, although substantial opportunities exist for further reductions in the burden of preventable disease. The gap in mortality rates between men and women has reduced, but marked health inequalities between the least deprived and most deprived areas remain". 

They go on to say that policies must address the causes of ill health and premature mortality. Action is needed to reduce risk exposures, support healthy behaviours, alleviate the severity of chronic disabling disorders, and mitigate the effects of socioeconomic deprivation.



This study used data to analyse the burden of disease and injury in England, and within each English region by level of deprivation. This was compared with the remaining constituent countries of the UK and with other comparable countries.

The researchers found an overall increase in life expectancy from 1990 to 2013. The decreased mortality gap between men and women is also encouraging. However, the inequality of life expectancy across regions of England has not improved. Those in more deprived areas have not yet reached the life expectancy of the less deprived in 1990.

Despite the overall decline in mortality, this has not been matched by a similar decline in the number of years people are living in poor health or with chronic illness.

The authors suggest the main reasons for improvement in life expectancy are reductions in: 

  • cardiovascular disease
  • cancer mortality
  • chronic respiratory disease
  • road injuries

However, they report that conditions still having a negative impact on life expectancy include:

  • cirrhosis of the liver (related to alcoholic liver disease)
  • mental disorders
  • substance use

Strengths of this study are the large amount of population data used and the long follow-up period. Some limitations are that data was not available for some diseases or by specific deprivation level. The relative level of deprivation of an area may also have changed since the measurement tool was created, and the cross-country comparisons may not be as straightforward as presented.

The findings have indicated areas where improvement has been made and possible areas that would benefit from more attention.

Though not all diseases are preventable, poor health can be caused by risk factors such as poor diet, low levels of physical activity, smoking and alcohol consumption.

Links To The Headlines

Life Expectancy in the UK: England's richest people 'live eight years longer than the country's poorest'. The Independent, September 15 2015

English life expectancy catches up with the west but poorest lag behind. The Guardian, September 15 2015

Huge increase in life expectancy: Britons now live average of 5.4 years longer than in 1990 - but only if they are wealthy. Mail Online, September 15 2015

Average life expectancy in England rises to 81 years but north-south divide remains. ITV News, September 15 2015

Where In England Do People Live The Longest? Sky News, September 15 2015

Links To Science

Newton JN, Briggs ADM, Murray CJL, et al. Changes in health in England, with analysis by English regions and areas of deprivation, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013. The Lancet. Published online September 14 2015

Categories: Medical News

Cannabis use may affect diabetes risk in the middle-aged

Medical News - Mon, 09/14/2015 - 14:30

"People who use marijuana may be more likely to develop pre-diabetes than those who have never smoked it," The Independent reports, after a US study found a link between long-term cannabis use and pre-diabetes.

Pre-diabetes is defined as having abnormally high blood sugar levels, but not high enough to meet criteria for diagnosis of type 2 diabetes.

The study enrolled around 3,000 healthy young US adults in the mid-1980s. Over the following years, researchers carried out regular medical assessments and questioned participants about their use of cannabis and other substances.

Cannabis use at the 25-year assessment, when the person was now in middle age, was associated with an increased risk of having pre-diabetes. However, there were no significant links between cannabis use and "full-blown" diabetes.

The main difficulty with this research is that the study design cannot prove direct cause and effect. Many other health and lifestyle factors could be linked to both cannabis use and diabetes risk, such as diet.

Cannabis is a notorious appetite stimulant – know as "the munchies", which often leads users to eat energy-rich, nutritiously poor snacks, such as crisps and sweets. If there is a link, it's possible that diet could be having an effect on diabetes risk, rather than cannabis itself.

While the short- and long-term effects of cannabis are not firmly established, the drug has been linked to mental health conditions such as psychosis and physical conditions such as lung cancer

Where did the story come from?

The study was carried out by researchers from the University of Minnesota and the University of California, San Francisco. It received various sources of financial support, including from the US National Institutes of Health.

The study was published in the peer-reviewed journal Diabetologia on an open-access basis, so it is free to read online as a PDF (384kb).

The Independent and the Mail Online's reporting of the study is accurate, although both articles could benefit from highlighting that this study cannot prove direct cause and effect. 

What kind of research was this?

This cohort study aimed to see whether cannabis use is associated with the presence or development of diabetes or pre-diabetes.

Pre-diabetes is when the person has blood glucose levels just below the threshold for meeting the criteria for diabetes. If the person doesn't make lifestyle changes, such as changing their diet, upping their physical activity and trying to lose weight, it can progress to type 2 diabetes.

Cannabis, or marijuana, has uncertain effects on a person's physical or mental health. In the US, where this study was based, it is the most frequently used illegal drug, with 18.9 million people over the age of 12 reportedly having used cannabis in 2012.

Recent studies have suggested that cannabis use may be associated with reduced odds of diabetes and other metabolic risk factors, such as a high body mass index (BMI) and waist circumference. The researchers report the possibility of bias with these studies, and the need for prospective studies to better examine these links.

In this study, researchers aimed to look at the link between self-reported cannabis use and the presence of diabetes or pre-diabetes (cross-sectional link) or the development of these conditions (prospective link).

The main limitation with this type of study is not being able to prove cannabis use has caused the diabetic conditions, as other factors may have had an influence – particularly with the cross-sectional association.   

What did the research involve?

This study involved participants of the Coronary Artery Risk Development in Young Adults (CARDIA) study. They were recruited from four urban areas in the US and aged 18 to 30 years at the time of enrolment in 1985-86.

At enrolment and each follow-up, the participants completed questionnaires and had clinical examinations, including blood tests and measurements of blood pressure and BMI. Questionnaires involved assessments of their health and lifestyle, including physical activity, alcohol, smoking and use of illegal substances.

The substance assessment asked specifically about the use of cannabis, crack or other cocaine, amphetamines or opiates in the person's lifetime or past 30 days, with frequency of once or twice, 3 to 9 times, 10 to 99 times, more than 100, or more than 500 times.

Pre-diabetes and diabetes were defined by blood glucose levels using American Diabetes Association criteria. For example, pre-diabetes was a fasting blood glucose of 5.6 to 6.9 millimole (mmol) per litre, and diabetes was a level of 7.0mmol per litre or greater.

The cross-sectional link between lifetime cannabis use and pre-diabetes or diabetes was assessed at the last follow-up assessment, around 25 years after enrolment.

The prospective link was examined between cannabis use seven years after enrolment and the later development of pre-diabetes or diabetes by year 25. The assessments included around 3,000 people.

When looking at the links between cannabis use and diabetes, the researchers took into account potential confounders – the use of other substances, smoking and alcohol, educational attainment, and examination findings, including BMI, blood pressure and cholesterol.  

What were the basic results?

Factors associated with cannabis use were being male, of white ethnicity, greater reported smoking, alcohol and other substance use, and greater physical activity.

Higher educational attainment and higher BMI were factors associated with less cannabis use. By the age of 24, 45% of the participants (1,193) had pre-diabetes and 357 had diabetes.

With full adjustment for all confounders, current use of cannabis was associated with about a two-thirds increased odds of pre-diabetes compared with never using the drug (hazard ratio [HR] 1.66, 95% confidence interval [CI] 1.15 to 2.38).

There were no significant links between pre-diabetes and former cannabis use. When broken down into frequency of use, there was a trend for increased lifetime use to be associated with an increased risk of pre-diabetes.

However, the only significant link was found for a lifetime use of 100 or more times being associated with a 40% increased risk of pre-diabetes (HR 1.40, 95% CI 1.13 to 1.72). There were no convincing links for a lower frequency use than this.

There was no statistically significant link between former, current or any lifetime use of cannabis and actual diabetes.  

How did the researchers interpret the results?

The researchers concluded that, "Marijuana [cannabis] use in young adulthood is associated with an increased risk of pre-diabetes by middle adulthood, but not with the development of diabetes by this age." 


This long-term study of healthy US adults found current cannabis use at the 25-year assessment – when the person had reached middle age – was associated with an increased likelihood of the person having pre-diabetes at this time.

Higher lifetime use of more than 100 times was also associated with an increased likelihood of pre-diabetes. However, there were no significant links between cannabis use and actual diabetes.

The main limitation of this study comes from the possibility of confounding. The researchers have attempted to take several confounders into account, including smoking and the use of alcohol and other substances.

However, various physical and mental health, lifestyle, personal and socioeconomic characteristics may be associated with both cannabis use and diabetes risk. For example, one possible factor that could be linked to both cannabis use and diabetes risk is poor diet.

Cannabis use can cause sudden and intense hunger pangs, nicknamed "the munchies". This can lead users to snack on foods with a high calorie and sugar content, but with little in the way of nutritional value. If maintained on a long-term basis, this type of diet can lead to obesity, which is a risk factor for type 2 diabetes.

This study is not able to account for the influence of all these factors, particularly as the main link was for the current use of cannabis at the 25-year assessment and pre-diabetes at the same time. This cannot prove that one thing has caused the other.

There was no link with type 2 diabetes itself. Pre-diabetes suggests the person may be on the border of developing diabetes, but they don't yet have the condition.

Another – admittedly unavoidable – limitation is that cannabis use was self-reported. This may be inaccurate, particularly when it comes to estimating the lifetime frequency of use. There is also the possibility when questioning people about their use of illegal substances that they may report never using them, when in fact they have.

This urban sample of US citizens may not be representative of everyone, particularly given they were enrolled 30 years ago. Patterns of cannabis use during the 80s and 90s may differ from use of the substance today. In particular, the strength of cannabis in terms of one of the active ingredients, tetrahydrocannabinol (THC), is thought to be much stronger than in the past.

The various possible effects of cannabis on physical and mental health – both in the immediate and longer term – are often debated. However, this study alone provides no proof that cannabis use will increase your risk of diabetes.

Cannabis remains a class B drug that is illegal to possess or distribute.  

Links To The Headlines

Marijuana users may be more likely to develop diabetes, research finds. The Independent, September 13 2015

Cannabis smokers are far more likely to develop early stages of diabetes, research finds. Mail Online, September 14 2015

Links To Science

Bancks MP, Pletcher MJ, Keresz SG, et al. Marijuana use and risk of prediabetes and diabetes by middle adulthood: the Coronary Artery Risk Development in Young Adults (CARDIA) study (PDF, 384kb). Published online September 12 2015

Categories: Medical News