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

GI diet 'debunked' claims are misleading

Medical News - Fri, 12/19/2014 - 13:29

Today, the Mail Online says, “The GI diet debunked: Glycaemic index is irrelevant for most healthy people”, explaining how “it doesn't matter if you eat white or wholewheat bread”.

This is overgeneralised and misleading, so the diet certainly hasn't been "debunked".

Glycaemic index (GI) measures how quickly foods containing carbohydrates raise blood sugar levels in the bloodstream. It’s used in some diets on the basis that foods that raise blood sugar slowly (low-GI) are considered better for you.

This small US study tried mainly obese people on different high- and low-carbohydrate versions of the GI diet for five weeks at a time.

It found that low-GI diets were no better than high-GI diets at reducing certain risk factors for cardiovascular disease and diabetes.

However, the results came from mainly obese adults, a quarter of whom had high blood pressure – so may not necessarily represent “most healthy people”. The very select group involved in this research makes it difficult to generalise the findings to the wider population.

What this trial tells us is that selecting low-GI foods as a way to reduce risk of diabetes and cardiovascular disease might not be any more beneficial than choosing high-GI foods.

This is food for thought for those aiming to reduce disease risk through dietary modifications, and for health professionals advising them.

 

Where did the story come from?

The study was carried out by researchers from Harvard Medical School and collaborators. It was funded by the (US) National Heart, Lung and Blood Institute; National Institute of Diabetes and Digestive and Kidney Diseases; the Harvard Clinical and Translational Science Center; the National Center for Advancing Translational Science; and the general clinical research center at Brigham and Women’s Hospital.

The study was published on an open -access basis in JAMA, a peer-reviewed medical journal.

The Mail Online got its headline a bit wrong when saying that the results applied to “most healthy people”, as the study had specific eligibility criteria to include people with a BMI over 25, some of whom had high blood pressure. It was also not correct to say that GI diets have been “debunked”, as the results may not be generalisable to the wider population.

 

What kind of research was this?

This was a randomised crossover trial (RCT) looking at the effect of different diets on cardiovascular disease and diabetes risk factors. The dietary elements of interest were carbohydrate content and GI.

GI is a measure of how quickly foods containing carbohydrates raise blood sugar levels in the bloodstream. High-GI foods cause a short-term spike in blood sugar level, while low-GI foods cause a more prolonged and smaller rise in blood sugar.

Some popular diets advocate the consumption of low-GI foods, based on the assumption that low-GI is healthier than high-GI. However, the researchers point out that the independent benefits of GI on health are uncertain.

An RCT is one of the best methods to isolate the effects of a dietary intervention such as this. Common issues reducing the reliability of RCTs are a lack of compliance to the diet, high levels of people dropping out of the study, or only recruiting small or highly specific numbers of people. Anything less than a couple of hundred is generally considered small. In this RCT, participants were assigned to trial at least two of the different diets, with a wash-out period in between.

 

What did the research involve?

Researchers recruited 189 overweight people (all had a body mass index (BMI) of 25 or above) and randomly allocated them to follow one of four strictly controlled diets for five weeks.

After this first phase, they were allowed a break to eat what they wanted for two weeks – called a wash-out period. After the wash-out period, they were randomly allocated a second time to a different diet for a further five weeks. 

To be eligible, people had to have a systolic (upper figure) blood pressure of 120 and 159mmHg and diastolic (lower figure) of 70 to 99mmHg. On this basis, some of the people could have had normal blood pressure, some borderline/pre-hypertension, and some high blood pressure (hypertension).

Other eligibility criteria included being aged 30 or above, and being free from diabetes or cardiovascular disease, and not taking medication related to these conditions.

The researchers aimed to ensure that everyone included in the trial went on two different strictly controlled diets for five weeks, with a two-week gap in the middle.

The background diets from which GI was manipulated were healthy dietary patterns established in the Dietary Approaches to Stop Hypertension (DASH) and Optimal Macronutrient Intake to Prevent Heart Disease (OmniHeart). These are diets that, the authors state, are being recommended in dietary guidelines to prevent cardiovascular disease (CVD).

Participants were randomised to one of four different diets:

  • high-GI, high-carbohydrate
  • low-GI, high-carbohydrate
  • high-GI, low-carbohydrate
  • low-GI, low-carbohydrate

All food and drink was provided and controlled by the researchers. The researchers directly monitored how people stuck to each diet through food diaries and the participants making daily visits to a centre, where the researchers directly observed them eating their main meal of the day. 

The main health measurements of interest were risk factors for diabetes and cardiovascular disease, including:

  • Insulin sensitivity. Taken via an oral glucose tolerance test, this shows how the body metabolises carbohydrates – specifically, how sensitive your body is to the effect of insulin. A tendency towards glucose intolerance can be a sign of higher risk of developing diabetes in the future.
  • LDL cholesterol – so-called “bad cholesterol”.
  • HDL cholesterol – so-called “good cholesterol”.
  • Blood fat levels.
  • Systolic blood pressure – the top number in a standard blood pressure measurement representing blood pressure as the heart contracts.

The analysis was restricted to people who had successfully completed the two diets, one after another, with the two-week gap in the middle.

 

What were the basic results?

Of the 189 randomised to start the trial, 163 completed enough of the study to be included in the final analysis. Compliance to the diets was high. The average BMI was 32 (BMI above 30 is classed as “obese”) – 92% of participants were obese or heavier. Around a quarter of people (26%) were defined as having high blood pressure. The main findings fell into three groups, summarised below.

Low-GI, high-carbohydrate diet, compared with high-GI, high-carbohydrate diet
  • insulin sensitivity worsened by 20%
  • bad cholesterol increased by 6%
  • good cholesterol, blood fat levels and systolic blood pressure were not any different between the groups
Low-GI, low-carbohydrate diet, compared with high-GI, low-carbohydrate diet
  • blood fat levels reduced by 5%
  • all other measures were not different between the groups
Low-GI, low-carbohydrate diet, compared with high-GI, high-carbohydrate diet
  • blood fat levels reduced by 23%
  • all other measures were not different between the groups

The researchers’ main conclusion was that: “In the context of an overall DASH-type diet [a diet to prevent or help people with high blood pressure], using GI to select specific foods may not improve cardiovascular risk factors or insulin resistance.”

 

Conclusion

This RCT showed that low-GI diets might not reduce risk factors for diabetes and cardiovascular disease in a group of mainly obese adults. All of these adults were free from diabetes or current cardiovascular disease, although a quarter of them had high blood pressure, and some may have had borderline high blood pressure.

As such, the trial’s participants were a specific group. This means that the results may not be relevant to the general population or other subgroups – for example, those who are a healthy weight or have an existing medical condition, such as diabetes.

However, compliance to the dietary interventions was high and the statistics seemed sound, thereby increasing our confidence in the results. If the findings were replicated in other studies, or if this trial had included more participants and/or been longer in duration, we could have some confidence in saying that for this group, the GI diet did not have the expected benefits. However, for example, if any of the effects of GI took longer than five weeks to occur, this study will not have picked them up. 

The authors themselves make the points that GI is only one attribute of carbohydrate-containing foods. They said: “Further, nutrients often cluster. Hence, the effects of GI, if any, might actually result from other nutrients, such as fibre, potassium and polyphenols, which favourably affect health.”

The study achieved a high compliance to the diets, through food diaries and observation. If this was attempted in real life, compliance would be much less. This would mean that any GI effects would probably be even smaller than was found in this study.

For this group of overweight people, the evidence of the GI diet reducing certain risk factors for cardiovascular disease and diabetes is lacking. The diet certainly haven’t been “debunked” for “most healthy people”, as the Mail Online claimed.

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

Links To The Headlines

The GI diet debunked: Glycaemic index is irrelevant for most healthy people - so it doesn't matter if you eat white or wholewheat bread, scientists claim. Mail Online, December 17 2014

Links To Science

Sacks FM, et al. Effects of High vs Low Glycemic Index of Dietary Carbohydrate on Cardiovascular Disease Risk Factors and Insulin Sensitivity. The OmniCarb Randomized Clinical Trial. JAMA. Published December 17 2014

Categories: Medical News

Ibuprofen unlikely to extend life

Medical News - Fri, 12/19/2014 - 12:54

The Daily Mirror today reports that, “taking ibuprofen every day could extend your life by up to 12 YEARS”. The Daily Express also has a similar front page headline, while the Mail Online suggests that these extra years would be of “good quality life”.

If you read these headlines and felt sceptical, you’d be right to do so.

The news has been extrapolated to humans, based on research in yeast, microscopic worms and fruit flies. These organisms are often used in longevity research due to their naturally short lifespans – even the longest-lived among them is measured in days, not decades. 

However, if a chemical does extend lifespan in these relatively simple organisms, this is not a guarantee that it will do the same in more complex organisms, such as mammals. We also have no idea whether any extension of life would be of “good quality”.

Even in the fruit flies, the effect was more complicated than in yeast or worms. Ibuprofen increased the flies’ average lifespan, but actually reduced the maximum lifespan in male flies.

We’re definitely not at a stage where taking ibuprofen every day could be recommended as a way to extend your lifespan. While some people might think “what harm can it do?" and "it might do some good”, ibuprofen is not risk-free. As with most drugs, ibuprofen can cause side effects, including gastrointestinal bleeding.

 

Where did the story come from?

The study was carried out by researchers from the Buck Institute for Research on Aging, and universities in the US and Russia. It was funded by the US National Institutes of Health and National Science Foundation.

The study was published in the peer-reviewed, open access journal PLOS Genetics.

The newspapers’ headlines are unwarranted over-extrapolations of this animal and laboratory research. Most later clarified that the research was in yeast, worms and flies – but read in isolation, the headlines are misleading.

This seems an irresponsible approach, given the potential harm that could result from people taking a cheap and readily-available drug unnecessarily.

 

What kind of research was this?

This was an animal and laboratory study looking at whether ibuprofen increases lifespan in flies, worms and yeast.

The researchers say that ibuprofen has been associated with a reduction in the risk of some age-related problems such as Alzheimer’s disease and Parkinson’s disease. However, whether it also has an effect on lifespan is unknown.

The organisms used in this study are often used in studies of lifespan, as their lives are short. This means that researchers can quickly find out if a chemical affects lifespan. If they find the same effect on lifespan in the multiple organisms tested, this suggests that the chemical is affecting a system that has been evolutionarily “conserved” across different organisms. This makes it more likely that the effect may also apply to other, untested, organisms.

However, flies, worms and yeast are relatively simple organisms, and things that affect their lifespans may not have the same impact on more complex organisms such as mammals. For example, while a chemical might double lifespan in a yeast, even if it also has an effect on lifespan in mice, it would be unlikely to have as dramatic an effect.

The researchers say that getting from chemicals that show promise in yeast and other organisms to drugs that are effective and safe in humans is a “significant hurdle”. For this reason, they wanted to look at a drug that was already used in humans, as they are already known to be safe enough for human use.

 

What did the research involve?

The researchers tested the effects of ibuprofen on one type of yeast, one type of microscopic worm, and fruit flies. In each case they exposed one group of yeast/worms/flies to ibuprofen and another group was not exposed (controls). They measured how long each group lived to see if it differed.

For yeast and worms, exposing them to ibuprofen involved growing them in a solution containing the drug. For yeast, the study looked at how long they were able to keep dividing to produce new yeast cells – a standard measure of their “active” lifespan. For flies, this involved feeding them with a solution that included ibuprofen. The organisms were grown in standard conditions, to make sure that the only thing that differed between them was whether or not they received ibuprofen.

The researchers then carried out a wide range of detailed experiments to determine how ibuprofen was having an effect.

 

What were the basic results?

The researchers found that yeast exposed to ibuprofen lived 17% longer on average than they did without it. Worms exposed to ibuprofen throughout their lives lived about 20 days, compared to about 18 days on average without ibuprofen. The researchers said that the levels of ibuprofen that extended the lifespan of worms and yeast were in the range of levels reached in people taking ibuprofen at typical doses.

In female fruit flies, ibuprofen extended the average lifespan and also the maximum lifespan. In male fruit flies, ibuprofen extended the average lifespan but, oddly, reduced the maximum lifespan. This meant that the shorter-lived flies were living longer with ibuprofen, but the longest-lived flies were not living as long.

The researchers found that ibuprofen seemed to be having its effect by reducing uptake of the amino acid tryptophan by cells.

 

How did the researchers interpret the results?

The researchers concluded that their results “identify a largely safe drug that extends lifespan across different kingdoms of life” and “implicate [tryptophan] import in aging”.

 

Conclusion

The current study has found that ibuprofen can extend lifespan in yeast, worms and flies.

This does not guarantee that it will extend the lives of humans – or indeed other animals more complex than flies. Even if a chemical was to have an effect on mammals, it would be unlikely to be as great an effect as in the simpler organisms that have been tested.

The results of the study themselves point to a more complicated story as organisms get more complex. While average lifespan was extended in all of the organisms, in male fruit flies (but not females) maximum lifespan was actually reduced with ibuprofen.

Doubtless these findings will lead to more research, as ways to fight the ravages of ageing are among the “holy grails” of drug development. The researchers point out in the news that there is probably already data available from observational studies in humans that could be used to assess whether ibuprofen use is associated with increased lifespan.

If you’re tempted to take a daily ibuprofen to extend your life because they’re cheap and readily available – don’t!

Ibuprofen, while safe enough for human consumption, is not risk-free. As with most drugs it can cause side effects, including gastrointestinal bleeding. While the benefits are likely to outweigh the harms for people taking the drug in the short term for its intended uses (such as pain relief), this is not the case when taking the drug on a daily basis for an unproven, and potentially non-existent, benefit.

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

Links To The Headlines

Is Ibuprofen the key to a longer life? Study finds it may provide 12 extra years of good health. Mail Online, December 18 2014

Taking ibuprofen every day could extend your life by up to 12 YEARS. Daily Mirror, December 18 2014

Ibuprofen adds 12 years to life! Cheap painkillers can slow ageing and fight disease. Daily Express, December 19 2014

Could ibuprofen be key to anti-ageing? Study finds painkiller extends life of flies and worms by equivalent of 12 human years. The Independent, December 19 2014

Hangover cure may aid a longer life. The Daily Telegraph, December 19 2014

Links To Science

He C, et al. Enhanced Longevity by Ibuprofen, Conserved in Multiple Species, Occurs in Yeast through Inhibition of Tryptophan Import. PLOS Genetics. Published December 18 2014

Categories: Medical News

Shift workers more likely to report poor health

Medical News - Thu, 12/18/2014 - 14:30

"Higher rates of obesity and ill-health have been found in shift workers than the general population," BBC News reports.

These are the key findings of a survey into health trends among shift workers; defined as any working pattern outside of the normal fixed eight-hour working day (though start and finish times may vary).

According to the survey (The Health Survey for England 2013), shift workers were more likely to report general ill-health, have a higher body mass index (BMI) and increased incidence of chronic diseases such as diabetes.

The Health Survey for England 2013 also monitored other trends in the nation’s health, including people’s weight, smoking habits, fruit and vegetable consumption, and prescribing patterns for drugs (a story we covered earlier this month). 
 

Who produced the data?

The report was produced by the Health & Social Care Information Centre (HSCIC), the official provider of national health and social care statistics. The HSCIC was set up by the government in April 2013. Its role is to provide information on a range of issues concerning health for use by commissioners, analysts and clinicians in driving patient services.

In the interests of transparency we should point out that the Behind the Headlines team, along with all NHS Choices staff, is employed by the HSCIC.

The HSCIC produces an annual Health Survey for England that monitors important aspects of the population’s health.

 

How was the data collected?

The data comes from interviews with a representative sample of the population. Participants aged 16 years and over who were in employment were asked whether they worked in shifts either "most of the time", "occasionally" or "never". Those who answered either "most of the time" or "occasionally" were then asked which type of shift work they were doing. Shift work was defined in the question as "work outside the hours of 7am to 7pm in your (main) job".

Participants were then grouped into shift workers (who reported that they did shift work "most of the time" or "occasionally") and non-shift workers.

Comparisons between shift workers and non-shift workers across a range of health and lifestyle factors were age-standardised, so that any differences in age profile are taken into account in the comparisons.

What were the key findings?
  • Men were more likely than women to report that they did shift work (33% of men and 22% of women).
  • Shift working was most prevalent in the 16-24 age group, and declined with age for both men and women. Almost half of men and over a third of women aged 16-24 did shift work compared with fewer than a third of men and a fifth of women aged 55 and over.
  • The prevalence of shift work varied significantly by household income, being highest in the lowest two income quintiles (42-43% among men, 27-28% among women, compared with 21% and 19% respectively in the highest income quintile). Similarly, the proportion of men and women in shift work was highest in the most deprived quintile compared with the least deprived.
  • Both men and women in shift work were more likely than non-shift workers to report fair or bad health.
  • Shift workers were more likely than non-shift workers to have a limiting longstanding illness; they were also more likely to have more than one longstanding illness.
  • Shift workers were more likely than non-shift workers to be obese. This is reflected in higher mean body mass index (BMI) measurements, higher proportions classified as obese, and greater proportions with a very high waist circumference.
  • Men and women in shift work were more likely than non shift workers to have diabetes (10% of both men and women in shift work, compared with 9% and 7% respectively of those not working shifts).
  • Current cigarette smoking prevalence was higher among shift workers than non-shift workers, with a larger difference among women than men. 28% of men in shift work currently smoked compared with 23% of men who did not do shift work. The equivalent figures for women were 26% and 15% respectively.
  • The proportion of both men and women who drank alcohol in the last year was slightly smaller among shift workers (84% of men, 81% of women) than among those who did not work shifts (88% and 83% respectively).
  • Daily fruit and vegetable consumption was lower among shift workers than non-shift workers. Men in shift work ate an average of 3.3 portions compared with 3.6 for non-shift workers. Among women the equivalent means were 3.6 and 3.8 respectively. Shift workers were also slightly less likely than non-shift workers to meet government recommendations of eating five or more portions per day.

 

Why do shift workers tend to be less healthy?

There are a number of potential underlying factors that may impact on health and wellbeing.

Firstly, shift working can disrupt what are known as circadian rhythms, the internal "body clock". This can disrupt the normal workings of a hormone called melatonin. This disruption can lead to poor sleep and chronic fatigue.

Persistent lack of good quality sleep has been linked to a range of chronic conditions such as obesity, depression, diabetes and heart disease.

While the body can slowly adapt to the changes in working patterns, many shift workers are on rotating shifts and suddenly switching from a night to day shift leads to further disruptions.

Rotating shift work can also disrupt the production of insulin, which may increase the risk of someone developing type 2 diabetes.

There is also the fact that shift workers tend to be on the lower end of the socioeconomic scale. And there is evidence that people on lower incomes have an increased tendency to smoke, drink excessive amounts of alcohol and eat a poor diet. There is also the stress and worry associated with trying to make ends meet.

 

What has previous research found?

There has a been a range of studies linking shift work to a number of different adverse outcomes; which we have looked at previously in Behind the Headlines. These include claims that:

The issue with all the studies is that due to the complex play of personal, environmental and socioeconomic factors, researchers were unable to prove a direct cause and effect link between shift work and the outcomes listed above; only an association.

Still, there seems to be a consensus that while shift work may not be actively dangerous, it is certainly not an ideal arrangement for healthy living.

 

So what can shift workers do?

Well, ideally, find another job. But that is often easier said than done. Most of us don’t have the luxury of quitting a job if the hours don’t suit us unless we have another job lined up.

That said, if you are unhappy with your current situation, it is worth spending a few hours every week signing up to job search sites. Along with commercial sites, the government also provides a service known as Universal Jobmatch.

The Health and Safety Executive also offers some useful and practical advice for people working shift work. This includes:

  • take extra care if you drive to and from work as your concentration may be impaired; if possible it may be a better idea to use public transport
  • identify a suitable sleep schedule of at least seven hours a day, you may find it useful to keep a diary to assess what sleep times suit you best
  • try to create an environment that promotes good sleep, for example heavy curtains or an eye mask may help you sleep during the day
  • making changes to your diet to improve both alertness and digestion; smaller healthy snacks during your shift may be a better idea than one big meal
  • limit your use of stimulants such as caffeine or energy drinks as well as sedatives such as alcohol; while they may bring short-term benefit they are unlikely to be of help in the long term
  • try to get regular exercise – at least 30 minutes per day

Read more Hints and tips for shift workers

.

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

Links To Science

Shift workers 'sicker and fatter'. BBC News, December 15 2014

Shift workers more likely to suffer from poor health, including diabetes and obesity. The Independent, December 15 2014

Categories: Medical News

'Electromagnetic smog' unlikely to harm humans

Medical News - Thu, 12/18/2014 - 14:30

The Daily Telegraph reports that “mobile phones are unlikely to harm human health”, adding to the ongoing, and often conflicting, coverage of the potential health impact of environmental exposure to what some commentators have called “electromagnetic smog”.

This is a term used to refer to a mix of low-level magnetic fields that exist in the modern environment. This "smog" is not just generated by mobile phones, but also by Wi-Fi routers, tablets, laptops, power lines and cell towers. In the modern world, you are never far away from a magnetic field.

Concerns regarding the impact of exposure to environmental magnetic fields (MFs) on human health have existed for decades. While observational studies have suggested that there is an association between such exposure and certain diseases, no studies have demonstrated a direct causal link. Part of the difficulty in determining whether there is a direct effect is the lack of an established mechanism of action by which magnetic fields could plausibly bring about changes in the biochemical processes that occur in the body.

The most plausible mechanism of action is known as the radical pair mechanism. A "radical" is an atom or molecule that is chemically reactive due to the presence of an unpaired electron. Some biochemical processes produce brief radicals as an intermediate step in the longer process. Processes that involve, or are thought to involve, pairs of these radicals were used in this research.  

This latest study investigated whether exposure to magnetic fields alters processes in a class of enzymes known or thought to involve radical pairs, which could potentially damage cells. The researchers found that these reactions were not sensitive to magnetic fields.

 

Where did the story come from?

The study was carried out by researchers from the University of Manchester and was funded by the EMF Biological Research Trust, in the UK.

The study was published in the peer-reviewed Journal of the Royal Society – Interface.

The research was reported well by the Daily Telegraph, which clearly stated that this was a lab-based study, and reported the need for further research to rule out other potential causal mechanisms.

 

What kind of research was this?

This was a lab-based study that systematically investigated the magnetic field sensitivity of a variety of enzymes. This research explored the impact of MFs in cells under lab conditions, to test the hypothesis that biological processes involving radical pairs are a plausible mechanism of action by which environmental MFs could affect biology.

It is important to note that the study did not assess the direct impact of MFs on the development of human disease.

 

What did the research involve?

The researchers tested the effect of exposure to a range of magnetic fields (MFE) on chemical reactions involving a group of enzymes called flavin-dependent enzymes. These are responsible for a variety of essential biological processes, including energy production, DNA repair, regulating natural cell death, neural development and detoxification. Several radical pairs can temporarily occur during reactions initiated by these enzymes, and the researchers were interested in magnetically-induced changes in these reactions arising from MF sensitivity.

 

What were the basic results?

The researchers found no magnetic field effects in the various reactions studied. They say that a number of conditions must be met for a radical pair reaction to be sensitive to magnetic fields, and that these conditions do not appear to be widespread in biology.

 

How did the researchers interpret the results?

The researchers concluded that we “should reconsider the likelihood of magnetic sensitivity as a result of the radical pair mechanism in biology”. That is, mechanism of action thought to be most plausible in explaining the observed association between magnetic field exposure and human disease was not seen.

 

Conclusion

This study adds to the literature suggesting that environmental magnetic field exposure is unlikely to cause human disease. It's important to note, however, that this study did not examine disease states directly, but instead investigated a mechanism of action thought to be the most likely candidate to explain the observed link between MFs and certain medical conditions. The results of this study suggest that radical pair mechanism is not likely to be sensitive to magnetic fields.

Further potential mechanisms of action will need to be studied before drawing firm conclusions on the risk (or lack thereof) presented by mobile phones, power lines and other sources of weak magnetic fields.

The results of this study do not conflict with the most recent guidance from the UK Health Protection Agency, which states that “there is no known mechanism or clear experimental evidence” that explains the association between MF exposure and diseases such as childhood leukaemia or Alzheimer’s disease.

Other agencies have released similar guidance on magnetic field exposure. In 2002, the International Agency for Research on Cancer (IARC) categorised extremely low-frequency magnetic fields as "possibly carcinogenic [i.e. cancer-causing] to humans". A later report from the same agency concluded that there is inadequate evidence to confirm the impact of these fields on human health.

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

Links To The Headlines

Mobile phones unlikely to harm human health, scientists find. The Daily Telegraph, December 10 2014

Links To Science

Messiha HL, Wongnate T, Chaiyen P, et al. Magnetic field effects as a result of the radical pair mechanism are unlikely in redox enzymes. Journal of the Royal Society - Interface. Published online December 10 2014 

Categories: Medical News

Fathers-to-be experience hormone changes

Medical News - Wed, 12/17/2014 - 16:00

“Men suffer pregnancy symptoms too: Fluctuating hormones make fathers-to-be … more caring,” the Mail Online reports. A small US study found evidence of changes in hormonal levels that may make fathers-to-be more able to cope with the demands of fatherhood.

The story comes from a study that looked at whether expectant fathers and their partners experience any changes in their hormone levels during pregnancy. It found that, as expected, women experienced a large increase in four hormones associated with pregnancy. Their male partners also experienced small changes in the hormones testosterone and oestradiol.

The researchers, as well as the media, speculate that these small changes in hormone levels could lead to men becoming less aggressive, less interested in sex, and more caring. Though whether such changes are linked to subsequent changes in their behaviour is unproven.

 

Where did the story come from?

The study was carried out by researchers from the University of Michigan. There is no information about external funding.

The study was published in the peer-reviewed American Journal of Human Biology.

The Mail Online overstated the results of the study, claiming that “men’s hormones go into a spin in the months before becoming a parent” and that this helps them prepare to bond with their babies – and stops them from straying. This is all speculation. The study did not look at men’s behaviour in the months before birth, only at their hormone levels. It is also misleading in that it claims that the men experienced “pregnancy symptoms”, when none were reported in the study.

 

What kind of research was this?

This study measured changes in levels of certain hormones in 29 first-time expectant couples at four points throughout the prenatal period. The authors point out that expectant mothers experience large increases in hormones such as testosterone, cortisol, oestradiol and progesterone. They say that these hormones are implicated in the neuroendocrine pathways (a complex connection of nerves that both respond to and also produce hormones) that affect maternal behaviour and may have long-term implications for women and their families.

They say that far less is known about changes in the hormone levels of expectant fathers, even though their behaviour may be influenced by the same neuroendocrine pathway. In addition, it is not known if there is any correlation between couples in changes in hormone levels.

The researchers focused on four hormones, which have large prenatal changes in women and which they say have important implications for parental behaviour. These are:

  • Testosterone – higher levels are associated with aggression and lower levels with parental care. Women’s testosterone levels increase during pregnancy and decline after birth.
  • Cortisol – associated with stress and challenges. In women, cortisol increases through pregnancy and declines after birth.
  • Oestradiol – associated with caregiving and bonding and thought to be important for maternal attachment. In women it increases during pregnancy and drops after birth.
  • Progesterone – associated with social closeness and maternal behaviour. In pregnant women it increases during pregnancy and drops after birth.

 

What did the research involve?

The researchers measured changes in all four hormones in 29 expectant couples. The couples, who were recruited online and in print, were paid $50 per session for participating. They had to be between 18 and 45, living together, expecting their first child and within the first two trimesters of pregnancy. Smokers, those with medical conditions that could influence hormone levels, and those taking hormone altering medications were excluded.

The couples’ hormone levels were assessed up to four times throughout the prenatal period, at approximately weeks 12, 20, 28 and 36 of pregnancy. Each couple came to the laboratory together and had their hormone levels measured at the same time and on the same day of the week. They provided two saliva samples on each visit. These were frozen until being tested for levels of testosterone, cortisol, oestradiol and progesterone, using commercially available kits.

The researchers analysed the results using standard statistical methods.

 

What were the basic results?
  • As expected, women showed large prenatal increases in all four hormones.
  • Men showed significant but small prenatal declines in testosterone and oestradiol, but there were no detectable changes in men’s cortisol or progesterone. 

 

How did the researchers interpret the results?

The researchers say their study is the first to demonstrate prenatal testosterone changes in expectant fathers.

They say the findings on testosterone and oestradiol support the idea that the same hormones may be involved in maternal and paternal care.

They say their findings provide some support for the theory that similar neuroendocrine pathways support both maternal and paternal behaviour.

 

Conclusion

This is an interesting study, but it was very small and, as the authors point out, found only limited evidence of small hormone changes among expectant fathers, so it is difficult to draw any conclusions from it.

One important limitation was the lack of a comparison group of non-expectant couples. This means the authors cannot say whether any hormone changes among the men occurred as a result of expectant fatherhood or other causes.

Nor did the researchers assess the men’s hormones before conception or postnatally, so they could not determine how men’s hormone levels change during the entire transition to parenthood.

In women, changes in hormone levels are vital to maintain the pregnancy and are also thought to affect maternal feelings and behaviour. This study does not provide conclusive results on the changes in hormone levels that occur in expectant fathers or whether these might be linked to changes in behaviour.

Becoming a dad for the first time can be an overwhelming and somewhat frightening experience, though most men quickly learn and adapt. The human race wouldn’t be here if that wasn’t the case.

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

Links To The Headlines

Men suffer pregnancy symptoms too: Fluctuating hormones make fathers-to-be less aggressive and more caring. Mail Online, December 16 2014

Links To Science

Edelstein RD, Wardecker BM, Chopik WJ, et al. Prenatal hormones in first-time expectant parents: Longitudinal changes and within-couple correlations. American Journal of Human Biology. Published online December 15 2014

Categories: Medical News

E-cigarettes could help some smokers quit

Medical News - Wed, 12/17/2014 - 15:00

“E-cigarettes can help smokers quit or cut down heavily,” The Guardian reports. An international review of the evidence, carried out by the well-respected Cochrane Collaboration, found evidence that they can help some smokers quit.

However, the available body of evidence was slim – just two randomised controlled trials (RCTs), involving around 950 participants.

The two studies found that 9% of people using e-cigarettes with nicotine quit smoking for at least six months, compared to 4% of people using placebo e-cigarettes. However, the results on quitting were only significant when the trials were added together, because so few people managed to quit. The individual trials found no difference in the number of people who quit smoking by at least six months when using e-cigarettes with nicotine compared to placebo e-cigarettes or nicotine patches. The researchers say that the pooled results should therefore be treated with caution.

Another concern is that while e-cigarettes are far safer than “real” cigarettes, they do nothing to tackle the underlying nicotine addiction.

A combination of methods may be the most effective method for people who are keen to stop. Other stop smoking treatments include nicotine gum, patches or inhalers, as well as medication that can reduce cravings, such as Zyban (bupropion).

 

Where did the story come from?

The study was carried out by researchers from Queen Mary University of London, the University of Auckland and the University of Oxford. There was no external funding.

The study was published in the peer-reviewed online medical journal The Cochrane Database of Systematic Review. As with all Cochrane research, the study has been made available on an open-access basis, so is free to read online or download as a PDF.

There were some inaccuracies in the media reporting of the study. There were not just 662 people in the two RCTs; this was the number of people randomised to have a type of e-cigarette. The actual number of participants was 957, as other people in these two trials were given nicotine patches.

The Times inaccurately reported that there were no side effects reported in the studies. This was not the case; there were no serious adverse events, but there were side effects. The most common side effects reported were irritation of the mouth and throat.

The Guardian (among other sources) printed some interesting reactions to the study.

Professor Robert West, editor-in-chief of the journal Addiction, was quoted as saying: “It’s early days, but it seems that these devices are already helping tens of thousands of smokers to stop each year.”

Dr John Middleton, the vice-president of the UK Faculty of Public Health, took a more cautious view and said: “It’s taken decades of sustained effort to create a society in the UK where smoking is now not seen as the norm. Our concern is that e-cigarettes could reverse this and create a new generation of customers for the tobacco industry, who might otherwise not have started smoking.”

 

What kind of research was this?

This was a systematic review and meta-analysis that aimed to assess how effective e-cigarettes are in helping people to stop smoking in the long term. The review also looked at whether e-cigarettes help to reduce the number of cigarettes smoked and if they are associated with any adverse events.

As this was a systematic review of all randomised controlled trials (RCTs)cohort studies and crossover trials (published and unpublished), this brings together the best available evidence on the subject.

 

What did the research involve?

The researchers searched all relevant medical databases for trials of at least six months' duration that compared e-cigarettes with a control condition. The RCTs, cohort studies and crossover trials were sorted using strict inclusion criteria, and from this they were able to estimate the effect of e-cigarettes.

The following databases were searched from 2004 to July 2014: the Cochrane Tobacco Addiction Group Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, PsycINFO and CINAHL.

In total, 21 studies were included in the review. Just two of them were RCTs and nine were ongoing studies that have not yet been completed.

One RCT was the ASCEND trial, in which 657 smokers in New Zealand were randomly assigned to have one of the following for 12 weeks after they chose to stop smoking:

  • e-cigarette with 16mg nicotine
  • nicotine patches with 21mg/24-hour nicotine
  • e-cigarette with no nicotine (placebo e-cigarette)

Their smoking status was assessed six months after the start of the trial (their target stop smoking date) using expired carbon monoxide readings. If they were still smoking, they were asked to report the amount of daily cigarette use.

In the other RCT, the ECLAT trial, 300 smokers in Italy who were not intending to quit smoking in the coming 30 days were randomly assigned to have access to one of the following for up to four times a day:

  • e-cigarette with 7.2mg nicotine
  • e-cigarette with 7.2mg nicotine for six weeks and then 5.2mg nicotine for six weeks
  • e-cigarette with no nicotine

They were followed up regularly over the next 12 months.

The 19 other studies were considered to be at high risk of bias and did not directly compare e-cigarettes with something else, so are not described in detail here.

 

What were the basic results?

In the ASCEND trial, there was no significant difference between the three groups. In the ECLAT trial, there was no significant difference between the two groups using e-cigarettes with nicotine and the group without nicotine.

Pooling the results of both RCTs:

  • using an e-cigarette with nicotine increased the chances of stopping smoking for at least six months (9% of participants) compared to using a placebo e-cigarette (4% of participants), (relative risk (RR) 2.29, 95% confidence interval (CI) 1.05 to 4.96)
  • a higher number of people were able to reduce cigarette consumption by at least half using e-cigarettes with nicotine (36% of participants) compared with placebo e-cigarettes (27% of participants) (RR 1.31, 95% CI 1.02 to 1.68)
  • a higher number of people were able to reduce cigarette consumption by at least half by using e-cigarettes with nicotine (61% of participants) compared with a nicotine patch (44% of participants) (RR 1.41, 95% CI 1.20 to 1.67)

There were no serious adverse events associated with e-cigarettes. The most common side effect was irritation of the throat and mouth.

 

How did the researchers interpret the results?

The researchers conclude that “there is evidence from two trials that ECs [e-cigarettes] help smokers to stop smoking long term compared with placebo ECs. However, the small number of trials, low event rates and wide confidence intervals around the estimates mean that our confidence in the result is rated ‘low’”. They go on to say that “ECs appear to help smokers unable to stop smoking altogether to reduce their cigarette consumption when compared with placebo ECs and nicotine patches”, but they also felt the evidence for this was of a low standard.

 

Conclusion

This comprehensive systematic review and meta-analysis has found some evidence that e-cigarettes with nicotine may help people to stop smoking, or at least reduce the amount they are smoking by over half.

That said, no matter how rigorously they are carried out, systematic reviews and meta-analyses can only be as good as the size and quality of evidence that go into them. In this case, the evidence was slim. 

The improvements were only apparent when the results of both RCTs were pooled together. There was no statistically significant result in either study on their own, despite having 657 and 300 participants respectively. This was mostly due to the low number of people who were able to stop smoking for at least six months in each study.

The researchers themselves are quick to point out that their confidence in the results is low because of this and the fact that they were only able to identify two relevant RCTs. (Cochrane researchers have a reputation for erring on the side of caution; their unofficial motto is “more research is needed on the topic”.)

The other types of studies identified did not directly compare e-cigarettes with another smoking cessation aid or no intervention, so they could not be included in the pooled meta-analysis.

Though the results show only a small benefit, it should be noted that in the first trial only a third of the participants accessed telephone support during their attempt to quit smoking, and increased support may have improved their success rates. In the second trial, none of the participants wanted to stop smoking in the first place, which is likely to have had a high impact on the number who quit.

Lastly, the studies did not report any serious adverse effects from the use of e-cigarettes, though mouth and throat irritation were commonly reported. As the studies were only of six months and just over a year's duration respectively, this research does not show what the long-term impact of e-cigarettes may be. Nicotine can increase the heart rate, and cause headaches and heartburn, to name just a few symptoms.

A combination of methods may be more effective for people who are keen to stop; using e-cigarettes to cope with the initial nicotine cravings and then weaning yourself of your addiction using gradually lower-dose patches or gum could be one way.

If you are determined to quit, it may be a good idea to make an appointment with an NHS stop smoking adviser. NHS stop smoking advisers are free, friendly and flexible, and can massively boost your chances of quitting for good.

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

Links To The Headlines

E-cigarettes can help smokers quit or cut down heavily, say researchers. The Guardian, December 17 2014

E-cigarettes 'help smokers quit or cut down'. BBC News, December 17 2014

E-cigarettes double chance of quitting. The Times, December 17 2014

E-cigarettes DO help people quit smoking: Review finds there are 'no serious adverse effects from short to medium term use'. Mail Online, December 17 2014

Links To Science

McRobbie H, Bullen C, Hartmann-Boyce J, et al. Cigarettes for smoking cessation and reduction. Cochrane Database of Systematic Reviews. Published December 17 2014

Categories: Medical News

Feeling 'young at heart' may increase lifespan

Medical News - Tue, 12/16/2014 - 14:55

“Feeling young at heart wards off death, scientists find,” The Daily Telegraph reports. A UK study found that people who reported feeling younger than their actual age were less likely to die than those who reported feeling their actual age or older.

The study in question asked almost 6,500 people in their 50s and over how old they actually felt, and followed them up over 99 months to identify any who died. It found that a quarter of people who feel considerably older than their actual age died over the following eight years, compared to only 14% of those who felt considerably younger. The difference remained even if the researchers took into account other factors (confounders) that could affect their risk of death, such as physical and mental health.

Still, the link between how old you feel and your health is likely to be very difficult to remove, even with the extensive efforts made in this study.

So, how do you feel younger? We would recommend staying as physically active as possibleconnecting with others (possibly through volunteering) and trying out new activities, such as yoga (which, by coincidence, was shown today to possibly reduce the risk of heart disease).

 

Where did the story come from?

The study was carried out by researchers from University College London (UCL). The study in which the data was collected was funded by the National Institute on Aging in the United States and a consortium of UK government departments coordinated by the Office for National Statistics. The researchers were supported by UCL, the International Longevity Centre UK and the British Heart Foundation.

The study was published as a letter in the peer-reviewed medical journal JAMA Internal Medicine.

The media covers this research reasonably well.

The Mail Online helpfully reports the actual risks of dying during the study in both groups (14.3% for the “young at heart”, 18.5% for those who felt their actual age and 24.6% who felt older than their age) rather than the relative difference in risk between them.

Just reporting the relative risk can give a distorted impression to the public on the size of a particular effect or trend.

There are also some minor inaccuracies in the coverage. The Mail Online stating that the report said "maintaining healthy weight helped increase life expectancy” – when the study authors actually noted that weight was not one of the factors assessed in their study – is one example. The Telegraph says that “those who felt younger than their actual age were 41% less likely to have died in the follow-up period” which is not quite right – it was actually those who felt older who were 41% more likely to die in the follow-up period than those who felt younger.

 

What kind of research was this?

This was an analysis of data from an ongoing prospective cohort study called the English Longitudinal Study of Ageing. Researchers looked at whether how old a person felt was related to how long they actually lived.

A cohort study is the best way to assess this question. However, as with all cohort studies, factors other than the factor in question (self-perceived age), known as confounders, can influence the results. The researchers in the current study took steps to remove the effect of such factors, but it is difficult to remove their effect entirely.

 

What did the research involve?

The researchers asked the participants how old they felt they were and then followed them for up to nine years to identify any deaths – specifically, deaths from cancer or heart disease, which are the two leading causes of preventable deaths. They then investigated if those who felt younger than they were lived any longer.

A total of 6,489 people aged 52 and over took part in the study. They answered the question about how old they felt in 2004-05. They also provided a lot of information about themselves and their health. The researchers classed them as:

  • those who felt at least one year older than their actual age
  • those who felt more than three years younger than their actual age
  • the remainder – who felt close to their actual age (from one year older to two years younger)

They recorded those who died up to March 2013 and their causes of death, and whether the proportion who died in the different “perceived age” categories differed. They took into account a range of confounders, which could affect risk of death, including:

  • age
  • gender
  • sociodemographic factors
  • depression
  • social engagement
  • cognitive function
  • physical health
  • mobility
  • lifestyle (smoking, alcohol consumption and physical activity)

 

What were the basic results?

The researchers found that most people (69.6%) felt younger than they were; 4.8% felt older; and about a quarter felt around their real age (25.6%). Their average actual age was around 66 years, while on average they felt only around 57 years old.

Participants were followed for just over eight years, on average. During the study, 15.9% of the participants died. More of the participants who felt older than their actual age died than those who felt their actual age or younger:

  • 24.6% of participants who felt older than their actual age died
  • 18.5% of those who felt about their actual age died
  • 14.3% of those who felt younger than their actual age died

When they took into account the factors that could affect risk of death, feeling older than your actual age was still associated with a 41% increase in risk of death during follow-up, relative to those who felt younger (hazard ratio (HR) 1.41, 95% confidence interval (CI) 1.10 to 1.82). They still found this association if they excluded people who died within a year of starting the study – to reduce the possibility that people who were feeling older than their age were doing so because they were already ill.

When looking at causes of death, feeling older than your age was associated with an increased risk of death from heart disease (HR 1.55, 95% CI 1.01 to 2.38), but not from cancer. After all of the other factors were taken into account, feeling your age was not associated with any greater risk of death, compared to those who felt younger.

 

How did the researchers interpret the results?

The researchers concluded that self-perceived age predicted deaths in the next eight years from any cause and deaths from heart disease. They say that self-perceived age can change, and that “individuals who feel older than their actual age could be targeted with health messages promoting positive health behaviours and attitudes toward ageing”.

 

Conclusion

This study has found that people in their 50s and over who feel considerably older than their actual age seem to be more likely to die over the next eight years than those who feel considerably younger. The study was large and collected data on how old people felt in a standard way, which strengthens its reliability.

It seems likely that how old people feel is related to how well they are. The researchers took this into account by adjusting for people’s physical and mental health in their analyses, and also by carrying out an analysis that removed people who died soon after they answered the question about how old they felt. They also took into account a wide range of factors that could affect risk, which also strengthens their results. However, the link between how you feel and your health is likely to be very difficult to remove, and there were some factors that could be having an effect that were not taken into account (such as weight).

The next question to ask is what can be done with this information? The researchers suggest that people who feel older than they are could be targeted for health improvements. They say that they may be able to change how old they feel, with the implication that this could help them live longer.

The findings are likely to need confirmation by other studies to make sure they are correct. Whether there are any longevity benefits of targeting people who feel older than they are would also need testing in a randomised controlled trial.

Making people feel younger is likely to involve socialphysical and mental activities, and can improve health – all of which have benefits. However, whether they prolong life is another question.

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

Links To The Headlines

Feeling young at heart wards off death, scientists find. The Daily Telegraph, December 15 2014

Being young at heart really CAN help you live longer: Researchers say those who feel younger die later. Mail Online, December 16 2014

People young at heart DO live longer says new research. Daily Express, December 15 2014

Links To Science

Rippon I, Steptoe A. Feeling Old vs Being Old - Associations Between Self-perceived Age and Mortality. JAMA Internal Medicine. Published online December 15 2014

Categories: Medical News

Yoga may help protect against heart disease

Medical News - Tue, 12/16/2014 - 14:05

“Yoga could be as effective as cycling or brisk walks in reducing the risk of a heart attack or stroke,” The Guardian reports.

Researchers have pooled the results of previous studies and report finding "promising evidence" of yoga’s health benefits, specifically in reducing the risk of cardiovascular disease (CVD), as well as metabolic syndrome.

Compared to doing nothing, or interventions that did not include exercise, yoga reduced body weight by 2.32kg, on average, and also improved body mass index (BMI), blood pressure and cholesterol levels, all of which have a protective effect against CVD.

It also found there was no significant difference between yoga and other types of exercise for improving risk factors for heart disease.

What is not clear from this review is which type of yoga could produce these results. Some types of yoga are more focused on physical activity, while others take a more meditative, slow-paced approach.

It should also be noted that there were some limitations to the evidence available. Most of the studies were small and rated as only of moderate quality. The results need confirmation in larger, more robust studies, ideally ones which assess heart disease, as well as its risk factors.

Hopefully, as the researchers suggest, yoga could be an ideal option for people unable to take part in exercises such as cycling or brisk walking because of mobility or other problems.

 

Where did the story come from?

The study was carried out by researchers from Harvard University and Erasmus MS in the Netherlands. There was no external funding.

The study was published in the peer-reviewed European Journal of Preventive Cardiology.

The UK media reported the results of the study reasonably accurately, but did not explain that they need to be treated with some caution as they are based on small studies. They have also not made it clear that the study does not pinpoint how much and what type of yoga is beneficial.

Only BBC News and the Daily Mail pointed out there are many different forms of yoga, some more strenuous than others.

 

What kind of research was this?

This was a systematic review and meta-analysis of all relevant randomised controlled trials (RCTs) that looked at the effect of yoga on risk factors for cardiovascular (heart and vascular system) disease. This type of study is the best way of identifying and pooling the results of all of the studies on a particular research question.

The current review only includes studies that have been published, which means that it can be open to finding a greater effect of the intervention than actually exists – this is called “publication bias”. This is because studies which do not show that an intervention is effective are less likely to be submitted to and chosen by journals for publication.

 

What did the research involve?

Medical databases were searched for all RCTs on the effectiveness of yoga at reducing risk factors for cardiovascular disease. The researchers assessed which of these RCTs met their inclusion criteria, and then pooled their results where possible to give an overall estimate of the effect of yoga.

These databases were MEDLINE, CINAHL, Cochrane Central Register of Controlled Trials (CENTRAL), Cochrane Database of Systematic Reviews, EMBASE, and PsycINFO. They found 37 relevant RCTs published up to December 2013, and they were able to pool the results of 32 of them.

In total, there were 2,768 adults (53% female) in the studies, with an average age of 50 years. A third of the studies were in healthy people, a fifth were specifically in people who already had cardiovascular risk factors, a quarter in people with diabetes or metabolic syndrome (a group of characteristics which increase cardiovascular risk) and just over a tenth in people with a specific type of heart disease (coronary artery disease).

The studies lasted from three to 52 weeks, during which yoga was compared to:

  • usual care or conventional medical therapy in 23% of the RCTs
  • waiting list or no intervention in 32%
  • exercise in 21% (physical training, cycling, running, brisk walking or resistance training)
  • education in 11%
  • a form of relaxation in 6%
  • diet alone in 4%
  • cognitive-based therapy in 2%

 

What were the basic results?

Overall, the individual studies tended to be small and of moderate quality.

There was no significant difference between yoga and other types of exercise for improving cardiovascular risk factors, such as body weight, BMI or cholesterol levels.

Compared to interventions which did not include exercise, yoga improved:

  • BMI -0.77kg/m2 (95% confidence interval (CI) -1.09 to -0.44)
  • systolic blood pressure (the higher number) by -5.21mmHg (95% CI -8.01 to -2.42)
  • low-density lipoprotein cholesterol by -12.14mg/dl (95% CI -21.8 to -2.48)
  • high-density lipoprotein cholesterol by 3.20mg/dl (95% CI 1.86 to 4.54)
  • body weight by -2.32kg (95% CI -4.33 to -0.37)

 

How did the researchers interpret the results?

The researchers conclude that this “review finds emerging evidence to support a role for yoga in improving common modifiable risk factors of CVD [cardiovascular disease] and metabolic syndrome”. They also highlight the “need for larger randomised controlled studies that meet explicit, high-quality methodological standards to ascertain the effects of yoga”.

 

Conclusion

Overall, this review suggests that yoga may be beneficial in reducing risk factors for cardiovascular disease and metabolic syndrome.

While these are encouraging findings, the authors also caution that these are based on trials with some limitations, including:

  • There was a wide variation in the type of yoga practised, the frequency and the length of each session across the studies. This means it is difficult to say what the actual effects of each approach are, as the overall effects are just an average across all of these approaches. Some may have more of an effect and some may have less.
  • The review does not report the amount of exercise yoga was compared to, and this could also affect their relative benefits.
  • The study participants could not be blinded to the fact that they were doing yoga, which could bias the results. However, this tends to be less of an issue when measuring things such as blood cholesterol levels, which participants can’t influence, as long as the people doing the measurements are blinded to whose samples they are testing.
  • Most of the studies only had around 20 to 60 participants, with one study having just nine people; the smaller a study, the more likely it is that results are affected by chance.

The government recommends that adults should do at least 150 minutes of moderate-intensity aerobic activity each week and muscle-strengthening activities on two or more days a week. Some forms of yoga could fit the bill for either of these exercise recommendations. 

Read more about getting started with a yoga plan.

Further, more robust RCTs are required to prove the specific cardiovascular benefits of yoga, and to assess its effects on heart disease events (such as heart attack or stroke), as well as risk factors.

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

Links To The Headlines

Yoga may provide similar health benefits to ‘cycling or brisk walking’. The Guardian, December 16 2014

Yoga is as healthy for your heart as cycling, says Harvard scientist: Analysis of studies finds discipline can cause weight loss and cut blood pressure. Mail Online, December 16 2014

Yoga may guard against heart disease, study finds. BBC News, December 16 2014

Yoga just as good as aerobics for cutting heart disease risk. The Daily Telegraph, December 16 2014

Links To Science

Chu P, Gotink RA, Yeh GY, et al. The effectiveness of yoga in modifying risk factors for cardiovascular disease and metabolic syndrome: A systematic review and meta-analysis of randomized controlled trials. European Journal of Preventive Cardiology. Published online December 15 2014

Categories: Medical News

Political hardliners 'fitter' than 'fence sitters'

Medical News - Mon, 12/15/2014 - 14:30

“Being an extremist is better for your health than holding moderate views,” the Mail Online reports.

A very much tongue-in-cheek study presents evidence that “armchair socialists” and their right-wing counterparts (“armchair generals?”) are more active than those with more moderate political views.

The study found that people at both ends of the political spectrum – left and right – were more physically active than those in the political centre.

People who sit on the fence, it seems, spend too much time sitting on the couch as well. 

This lighthearted look at the association between political beliefs and activity levels was based on people self-reporting both, which tends to make it less reliable. It is quite possible, for example, that “political extremists” tend to be self-deluded about how active they actually are.

There is also a case to make that the term “political extremist” used in the media is neither helpful nor accurate as it conjures up images of violence. This use of extreme in the study referred to people who self-identified as “very far right” or “very far left” on the political spectrum. Being a democratic socialist is not the same thing as being a 70s-style “Freedom for Tooting” Trotskyist revolutionary. Similarly, wanting to pull out of the EU and restrict immigration doesn’t mean you want to goose step through Trafalgar Square.

Despite the end-of-term tone of the study, there could be some relevance to its findings. Political activists, especially during elections, do spend significant time plodding the pavements, delivering leaflets and knocking on the doors of potential voters.

 

Where did the story come from?

The study was carried out by researchers from the University of Sydney. There is no information about external funding.

The study was published in the Christmas issue of the peer-reviewed British Medical Journal, which publishes a few lighthearted “studies” around the festive period. The study is open access so it is free to read online or download as a PDF.

The Mail Online’s picture desk went to town on this study, with photos of UKIP leader Nigel Farage, comedian Russell Brand, London mayor Boris Johnson and Shadow Chancellor Ed Balls; all used as examples of “extremists”.

More seriously, it is debatable whether left- and right-wingers, especially those who are members of democratic parties, can all be classified as “extremist”. When the study used the term extreme they were referring only to the extreme ends of the political spectrum in views, not in necessarily in actions.

 

What kind of research was this?

This was a cross-sectional study of nearly 30,000 European adults, looking at the relationship between political beliefs, activity levels and sitting-down time.

The authors point out that the term “armchair socialist”, which originated in 19th century Germany, is used to characterise middle class people who make political pronouncements without engaging in political activism. Similar terms are “limousine liberal” (in the US), “champagne socialist” and “armchair revolutionary”.

A right-wing alternative could be “armchair general”; somebody who is happy to fight for a better world as long as somebody else is doing the fighting.

Their purpose, they say, was to find out whether this is literally true – whether people who identify themselves as left wing spend more time sitting than other groups. They point out that if this is true, their health could be compromised. 

In the interest of balance they also looked at people who identified themselves with right-wing views.

 

What did the research involve?

The data analysed in the study came from a survey in 2005 of 29,193 adults from 32 European countries, conducted on behalf of the European Commission. The survey included a question on political affiliation as well as a questionnaire that assessed physical activity and sitting time at work, home, at leisure and when travelling.

The question on political leaning asked respondents to rate their political orientation from 1 (far left wing) to 10 (far right wing). (In this the authors perhaps mistakenly assumed that socialists would define themselves as far left). The far left wing were defined as having scores of 1 or 2,  far right-wingers were those with scores of 9 or 10 and people with scores of 3-8 were described as politically centrist.

They used the data people gave on weekly minutes of vigorous intensity activity, moderate intensity activity, walking, and sitting time, to summarise their total physical activity.

 

What were the basic results?

The authors say their findings refute the existence of a (literal) “armchair socialist” and that people at the extremes of both ends of the political spectrum were more physically active than those in the centre.

Those who described themselves as on the right reported doing 62.2 more weekly minutes of physical activity (95% confidence interval (CI) 23.9 to 100.5) than those in the political centre, and those who were on the left did 57.8 more minutes (95% CI, 20.6 to 95.1).

People with right-wing political affiliations reported 12.8 minutes less time sitting a day (95% CI, 3.8 to 21.9) than the centrists.

Data was missing from a lot of respondents (26.2%).

 

How did the researchers interpret the results?

There is little evidence to support the literal notion of armchair socialists, say the authors, as socialists – defined here as being on the far left – are more active than the mainstream in the political centre.

“It is those sitting in the middle (politically) that are moving less, and possibly sitting more, both on the fence and elsewhere, making them a defined at-risk group.”

Perhaps they are suggesting (not entirely seriously) that centrists and the politically uncommitted should be encouraged to move off the fence and adopt stronger political views in either direction, to improve their activity levels and therefore their health.

The authors do conclude with the following disclaimer “the research … was not intended to imply epidemiologically credible health risks of political centrism”.

 

Conclusion

As the authors point out, all the data used in this study was self-reported, which makes the results less reliable. The high percentage of missing data also reduces confidence in this study.

This was a cross-sectional study, which means we cannot be sure which came first – people’s political views or their exercise levels. Perhaps being very active leads to stronger political views rather than vice versa; or perhaps the type of personality who adopts strong views also goes overboard on exercise.

Despite the lighthearted tone of the study there could be a ring of truth about its results. As anyone who had been involved in grassroots politics (or any other type of campaigning work) can tell you, most political activity consists of stuffing envelopes, delivering said envelopes to hundreds of houses (and trying not to get your fingers bitten in the process) and standing around in community centres waiting for votes to be counted.

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

Links To The Headlines

Being an extremist is BETTER for your health than holding moderate views: 'People with stronger political opinions do more exercise'. Mail Online, December 12 2014

Links To Science

Bauman A, Gale J, Milton K. Are “armchair socialists” still sitting? Cross sectional study of political affiliation and physical activity. BMJ. Published online December 11 2014

Categories: Medical News

Spicy food 'curries favour' with alpha males

Medical News - Mon, 12/15/2014 - 14:10

“Men who like spicier food are 'alpha males' with higher levels of testosterone,” The Daily Telegraph reports. A small French study found an association between a preference for spicy foods and elevated testosterone levels; but no evidence of a direct link.

Testosterone is a steroid hormone that in popular culture has long been associated with male virility. Men with high levels of testosterone are alleged to be more sexually active, domineering, brave and willing to take risks – the so-called “alpha male”.

So, is a liking for spicy foods a sign of “alpha male” risk taking and bravery? Is ordering the hottest thing on the menu a 21st Century equivalent of a tribal initiation ceremony? The quick answer is that we don’t know.

The study in question measured spice preference and testosterone level at the same time. This means it cannot prove cause and effect. It is possible that spicy food, or anticipation of spicy food, leads to higher testosterone levels. An effect that has been seen in rats.

Food preferences probably have genetic, psychological and social elements of influence. So actual behaviour regarding spice preference is likely to differ, depending on the situation. A man might be more likely to tackle a vindaloo while on a lively stag do than on his wedding day, for instance, not least to prevent any adverse effects on the wedding night.

 

Where did the story come from?

The study was carried out by researchers from The University of Grenoble, France. No funding source was stated.

The study was published in the peer-reviewed science journal Physiology and Behavior.

The UK media generally reported the study accurately, but failed to discuss any of the limitations and so took the findings at face value.

 

What kind of research was this?

This was a laboratory study testing human preferences for spicy food and how they might relate to testosterone levels in men.

Testosterone is a hormone released by the testicles of men and the ovaries of women. Although both genders secrete it, men secrete much more. It plays a key role in sexual growth and development and some research has linked high levels to financial, sexual and behavioural risk taking. They have also linked it to so-called “alpha male” behaviour, which can include domination and aggression.

This study ignored social influences and focused on whether there was a link between spice preference and testosterone level.

 

What did the research involve?

The study recruited 144 men aged between 18 and 44 living in Grenoble, France, and tested their preference for salt and spice in a number of ways under controlled conditions.

Recruits visited a testing centre and were first asked to rate how much they liked spicy and salty foods on a four point scale. They then sat down to a plate of mashed potato and were asked to flavour the mash to their taste with little sachets of Tabasco sauce (a hot sauce made from tabasco peppers) and salt, which was recorded.

They ate the mash and again rated how hot and salty the food was on a six point scale. Interestingly, the scale went up to “excessive burning sensation” for salt and “risks of temporary extinction of the sense of taste, risks of vomiting” for Tabasco. Finally, after finishing they were asked if their meal was too spicy or salty on a five point scale.

At some point all participants gave a saliva sample, which was used to measure their testosterone levels. It wasn’t clear whether this was tested before, during or after the meal.

The analysis looked for correlations between the different ratings of spice preference and level of testosterone.

As far as we can tell the tests were conducted in isolation so there was no social element to the study.

 

What were the basic results?

There was a positive and statistically significant correlation between testosterone and the quantity of hot sauce that individuals voluntarily and spontaneously ate (r=0.294). This means the more testosterone men had, the more hot sauce they put on the mash. A correlation of 0.29, is generally considered a weak correlation, as positive correlations can vary from 0 (no correlation at all) to 1 (perfect correlation).

Correlation between reported preference for spicy food (before the task) and testosterone was not statistically significant.

Age affected many of the results. Once this was accounted for, the only significant correlations were:

  • number of spicy doses put on the mash (r=0.32)
  • evaluation of the meal’s spiciness after eating (r=0.30)
  • preference for spicy food (r=0.19)

There was no correlation between testosterone levels and preference for salt for any measures.

 

How did the researchers interpret the results?

The authors concluded simply: “This study suggests that behavioural preference for spicy food among men is related to endogenous testosterone levels.”

Furthermore they indicated that: “To our knowledge, this is the first study in which a behavioural preference for spicy food has been linked to endogenous testosterone in a laboratory setting. The juxtaposition of using highly accurate laboratory measurement with a diverse community sample of male participants ensures adequate levels of both internal and external validity. This study provides new insights into the biology of food preference by expanding our understanding of the link between hormonal processes and food intake”.

 

Conclusion

This small human laboratory study found higher testosterone levels were linked to adding more spice to food in adult men. However, due to the study’s design, and a number of limitations cited below, it does not prove this link.

Many factors probably influence preference for spicy food. These could include physiological measures such as testosterone, but also involve social, genetic and psychological elements. For example, adding spice to food could be a learned habit, for example from family, or innate, passed on in genetics due to difference in the way spice is tasted on the tongue. We do not know how important each of these factors is in spice preference, relative to one another.

The study measured spice preference and testosterone level at the same time. This means it cannot prove cause and effect. It is possible that spicy food, or anticipation of spicy food, leads to higher testosterone levels. This sort of effect has been observed in rats, the study authors tell us.

The research team also highlighted a less obvious limitation in their research: colour. They indicated they used a red Tabasco spice sachet. Intriguingly, previous studies have shown a link between higher testosterone in men and a preference for colours signifying dominance and aggression, such as red. This could have played a role in influencing the results, but we don’t know how strongly.

Overall, the study suggests there might be a physiological reason for spice preference (testosterone level), but does not prove it. There are likely to be many factors involved and we do not yet know which are the most important. On further investigation testosterone might turn out be a very important factor, or more marginal. Given the weak correlations in this study, we would suspect it might be on the weaker side. 

A final word of advice would be that while spice can be nice, we would never recommend eating food that causes you actual physical pain.

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

Links To The Headlines

Men who like spicier food are 'alpha males' with higher levels of testosterone. The Daily Telegraph, December 14 2014

Men who like spicy food 'have higher testosterone levels'. Daily Mirror, December 14 2014

Why liking hot curries really does make you the alpha male: Men who enjoy spicy food have higher testosterone levels. Mail Online, December 15 2014

Links To Science

Bègue L, Bricout V, Boudesseul J.  Some like it hot: Testosterone predicts laboratory eating behavior of spicy food. Physiology and Behavior. Published online November 25 2014

Categories: Medical News

Could a '10 to 6' working day help you sleep better?

Medical News - Fri, 12/12/2014 - 15:30

A major new study of American workers has recommended “later start times to improve on health,” the Mail Online reports.

To improve people’s sleep patterns the research team suggested work start times could be moved later, such as 10am. This was just a suggestion, and was not backed up with any new evidence from this study itself.

This research didn’t actually look at any health effects of sleep, but explored possible reasons for why people might sleep less. Most of the findings seemed common sense, such as having to get up to go to work.

Still, fatigue appears to be a common problem. As our website reports in the Living with insomnia section one in three Britons suffers from poor sleep, with stress, computers and taking work home often blamed for the lack of quality slumber.

And two of the most widely visited topics on the NHS Choices website are “10 medical reasons for feeling tired” and “Why am I tired all the time?” 

If you are struggling to stay awake during your morning commute it may be an idea to discuss if there is any possibility of flexible working times.

 

Where did the story come from?

The study was carried out by researchers from the University of Pennsylvania and was funded by the US National Institutes of Health and NASA.

The study was published in the peer-reviewed science journal Sleep.

One of the authors is on a paid science advisory council for Mars Inc (the chocolate bar people). The same person and a colleague are editors and deputy editors of the journal in which the article was published. None declare a financial conflict of interest.

The coverage in the Mail Online was accurate, although seemed more excited by the findings than we were. Claims that a lie-in “could dramatically improve your life” were not backed up by new evidence uncovered as part of this study.

 

What kind of research was this?

This was a secondary analysis of data collected from a previous cross-sectional survey.

The research team was looking for reasons why some people sleep less than others. They highlight that sleep is essential for memory consolidation and alertness, while lack of sleep is linked with poorer health.

Regular poor sleep puts you at risk of serious medical conditions, including obesity, heart disease and diabetes – it also shortens your life expectancy.

 

What did the research involve?

The research team analysed information on what people did each day, and how long they spent doing it, including sleep patterns. They compared the habits of short sleepers (less than 6 hours a night) with normal sleepers (6 to 11 hours) and longer sleeps (over 12 hours) to uncover possible reasons for the sleep differences.

The information was already collected for them as part of the “American Time Use Survey”. This gave them access to detailed information on the daily habits of 124,517 adult Americans over 15 years of age.

The definition of sleep in the study included a range of rest and napping type behaviours such as “dozing off”, “catnapping” and “getting some shuteye”. This is different from most studies recording sleep, which tend to ask how much sleep people get on average over the week and or weekends.

The analysis looked for links between sleep duration and the wide range of daily activities reported during the survey, such as going to work, socialising, self-grooming and watching TV.

The analysis was adjusted to reflect the general American population in terms of demographics and took account of where and when the surveys took place.

 

What were the basic results?

One of the main findings was that people slept less if they had to go to work. A good example of science confirming common sense. With every hour that work or education started later in the morning, people slept 20 minutes more.

Working multiple jobs was linked with the highest chance of sleeping less than six hours a night on weekdays.

Self-employed people were less likely to be short sleepers compared to private sector employees.

Short sleep was consistently linked to the following factors:

  • being 25 to 64
  • being a man
  • having a high income
  • being employed

How did the researchers interpret the results?

The researchers suggested: “Interventions to increase sleep time should concentrate on delaying the morning start time of work and educational activities (or making them more flexible), increasing sleep opportunities and shortening evening and commute times.

“Reducing the need for multiple jobs may increase sleep time, but economics disincentives from working fewer hours will need to be offset.

“Raising awareness of the importance of sufficient sleep for health and safety may be necessary to positively influence discretionary behaviours that reduce sleep time, including television viewing and morning grooming.”

 

Conclusion

This cross-sectional study highlights possible reasons why people might sleep less, most of which seem common sense, such as having to get up to go to work. The data were collected as part of a large cross-sectional survey in the US, but the findings are likely to be relevant here in the UK. The study does not provide any new information on whether, or how, poor sleep leads to poorer health, directly or indirectly.

The study did not have detailed information on some factors that affect sleep, such as alcohol or caffeine, or, as far as we could tell, the quality of sleep. Similarly, their definition of sleep, which included napping, was a little different to what you might expect. These limitations reduce the reliability of the findings but, in our view, are unlikely to affect the overall conclusions reached.

The researchers’ interpretation was that people’s sleep patterns may be improved if the working day started later, such as 10am, or was flexible. This was raised in the discussion but was not built on evidence collected from the study itself. Many work places will have such arrangements, but they may be practically difficult in many time-bound industries.

The study serves to point out possible solutions to low sleep hours. However, the solutions of less work, more rest and flexible hours may be somewhat at odds with current trends of economic development based on consumerist principles. The reasons people sleep less seem deeply entrenched in financial, cultural and societal pressures and changing these is likely to be challenging in increasingly globalised economies of the modern age.

The economist John Maynard Keynes famously predicted that by the early 21st century we would all be working just 15 hours a week due to efficiency gains through technology. How wrong he was.

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

Links To The Headlines

Could a lie in dramatically improve your life? Experts call for workers to start at 10AM to improve sleep quality. Mail Online, December 11 2014

Links To Science

Basner M, Spaeth Am, Dinges DF. Sociodemographic Characteristics and Waking Activities and their Role in the Timing and Duration of Sleep. Sleep. Published online December 10 2014

Categories: Medical News

Memory gaps in graduates a 'stroke warning sign'

Medical News - Fri, 12/12/2014 - 14:00

“People with memory problems who have a university education could be at greater risk of a stroke,” BBC News reports. The hypothesis is that the gaps in memory could be the result of reduced blood flow to the brain, which may then trigger a stroke at some point in the future.

Researchers documented memory complaints and occurrences of stroke in a group of 9,152 adults aged over 55 living in the Netherlands, for an average of 12.2 years.

This showed that replying “yes” to the question “Do you have any memory complaints” was associated with a 20% higher risk of stroke overall compared with those saying “no”. This relative risk was higher in people categorised as educated – holding a university degree or higher vocational qualification.

This shouldn’t be interpreted as meaning that having a higher education increases your risk of stroke. The explanation put forward by the experts was that people with a higher education may have higher levels of cognitive awareness, so they may be more likely to be aware of worsening.

The study had a number of strengths, such as its long follow-up. However, its results were only significant using a subjective, self-reported measure of mental ability. A more objective assessment showed no link. There are many potential explanations for this, including the possibility that higher education compensates in some way.

Still, knowing what we do about blood flow and brain function, a link between memory problems and stroke is plausible.

 

Where did the story come from?

The study was carried out by researchers based in the Netherlands and was funded by a range of medical, science and academic research funding bodies from the Netherlands and the European Commission. There were no conflicts of interest reported.

The study was published in Stroke, a peer-reviewed Journal of the American Heart Association. The study has been published on an open-access basis so it is free to read online or download as a PDF.

BBC News reported the study accurately and although it outlined potential implications of the results, it did not discuss any of its limitations.

 

What kind of research was this?

This was a cohort study (Rotterdam Study) investigating whether memory complaints earlier in life were linked to occurrence of a stroke in later life.

The researchers say that people with cognitive impairment – some impairment of their brain’s ability to function – are at a higher risk of having a stroke.  

A stroke is a serious and potentially fatal condition in which the flow of blood to the brain is disrupted. Strokes have two main causes

  • a blood clot blocks the supply of blood to the brain (ischaemic stroke)
  • bleeding occurs inside the brain, usually due to a weakened blood vessel bursting (haemorrhagic stroke)

Both types of stroke can occur in people with cardiovascular disease:

The research team wanted to know whether there were early signs of cognitive impairment, such as memory lapses, that could help them identify people at higher risk of stroke. If they knew who the high risk people were, they could focus efforts on minimising their risk, potentially preventing some occurrences of stroke. 

 

What did the research involve?

The researchers documented memory complaints and any occurrences of stroke in a group of 9,152 adults over 55 living in Rotterdam, the Netherlands, for an average of 12.2 years.

Trained investigators interviewed all participants at home. The presence of subjective memory complaints was assessed by the question, “Do you have memory complaints?” Cognitive function was assessed using the standard objective measure of the Mini-Mental State Examination. This assesses orientation, memory, attention, language, and visuospatial construction (the ability to recognise a pattern or set of objects and then replicate the pattern or set). It wasn’t clear when the assessment of memory complaints occurred, or whether it was reported over time.

Once enrolled in the study, participants were left to their own devices while the researchers were notified of any reports of stroke in the following years.

People who already had a stroke or had dementia at enrolment into the study were excluded. The number of participants available for analysis was 9,152.

The research team analysed links between memory complaints and incidence of stroke. They also looked at whether education level influenced this link. The analysis took account of a range of known confounders for stroke risk, including:  

  • age
  • gender
  • smoking
  • body mass index
  • blood cholesterol levels
  • diabetes
  • blood pressure and blood pressure medications
  • ability to perform activities of daily living – a type of older age disability test

 

What were the basic results?

Over the study period 1,134 strokes occurred, average follow up was 12.2 years.

One of the main findings was that people reporting subjective memory complaints were 20% more likely to have a stroke than those who didn’t (Hazard ratio [HR] 1.20, 95% Confidence interval [CI] 1.04 to 1.39). However, this result was not found using the more objective measure of mental ability, the Mini-Mental State Examination. Better point scores on the test were not significantly linked to stroke occurrence (HR 0.99, 95% CI 0.95 to 1.02). These figures come from the analyses that took account of the largest list of confounders.

The second important finding was that level of education was significantly influencing the results. Subjective memory complaints were linked with stroke only in those with high education – defined in this study as higher vocational education or university training (HR 1.39, 95% CI 1.07 to 1.81).

Participants with missing information tended to be older, had more memory complaints, more likely to be female and had slightly worse scores on the assessments of mental abilities. These people were still included in the analysis.

 

How did the researchers interpret the results?

The researchers concluded “Subjective memory complaints might be an early indicator of stroke risk, especially in highly educated individuals”.

 

Conclusion

This study showed that highly educated people who notice memory complaints in themselves may be more likely to develop stroke than those who don’t, over an average of 12 years.

The study had a number of strengths, such as its population-based prospective design and availability of data on more than 9,000 participants at baseline with a long follow-up. However, there were also a number of limitations that weaken the strength of the conclusions.

It was not clear whether the memory complaints were assessed just once at the start of the study or an ongoing basis. Some people may report memory complaints that are only temporary, while others not initially reporting complaints may have done so in later years. This could have altered the results, but is only likely to have had a minor influence.

The results were only significant using the subject measure of mental ability. It would be interesting to explore whether other subjective and objective assessments show a link or not. Results tend to be more reliable if there is consistency between different measures of the same thing, objective or subjective. This was not the case in this study. 

The Mini-Mental State Examination is known to be less sensitive in well-educated patients. Possibly a different type of test is required.

Although the study adjusted for a range of confounders, it is difficult to exclude the possibility that residual confounding by measurement error or unmeasured factors biased the results to an unknown degree.

Data on depression and depressive symptoms was not available. The researchers highlight that this was a major limitation, “because it has been suggested that the associations with subjective indicators of health, especially memory, may be confounded by prevalence of depression”.

The bottom line is that this study suggests a link between memory complaints in the highly educated and stroke but does not prove one causes the other. The study authors point to a plausible biological explanation but this was not tested in this study.

The results may warrant further investigation and confirmation in different studies, using different ways of assessing memory. If the link is real, we’d expect to see somewhat consistent results across different measures. Based on this study we can’t say that educated people with memory complaints are definitely at a higher risk of stroke.

Nevertheless, vascular dementia (where reduced blood flow to the brain causes cognitive dysfunction) and stroke are both linked to the same underlying cardiovascular disease process, so a link between memory problems and stroke is plausible – particularly for this specific type of dementia.

Methods you can use to reduce your stroke risk include eating a healthy diet, taking regular exercise, quitting smoking if you smoke, moderating your consumption of alcohol. Read more about stroke prevention.

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

Links To The Headlines

Memory lapses in well-educated may signal stroke risk. BBC News, December 12 2014

Links To Science

Sajjad A, Saeed S, Portegies LP, et al. Subjective Memory Complaints and the Risk of Stroke. Stroke. Published online December 11 2014

Categories: Medical News

Almost half of all adults take prescription drugs

Medical News - Thu, 12/11/2014 - 13:30

“Half of women and 43% of men in England are now regularly taking prescription drugs,” BBC News reports. The figures have come to light as part of a new survey into drug prescribing patterns.

According to the survey (The Health Survey for England 2013), commonly prescribed medications included:

There was also media controversy over the number of antidepressants being prescribed – particularly for women on a low income. Nearly one in five women from economically deprived areas were taking antidepressants.

The Health Survey for England 2013 also monitored other trends in the nation’s health, including people’s weight, smoking habits, fruit and vegetable consumption, and shift work. 

 

Who produced the data?

The report was produced by the Health and Social Care Information Centre (HSCIC), the official provider of national health and social care statistics. The HSCIC was set up by the government in April 2013. Its role is to provide information on a range of aspects concerning health for use by commissioners, analysts and clinicians in driving patient services.

In the interests of transparency we should point out that the Behind the Headlines team, along with all NHS Choices staff, is employed by the HSCIC.

The HSCIC produces an annual Health Survey for England that monitors important aspects of the population’s health.

 

How was the data collected?

The data comes from interviews with a representative sample of the population, carried out by the Joint Health Surveys Unit of NatCen Social Research and the Research Department of Epidemiology and Public Health, at the University of London. The interviews consisted of core questions and groups of questions on specific issues. Measurements such as blood pressure and waist circumference, and analysis of blood and saliva samples, were taken by a nurse.

The researchers interviewed 8,795 adults and 2,185 children for the 2013 survey.

 

What were the key findings?

Below are the key findings from the survey on prescription medication.

  • 43% of men and 50% of women reported that they had taken at least one prescribed medicine in the last week. Almost a quarter of men (22%) and women (24%) reported that they had taken at least three prescribed medicines in the last week. This proportion increased with age, with more than half of participants aged 65-74, and more than 70% of those aged 75 and over, having taken at least three prescribed medicines.
  • On average, 18.7 prescription medicines were dispensed per head of population in 2013.
  • The most frequently reported prescribed classes of medicines were cholesterol-lowering drugs (16% of men and 12% of women), drugs to lower blood pressure (14% and 15% respectively) and for women, painkillers including NSAIDs (12%).
  • Women (11%) were also more likely than men (6%) to be taking antidepressants. Women also demonstrated a significant variation by income class. 7% of women in the highest two quintiles of income were taking antidepressants, which rose to 17% of women in the lowest quintiles.
  • The cost of medicines in 2013, including costs for use in hospitals, was more than £15 billion. More than 1 billion prescription items were dispensed in the community in England, an average of 2.7 million items every day. The Net Ingredient Cost in 2013 was £8.6 billion, an increase of £102 million from the 2012 cost.

 

What did the media say?

Not surprisingly, the report was widely covered in the media, with many papers focusing on the numbers of people taking prescription drugs. Much of the reporting took a negative tone.

For example, the headline in The Times was “nation hooked on prescription medicine”. This is not particularly useful language as it implies that people are addicted to their medications. Medicines such as statins and ACE inhibitors are not addictive; though people often have to take them on a long-term basis to reduce the risk of serious complications such as heart attacks or strokes.

BBC News and the Daily Mail were relatively more balanced, as they carried comments from Dr Jennifer Mindell, one of the report’s authors. Dr Mindell explained there had been big changes in the use of statins (which lower cholesterol), with millions more people eligible to take them today than a decade ago. This increase in eligibility for these drugs is likely to be the result of new evidence on cost and effectiveness, which has suggested that the benefits in terms of preventing cardiovascular disease may outweigh the risks for many people.

Depression rates were generally higher among women than men because they were more willing to seek medical help, she reportedly said. The link between poverty and depression is also not particularly surprising, and is consistent with other observations from national reports and surveys in recent years that tend to show greater prevalence of both chronic mental and physical health conditions in more deprived areas. How to address this socioeconomic health divide is another matter.

The Mail also quoted Dr Maureen Baker, of the Royal College of General Practitioners, who said: “We have an ageing population and more patients are presenting with complex and multiple conditions including mental health issues and this is reflected in today’s figures.”

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

Links To The Headlines

Nearly 50% take prescription drugs. BBC News, December 10 2014

Half of women are taking drugs on prescription... and four in ten men are doing the same. Daily Mail, December 11 2014

Almost half of all English on prescription medication. The Times, December 10 2014

HALF of women are taking prescription drugs EVERY week, new study reveals. Daily Mirror, December 10 2014

Links To Science

Health & Social Care Information Centre. Use of prescribed medicines (PDF, 647kb). December 2014

Categories: Medical News

Food additive that could reduce appetite

Medical News - Thu, 12/11/2014 - 12:54

“Appetite suppressing additive could be added to food to create 'slimming bread'," ITV News reports.

This reports on a study that showed that short-chain fatty acids (SCFAs) are released from gut bacteria as they break down dietary fibre. These SCFAs then stimulate the release of hormones that signal to the brain that we are full.

The problem is that many people don’t eat a high-fibre diet, despite the numerous benefits. Therefore, finding new ways to increase SCFAs in people’s diets would be useful.

This study looked at an SCFA called propionate. Eaten by itself, propionate is said to taste like vinegar, and is broken down by the small bowel.

In this study, researchers managed to bind propionate to a polymer, helping to mask the taste and deliver it to the large bowel intact.

60 healthy overweight adults were given either this chemical or a control daily for 24 weeks. The chemical reduced further weight gain compared to the control, and also reduced the proportion of body fat around the tummy.

This is promising proof-of-concept research. However, more research is needed to see if this supplement is effective and safe enough to become more widely available.

 

Where did the story come from?

The study was carried out by researchers from Imperial College London, University of Glasgow, and other research institutions in the UK and Australia, and was funded by the UK Biotechnology and Biological Sciences Research Council.

The study was published in the peer-reviewed medical journal Gut on an open-access basis, so can be read for free or downloaded as a PDF.

The UK’s media reported the study accurately, though it is a little too early to suggest that this discovery could combat the obesity crisis.

 

What kind of research was this?

This was a preliminary laboratory study, followed by a randomised controlled trial (RCT).

The study aimed to investigate whether giving a particular chemical to humans can satisfy appetite and reduce weight gain.

The researchers explained how the normal bacteria in the large bowel help to break down fibre in the food we eat, and in so doing produce SCFAs. These SCFAs stimulate the release of certain gut hormones, called peptide YY (PYY) and glucagon-like peptide-1 (GLP-1). These hormones signal to the appetite centres in the brain that we are full. This is why high-fibre foods – such as wholemeal bread and root vegetables such as carrots – make us feel much fuller than processed foods such as burgers.

Previous studies have found that giving these hormones to humans and animals enhances feelings of fullness and reduces food intake.

Research has shown that SCFAs stimulate the release of these hormones by stimulating a particular bowel receptor called FFAR2. Of all the SCFAs produced by the breakdown of dietary fibre, one called propionate has been shown to have the highest affinity for this receptor.

Therefore, researchers wanted to see whether giving propionate could help to regulate the appetite. Giving SCFAs by mouth is unpalatable. They are said to have an extremely bitter taste, similar to drinking very strong vinegar.

SCFAs are rapidly absorbed by the small bowel before they even get to the large bowel. Therefore, the researchers developed a novel delivery system that would release small quantities of propionate into the first part of the large bowel. The researchers expected this to stimulate the release of the PYY and GLP-1 hormones, which suppress appetite.

 

What did the research involve?

The researchers first carried out laboratory tests to confirm that propionate did indeed cause a release of PYY and GLP-1 hormones from large bowel cells.

They then produced a “carrier molecule”, which could deliver propionate to the large bowel intact. This involved propionate being chemically bound to a natural dietary fibre called inulin.

Their first human test involved looking at the effect of single doses of inulin-propionate upon energy intake and the release of PYY and GLP-1 hormones in 20 volunteers. They then examined the effect on stomach emptying in another 14 volunteers.

The researchers then went on to conduct an RCT to investigate whether giving inulin-propionate over 24 weeks to overweight adults would decrease weight gain. They included 60 people who were aged between 40 and 65, with a BMI of 25 to 40, and who didn’t have any significant physical or mental health illness, including diabetes. These people were randomly assigned to supplementation with either inulin-propionate or inulin-control.

The trial was double blinded, meaning participants and researchers didn’t know which had been given.

These supplements were supplied in 10g ready-to-use sachets that, once a day, could be mixed into the content of their normal diet. Participants were advised to maintain their normal diet and activity patterns.

At the start of the study and after 24 weeks, participants completed self-reported diet and physical activity records, in addition to having their weight and other body measurements taken. These measures included having blood samples taken to measure PYY and GLP-1 concentration. The main outcome they looked at was change in body weight and food intake.

 

What were the basic results?

In the trial, 49 of the 60 participants (82%) who completed the 24-week study were analysed. There was no difference between the two groups in compliance or completion, and ratings of nausea were also no different.

Flatulence was the only other adverse effect reported, which was experienced more than half of the time in the control group, compared to a quarter of the time in the propionate group.

Weight gain was significantly less in the intervention group: 1 out of 25 participants in the inulin-propionate group (4%) gained 3% or more of their baseline body weight, compared with 6 out of 24 in the control group (25%). None of the participants in the inulin-propionate group had substantial weight gain (defined as 5% or more gain) compared with 4 out of 24 (17%) of the control group. There was a trend towards greater weight loss in the inulin-propionate group, but this was not significant compared to the control group. The intervention group also had a significantly lower proportion of their body fat tissue distributed in the abdomen compared to the control group.

When looking at food intake, there was no significant difference between the groups in terms of food intake at the end of the trial. There was a trend towards reduced food intake in the inulin-propionate group, but this was not significant. There was no difference in blood glucose control between the two groups. Total blood cholesterol and HDL (“good”) cholesterol were found to reduce in both groups, though LDL (“bad”) cholesterol was only reduced in the intervention group.

 

How did the researchers interpret the results?

The researchers say that their data “demonstrate for the first time that increasing [large bowel] propionate prevents weight gain in overweight adult humans”.

 

Conclusion

This interesting study has developed from the understanding that SCFAs are released from gut bacteria as they break down dietary fibre. These SCFAs then stimulate the release of hormones that signal to the appetite centres in the brain that we are full.

Of the SCFAs, propionate demonstrated the greatest affinity for receptors in the bowel, so therefore seemed the best candidate for study. The researchers then managed to develop a novel system that would deliver propionate intact to the large bowel, without the molecule first broken down in the small bowel.

In their first 24-week trial in 60 overweight adults, they found that it reduced further weight gain compared to the control group, which was the main outcome they set out to investigate. The trial benefits from being fairly long in duration and that it was double blind, which should remove the risk of biased reporting of outcomes from either participants or investigators.

However, there are various points to consider:

  • The trial was quite small, including only 60 people; just 49 completed it. Participants were middle-aged, overweight adults with no significant health problems. Therefore, the results may not be applicable to other groups.
  • We don’t know how this supplement could be taken practically outside of this trial's context – for example, whether this would be taken in the long term or just for short periods. If taken continuously in the longer term, we don’t know whether it would continue to prevent weight gain, or lead to significant weight loss.
  • This trial studied effects alongside the continuation of previous diet and activity patterns. We don’t know how the effects may differ if other lifestyle aspects were also altered.
  • The way this drug works needs to be studied further. For example, despite the treatment reducing weight gain, there was no difference in reported food intake between the treatment and control groups. Given that the proposed method of action of this treatment was to tell our brains we are full and so suppress appetite, this doesn’t seem to correlate. 
  • The trial only briefly reported on gastrointestinal adverse effects, though increased flatulence was frequently reported. If this supplement were to be used more widely, safety needs to be studied further. This includes looking at effects on body biochemistry and other aspects of health. Possible interactions with other medical drugs would also need to be considered. 

Overall, this is promising proof-of-concept research into the use of a novel chemical to try to prevent weight gain. However, further study is needed before this supplement could ever become more widely available.

For the time being, if you want to eat foods that make you feel fuller without adding lots of calories to your diet, a high-fibre diet – such as wholemeal bread, bran, cereals, nuts and seeds, as well as fruit, such as bananas and apples – is recommended. 

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

Links To The Headlines

Appetite suppressing additive could be added to food to create 'slimming bread'. ITV News, December 11 2014

Scientists discover a secret ingredient 'to make you slim' and combat UK's obesity crisis. Daily Mirror, December 10 2014

Scientists make 'feel full' chemical. BBC News, December 11 2014

Scientists find natural food ingredient makes you eat less - but it tastes 'foul'. The Independent, December 11 2014

Links To Science

Chambers ES, Viardot A, Psichas A, et al. Effects of targeted delivery of propionate to the human colon on appetite regulation, body weight maintenance and adiposity in overweight adults. Gut. Published online December 10 2014

Categories: Medical News

Gene therapy could help with inherited blindness

Medical News - Wed, 12/10/2014 - 14:25

"Procedure to restore sight in dogs gives hope for future blindness cure," The Independent reports.

Researchers have restored some modest degree of light sensitivity (though not full vision) in animals who have a similar condition to retinitis pigmentosa.

Retinitis pigmentosa is an umbrella term for a group of human inherited eye conditions, affecting around 1 in 4,000 people, in which the normal light-sensing cells contained in the retina become damaged or die.

Experiments on blind mice and dogs have found cells in the retina that are not normally light-sensing (retinal ganglion cells) can be genetically modified to respond to light.

The researchers used gene therapy to modify these cells. The cells responded to light after they were activated with an injection of a chemical called MAG, with the effects lasting up to nine days.

In some of the experiments, blind mice treated in this way were able to see light again and move around like sighted mice in a maze.

The researchers also carried out similar experiments using blind dogs to see if the method would work in a large animal.

Laboratory experiments were able to show ganglion cells in dogs could also respond to light. However, there were no experiments that showed whether the dogs could see again.

No human trials have been performed yet, but the researchers hope this will not be too far off.

 

Where did the story come from?

The study was carried out by researchers from the University of California, the University of Pennsylvania, and the Lawrence Berkeley National Laboratory.

It was funded by the US National Institutes for Health, the National Eye Institute, and the Foundation Fighting Blindness.

The study was published in the peer-reviewed medical journal Proceedings of the National Academy of Sciences of the United States of America.

The Independent and the Mail Online accurately reported the study, although the headline writers took the usual liberties. While both acknowledged the research involved dogs and mice, claims the animals had their sight "restored" is an overstatement.

The headlines also failed to point out this technique would only have a potential application in cases of retinitis pigmentosa and not more common causes of visual impairment, such as age-related macular degeneration.

 

What kind of research was this?

This animal study tested whether cells in the retina that do not respond to light could be made to respond. They used genetic modification to produce a light receptor protein and a light-sensing chemical compound. This two-step process was tested on the retinas of blind mice and dogs.

In the inherited human condition retinitis pigmentosa, there is a progressive loss of rod receptors (light-sensitive cells) and cone receptors (colour-sensitive cells). This causes tunnel vision and, eventually, blindness.

Previous research found that although there is loss of these photoreceptors on the outer level of the retina, the connecting nerves underneath still function.

Researchers were interested in whether they could get these connecting nerves (retinal ganglion cells) to act as light-sensing cells, which could restore some vision.

 

What did the research involve?

The researchers first used genetic engineering to insert a gene for a receptor that responds to light in the presence of a chemical called maleimide-azobenzene-glutamate (MAG).

This process uses a modified virus called adenovirus to carry the gene into cells. The genetically modified virus is injected into the retina. The scientists were able to get retinal ganglion cells to produce this receptor.

Afterwards, an injection of MAG could turn on the light receptors when they are exposed to light. However, the first set of laboratory experiments did not work well because the level of light required to activate the new light receptors was so high that it damaged the retina.

After modifications, they produced a slightly altered chemical compound called MAG460, which responded to a less damaging wavelength of light, and performed a set of experiments.

Mice genetically engineered to lose the function of rods and cones by the age of 90 days were used. The researchers injected the mice's retinas with the adenovirus containing the light receptor gene.

Afterwards, they injected the retinas with MAG460 and then measured the ability of the retinal cells to respond to light in the laboratory.

As mice naturally avoid light, they compared the behaviour of the blind mice in a box that had light and dark compartments before and after the injections into the retina of the light receptors and MAG460.

To more accurately assess the ability to see, the researchers created a maze for the mice. They compared the ability to exit the maze of wild mice and blind mice injected with either the light receptors and MAG460, or an inactive placebo injection.

Finally, the researchers injected a canine version of the adenovirus and light receptor mixture and MAG460 into the retinas of three blind dogs and one normal dog.

They euthanised at least one of the dogs so they could look at the retinas in the laboratory to see if the light receptors had joined to the retinal ganglion cells. They also took retinal biopsies from the other dogs to measure if the cells could respond to light.

 

What were the basic results?

The light receptors were successfully produced by most of the retinal ganglion cells. The chemical compound MAG460 they developed was able to cause the cells to react to blue or white light without causing retinal damage. The light receptor was also able to "switch off" in darkness.

The retinas of blind mice that had been injected with the light receptors and then MAG460 became responsive to blue and white light. The treated retinal cells were able to detect different levels of light.

After injecting the retina with light receptors and MAG460, the blind mice had a strong avoidance of the light compartment of a plastic box, similar to normal-sighted mice. This effect lasted about nine days.

The sighted mice and blind mice injected with light receptors and MAG460 were able to learn how to exit the maze with increasing speed over the course of eight days. The blind mice injected with placebo were not able to learn how to do the task.

Experiments using the retinas of dogs showed that after the injections, retinal ganglion cells produced the light receptor and this, with MAG460, was able to make these cells respond to light.

 

How did the researchers interpret the results?

The researchers concluded they have been able "to restore retinal light responses and enable innate and learned light-guided behaviour in blind mice".

They say the system is equally effective in the retinas of genetically engineered blind dogs when tested in the laboratory.

These results will pave "the way for extensive testing of high-resolution vision in a preclinical setting and for clinical development," they say.

 

Conclusion

This innovative set of experiments has shown retinal ganglion cells can be genetically modified to produce a receptor on their surface that can respond to light in the presence of a chemical compound called MAG460. This light receptor can be activated for up to nine days.

This was shown in laboratory experiments on the retinas of mice and dogs, and in sight-testing experiments using mice. The mice had been genetically engineered to lose both types of photoreceptors, rods and cones by 90 days.

This model mimics what occurs over a much longer timescale in the human condition retinitis pigmentosa.

It appears from this research that other cells that are not damaged in the retina, such as retinal ganglion cells, can be genetically reprogrammed to respond to light.

These experiments provide hope that, despite the original photoreceptors being damaged or dying, some function can be restored if other cells are undamaged.

This could help people with conditions such as retinitis pigmentosa, but would not be suitable for people with age-related macular degeneration or diabetic retinopathy, where the damage is more extensive.

The experiments so far show there is some ability to respond to light, but these behavioural tests are at an early stage. More sophisticated experiments are needed to further assess the extent of visual ability this process can restore.

No human trials have yet been performed, but the researchers hope this will not be too far off.

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

Links To The Headlines

Procedure to restore sight in dogs gives hope for future blindness cure. The Independent, December 8 2014

Have scientists found a cure for blindness? Radical gene therapy that restores sight in mice and dogs could be used on humans. Mail Online, December 9 2014

Links To Science

Gaub BM, Berry MH, Holt AE, et al. Restoration of visual function by expression of a light-gated mammalian ion channel in retinal ganglion cells or ON-bipolar cells. PNAS. Published online December 8 2014

Categories: Medical News

Academic hype 'distorting' health news

Medical News - Wed, 12/10/2014 - 13:29

"Science and health news hype: where does it come from?," The Guardian asks. A new study suggests a lot of the hype comes from academics themselves, or at least their press offices, as many press releases contain exaggerations.

Researchers looked back at all health-related press releases issued by 20 major UK universities during 2011.

They found many spurious health news reports were based on misleading press releases – normally part written, or at least approved by, the scientists themselves. For example, 36% of press releases they studied made exaggerated claims about human health from research actually carried out on animals. 

But somewhat ironically, the study found press releases containing exaggerated claims were actually less likely to generate news coverage.

So the study asks who's to blame – journalists for not bothering to read the actual studies they are reporting on, or academic press releases for hyping results? Or possibly a 24/7 media culture in which the amount of content produced is seen as more important than the quality?

It would seem misrepresentations can occur at all levels. While there are many dedicated journalists and press officers who strive for transparency and accuracy, a minority are letting the side down.

 

Where did the story come from?

The study was carried out by researchers from Cardiff and Swansea Universities in the UK and the universities of New South Wales and Wollongong in Australia.

It was funded by the British Psychological Society, the Experimental Psychology Society, the Wales Institute of Cognitive Neuroscience, the Wellcome Trust, the Economic and Social Research Council, the Biotechnology and Biological Sciences Research Council, and Cardiff University.

The study was published in the peer-reviewed British Medical Journal on an open access basis, so it is free to read online or download as a PDF (1.5Mb).

Not surprisingly, the study was not covered widely by most of the papers, especially those whose content is often dominated by health news.

While nobody is covered in glory by this research, journalists come out of it slightly better, as the researchers found hype invented by reporters was relatively uncommon.

But some journalists would seem to be guilty of recycling press releases rather than carrying out any independent reporting (or as it is known in the trade, "Churnalism").

The Guardian did publish a blog by the scientists who conducted the study, and The Independent provided an accurate summary of the study's findings.

And the BMJ put out a press release – on the exaggerations made in press releases. 

 

What kind of research was this?

This was a retrospective observational study, which looked at the content of all press releases about health-related science issued in 2011 by 20 major UK universities, together with the peer-reviewed journals they originated from and the printed news stories that followed.

It aimed to identify how often news stories contain claims or advice that go beyond those in the journal articles or if they try to identify the likely source – whether press releases or the news stories themselves.

The scientists point out health-related news has the widespread potential to influence health-related behaviour, but studies they are based on are often misreported.

It is often unclear whether inaccuracies and exaggerations originate in the news stories themselves or in the press releases issued by the academic institutions producing the research.

They also point out how journalists are increasingly expected to produce more copy in less time. This means press releases have become increasingly important, and the information they provide often makes up the core of the story.

Previous research, such as a study we covered in 2012, has suggested press releases can be a source of misinformation.

 

What did the research involve?

Using publicly accessible information from 20 leading research universities, the researchers identified all press releases based on published studies with possible relevance to human health, which had been issued in 2011 – they found 462 press releases.

For each press release, they sourced the original study and all relevant print or online news stories from the national press (not including broadcast news) – they found 668 news stories.

They coded each journal article, press release and news story.

They focused on three different types of exaggeration:

  • advice to readers to change their behaviour because of the study
  • claims that one thing causes another, but made from observational data only – they used a seven-point scale to rate the strength of such statements
  • inferring there was a relevance to humans from findings in animals beyond (or different to) that stated in the associated peer-reviewed paper

For each category of exaggeration, both news stories and press releases were coded for the strength of their statements.

Taking the peer-reviewed study as a baseline, the researchers then asked to what extent exaggerated statements in news stories were present in each press release.

For example, if a journal article reported an association between eating biscuits and cancer risk and the news story claimed the biscuits caused cancer – a common type of exaggeration – they looked at what the press release said, too.

Or if a news story claimed a treatment for humans but the actual study was on rodents – another common problem – they examined statements in the press release.

They also searched press releases and news stories for any caveats or qualifications to the claims being made.

They analysed their results using standard statistical methods.

 

What were the basic results?

Below are the study's main findings:

Exaggerated advice

Forty per cent of the press releases contained more direct or explicit advice than the journal article (95% confidence interval [CI] 33% to 46%).

Exaggerated causal claims

Thirty-three per cent of the claims in press releases were more "strongly deterministic" than those present in the associated journal article (95% CI 26% to 40%).

Exaggerated claims from animal or cell research

Thirty-six per cent of press releases exhibited inflated inference to humans compared with the journal article (95% CI 28% to 46%).

They also found when press releases contained exaggerations, it was more likely that news stories would, too (58% for advice, 81% for causal claims and 86% for inference to humans).

But when press releases did not contain exaggeration, rates of exaggeration in news stories were only 17%, 18% and 10% respectively.

Exaggeration was not significantly associated with increased news coverage compared with press releases, which were more accurate. So it would seem that not only is exaggeration "bending the truth", it is also ineffective.

 

How did the researchers interpret the results?

The researchers say it is common to blame media outlets and their journalists for exaggerated or sensationalised news stories about health – but their main finding was most exaggeration in health news is already present in academic press releases.

The blame, they say, "lies mainly with the increasing culture of university competition and self promotion, interacting with the increasing pressures on journalists to do more with less time."

The scientific community has the ability to improve this situation, they conclude. Press releases could be a primary target to improve the accuracy of science news, with potential benefit for public health.

In an accompanying editorial, Ben Goldacre, Research Fellow at the London School of Hygiene and Tropical Medicine and author of the book Bad Science, argues academics should be made accountable for exaggerations made about their own work in press releases.

 

Conclusion

As the authors point out, this was a retrospective observational study, so it cannot prove exaggeration in press releases accompanying health studies causes exaggeration in news stories.

To find out more, they are now planning a randomised trial on how different styles of press release influence the accuracy of science news stories.

However, it does chime with anecdotal evidence on the exaggerations in press releases that are then taken up by the media. It can only be a good thing if, as a result of this and future research, scientists themselves take more responsibility for the accuracy of press releases related to their studies. 

There is always the danger of creating a "boy who cried wolf" scenario. Readers may become so mistrustful of what they perceive as hype and exaggeration in health news that they ignore valid, evidence-based advice, which could lead to real harms. 

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

Links To The Headlines

Science and health news hype: where does it come from? The Guardian, December 10 2014

Bad science reporting blamed on exaggerations in university press releases. The Independent, December 10 2014

Links To Science

Sumner P, Vivian-Griffiths S, Boivin J, et al. The association between exaggeration in health related science news and academic press releases: retrospective observational study. BMJ. Published online December 10 2014

Categories: Medical News

Around 1 in 10 maternal deaths due to flu

Medical News - Tue, 12/09/2014 - 15:25

“Nearly one in ten pregnant deaths caused by flu,” The Daily Telegraph reports. A review into maternal deaths, which thankfully remain rare, found that conditions such as the flu and sepsis account for many of the deaths. Maternal deaths are deaths in women that occur during their pregnancy or within six weeks after the end of their pregnancy.

Other headlines prompted by the review included the Mail Online’s “Half of deaths in pregnancy are 'avoidable'”, pointing out that mental health and heart problems take a “heavy toll”.

BBC News took a more positive approach, pointing out that “Maternal death rates 'are falling'”. Maternal death rates dropped from 11 per every 100,000 women giving birth during the 2006-08 period to 10 per every 100,000 women during the 2010-12 period.

 

What are the news stories based on?

The news stories are based on a report by researchers at the University of Oxford. It aimed to find the reasons for maternal deaths and illness (morbidity) between 2009 and 2012 in the UK and Ireland, and what lessons can be learned. They note that the focus is not on attributing blame, but on using these lessons to improve future maternity care. The UK’s maternal death rates are now among the lowest in the world.

This is part of a programme of Confidential Enquiries into Maternal Deaths, which has been running since 1952. The current programme, called the “Maternal Newborn and Infant Clinical Outcome Review Programme”, is provided by the MBRRACE-UK collaboration. MBRRACE-UK stands for Mothers and Babies: Reducing Risk through Audits and Confidential Enquiries across the UK.

 

What data do they look at and how do they collect it?

The current data covers the UK and, for the first time, the Republic of Ireland.

Data on maternal deaths is collected from various sources, including direct notification by individual maternity units, coroners, pathologists, midwives or members of the public, or though media reports. This is cross-checked with data from the Office for National Statistics and National Records of Scotland. The researchers also search for records of deaths in women of childbearing age, and compare these with birth records to identify any missing deaths.

The researchers send forms to the units in which the deaths occurred to find out demographic and medical details, causes of death, and provide contact details for the clinicians involved in their care. They then send questionnaires to the clinicians to ask about their views on the women’s care. All of these details and copies of the women’s medical records are provided to the MBRRACE-UK assessors for review, but only after any details that could identify the women are removed – so the records are anonymous.

 

What are the main findings and trends?

Their main findings were:

  • 357 women died during or within six weeks of the end of their pregnancy in 2009-12; this was equivalent to 10 in every 100,000 women giving birth.
  • This was a significant reduction from 11 deaths in every 100,000 women giving birth in 2006-08.
  • The reduction was largely due to a reduction in deaths as a direct result of a pregnancy complication such as bleeding.
  • In 2009-12, one third of mothers who died did so as a direct result of a pregnancy complication.
  • Two-thirds of the deaths were from medical or mental health problems that were not directly linked to pregnancy, but got worse during pregnancy.
  • Three-quarters of mothers who died had pre-existing medical or mental health problems when they became pregnant.
  • More than two-thirds of women who died did not receive the nationally recommended level of care during their pregnancy (antenatal care), and a quarter did not receive the recommended minimum level of care.
  • Almost a quarter of women who died had a severe infection (sepsis).
  • One in 11 of the mothers who died did so from flu, and more than half of these could have been prevented by a flu vaccination.

 

What recommendations do they make?

The report’s basic recommendations are that:

  • Women with pre-existing medical and mental health conditions need pre-pregnancy advice and joint care from specialists in their condition and maternity staff.
  • Women with a severe infection need early diagnosis, rapid antibiotic treatment and a review by senior doctors and midwives.
  • More women need to receive the seasonal flu vaccine in pregnancy.

The report expands on these to make more detailed recommendations for various groups of staff in the healthcare system and professional organisations.

This included, for example, keeping the possibility of sepsis in mind at all times, ensuring women with any symptoms or signs of ill health in pregnancy have a full set of basic observations – such as temperature, blood pressure and breathing rate – and ensuring that women get access to  available care. They also recommended that any maternal deaths should be reviewed locally by a multidisciplinary group.

A full version of the report is available in the further reading section below.

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

Links To The Headlines

Nearly one in ten pregnant deaths caused by flu. The Daily Telegraph, December 8 2014

Maternal death rates 'are falling'. BBC News, December 9 2014

Better care urged for pregnant women with mental health problems – study. The Guardian, December 9 2014

Half of deaths in pregnancy are 'avoidable': Oxford study lays bare heavy toll of mental health and heart problems. Mail Online, December 9 2014

Categories: Medical News

Hopes for chemicals that turn 'bad' fat 'good'

Medical News - Tue, 12/09/2014 - 14:00

"Scientists discovered how to trigger a molecule which can turn 'bad' white fat cells into 'good' energy-burning brown fat cells," The Daily Telegraph reports, saying that it could "replace the treadmill". But this proof of concept lab research didn't involve any humans.

White fat is what most people think of when they are talking about fat – it stores energy, adds bulk to the body, and too much can lead to obesity.

Brown fat helps to keep body temperature stable by burning energy, and this uses up calories. Brown fat is mostly found in newborns, but researchers think if they could convert white fat cells into brown fat cells in adults, this could lead to weight loss.

In this study, researchers have identified a number of potentially promising chemicals that could be used to create a drug that can turn white fat into brown fat.

A pill that allows us to eat what we want and not gain weight might become a reality at some point in the future, but this is unlikely to be an option in the short term.

Researchers have only done tests on cells in the lab so far. They do not yet know whether the chemicals will be effective and safe in humans.

Even if an obesity-busting pill becomes a reality, it is unlikely to replace all of the benefits of keeping active and eating a healthy balanced diet – so do still ask Father Christmas for that treadmill.

 

Where did the story come from?

The study was carried out by researchers from the drug company Roche, Harvard University and Massachusetts General Hospital in the US.

The research was funded by F. Hoffmann-La Roche, the US Institutes of Health and Harvard University, and was published in the peer-reviewed journal, Nature Cell Biology.

Both The Daily Telegraph's and the Mail Online's reporting of the study was broadly accurate. But claims made in the headlines that the pill could replace exercise, which is reported in a quote from one researcher, are probably overly optimistic.

Even if a drug was successful in leading to weight loss without the need for exercise, exercise brings additional health benefits.

These include enhanced cardiovascular health and a reduction in the risk of some cancers, bone fractures and dementia, as well as an improvement in symptoms of mild depression.

To be fair to the Mail Online, their article does say the research team pointed this out, but not until the end of the story.

 

What kind of research was this?

This was laboratory research looking for chemicals that can convert fat-storing cells (white fat cells) into energy-burning cells (brown fat cells).

Mammals have two types of fat – white and brown fat. White fat stores excess energy and helps regulate feelings of fullness. Brown fat keeps body temperature stable by burning fat to produce heat.

In humans, brown fat cells are mostly found in newborn infants to help keep them warm before they are able to shiver.

As we grow, most brown fat cells are replaced by white as we have less need for them, but studies have found the more brown fat we have the less likely we are to be overweight.

Animal studies have suggested white fat cells can be prompted to change into brown fat cells by exposing them to certain conditions (such as cold) or certain molecules.

The researchers say if they could find a way to convert white fat cells to brown fat cells in humans, it could be a promising way to combat obesity.

In particular, the researchers wanted to develop a way to rapidly assess a wide range of chemicals for this fat cell-converting ability, and test any chemicals they identified as showing potential.

This is a common way to start looking for chemicals that could be developed into useful drugs. It is a very early stage of drug development, and many of the chemicals identified will never make it to the pharmacy shelf.

And those that do can take a long time to get there. If the process of creating a successful drug was similar to an X-Factor-style reality talent show, the work being done in this study would be akin to the first round of public auditions.

 

What did the research involve?

The researchers started with human stem cells in the lab and treated the cells with chemicals that induce them to develop into white fat cells.

Brown fat cells produce a special protein called UCP1, which white fat cells do not. The researchers used this protein as a "marker" for identifying cells that had started to behave like brown fat cells.

They tested 867 different chemicals to see if they could cause the cells to "switch" to being like brown fat cells. They also looked at whether these chemicals caused the cells to look more like brown fat cells under the microscope.

White fat cells have one or a few large drops of fat inside them, while brown fat cells contain many small droplets of fat. Brown fat cells also possess more of the energy-producing "powerhouses" of the cells called mitochondria.

The researchers also looked at whether the switched cells were producing more mitochondria and were more metabolically active, and what happened if the chemicals were removed from the cells.

They tested whether the chemicals identified could cause cells collected directly from human fatty tissue and white fat tissue from mice to turn into brown fat cells.

They also looked at whether the genes that were active in the switched cells were more like white fat cells or brown fat cells.

The researchers also carried out other experiments to look at how the chemicals they identified had their effect. This could also help them to identify other ways to get white fat cells to switch.

 

What were the basic results?

The researchers identified 83 chemicals that caused white fat cells to become brown fat cells, producing the brown cell-specific protein UCP1 in the laboratory. These switched cells also looked like brown fat cells under the microscope.

Three of these chemicals showed the greatest ability to get white fat cells to switch to UCP1-producing brown fat cells.

The switched cells were also producing more mitochondria and were more metabolically active, burning more fats to make heat.

Two of these chemicals inhibited proteins called JAK and SYK. One was a drug called tofacitinib, which is currently used to treat rheumatoid arthritis.

Even after these inhibitors were removed from the switched cells, they were still behaving like brown fat cells 28 days later.

The researchers carried out further tests on these compounds and found they could cause cells collected directly from human fatty tissue to turn into brown fat cells.

They could also cause white fat cells from under the skin of mice to convert into brown fat cells in the lab, but not fat cells from the abdomen.

Finally, they found although the switched cells were acting more like brown cells, they still had patterns of gene activity that were more like white fat cells. This suggested the cells had not entirely converted to brown fat cells.

 

How did the researchers interpret the results?

The researchers concluded they have developed a way to identify chemicals that can get fat-storing white fat cells to switch to behaving like energy-burning brown fat cells.

Using this system, they identified two inhibitors of the JAK protein, which can cause white fat cells to take on brown fat cell-like characteristics and metabolism in the lab.

They say a role for the JAK pathway in controlling fat cells was not previously known about, and this knowledge could help identify chemicals that could be used to treat obesity.

 

Conclusion

This laboratory research has identified chemicals that can make fat-storing white fat cells behave more like energy-burning brown fat cells in the lab.

They hope these or other chemicals identified using their new method could eventually help combat obesity.

A pill that allows us to eat what we want and not gain weight is a holy grail for many. While it might become a reality at some point in the future, this is unlikely to happen any time soon.

As the authors themselves note, they have only done tests on cells in the lab so far. They do not yet know whether the chemicals will have the same effect within the body or, more importantly, whether they would be safe to use.

The researchers are right in sounding a note of caution. The chemicals they have identified as working best so far inhibit a protein called JAK, which plays an important role in the immune system.

This could make using JAK inhibitors to treat obesity more difficult, as it could mean side effects for the immune system.

This research is at a very early stage, and the pill will certainly not be in the stores in time for Christmas, so you are still going have to hit the gym if you want to get rid of any excess calories you consume over the festive period.

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

Links To The Headlines

Obesity pill to 'replace treadmill' being developed by Harvard University. The Daily Telegraph, December 8 2014

The obesity pill that could replace exercise by turning 'bad' fat to 'good'. Mail Online, December 8 2014

Links To Science

Moisan A, Lee Y, Zhang JD, et al. White-to-brown metabolic conversion of human adipocytes by JAK inhibition. Nature Cell Biology. Published online December 8 2014

Categories: Medical News

Lack of sleep linked to negative thinking

Medical News - Mon, 12/08/2014 - 14:30

“Feeling anxious? Go to bed earlier: Getting more sleep really can calm the mind,” reports the Mail Online. 

However, if you’re more of a "glass half-empty" sort of person, the headline could have read “feeling anxious affects your sleep” – which is an equally valid interpretation of the same results.

A study of 100 university students has found that shorter sleep and delayed ability to get to sleep are associated with repeated negative thoughts (RNT). RNT are unwanted, unhelpful and distressing thoughts that are repeated over and over again, such as “my life is pointless”.

RNT can be a common problem in people with mental health issues such as generalised anxiety disorder and obsessive compulsive disorder (OCD).

Students filled in surveys assessing their sleep patterns, mood, anxiety levels and how often they experienced RNT. There was a clear correlation between poor sleep quality and RNT but the “direction of travel” is unclear. Does poor sleep lead to RNT or does RNT lead to poor sleep?

It’s plausible that lack of sleep might make negative thoughts or mood worse, as it does for concentration. Similarly, it’s easy to imagine that worrying about issues can stop someone sleeping well.

If you are troubled by persistent insomnia and unwelcome thoughts that you feel you cannot control, see your GP. Talking therapies such as cognitive behavioural therapy can often help with both of these issues.

 

Where did the story come from?

The study was carried out by researchers from Binghamton University, US. Sources of funding were not reported.

The study was published in the peer-reviewed medical journal Cognitive Therapy and Research.

The Mail Online accurately reported on the study (and somewhat unusually for the Mail, put a positive spin on the results), though it did not make it clear that the study was conducted on apparently healthy student volunteers. Similarly, it did not highlight the most important limitation of the study, the possibility of reverse causation or what is known in academic circles as “the chicken egg problem”.

The Mail also reported “a spate of studies [that] suggested getting between seven and eight hours is essential for good health”. This refers to separate research, which we have not appraised. Consequently, we cannot comment on the accuracy of these specific statements.

That said, there is a general consensus of expert opinion that persistent lack of sleep can be detrimental for both your physical and mental health.

 

What kind of research was this?

This was a cross-sectional study that aimed to see if the student responses to a variety of questionnaires indicated any association between repetitive negative thinking (RNT) and sleep. RNT describes when a person has distressing or worrying thoughts that are repeated over and over again and are difficult to control.

RNT occurs in a variety of mental illnesses, including generalised anxiety disorder, major depression, post-traumatic stress disorder (PTSD) and obsessive compulsive disorder (OCD). It can also occur in people who do not currently have a mental illness and generally causes increased feelings of anxiety and a lowering of mood. The researchers wanted to explore the relationship between RNT and a lack of sleep or delay in getting to sleep.

As this was a cross-sectional study, it cannot prove causation. That is, whether poor sleep causes RNT or RNT causes poor sleep. Both scenarios seem plausible.

 

What did the research involve?

The researchers recruited 100 US university students who had volunteered to participate in any research studies. They were on average 19 years old and 58% of them were female.

The students completed a variety of questionnaires assessing their levels of worry, thought patterns, sleep patterns and whether they were more of a morning or an evening person. This included the:

  • Worry Domain Questionnaire (WDQ)
  • Ruminative Response Scale of the Response Style Questionnaire (RRS)
  • Obsessive Compulsive Inventory (OCI)
  • Perseverative Thinking Questionnaire (PTQ)
  • Positive and Negative Affective Schedule (PANAS)
  • Negative Affect scale (PANAS-NA)
  • Pittsburgh Sleep Quality Index (PSQI)
  • Horne Ostberg Morningness-Eveningness Questionnaire (MEQ)

The researchers then performed statistical analyses to look for any associations between sleep and repetitive negative thinking from the answers to these questionnaires.

 

What were the basic results?

The main findings were:

  • increased RNT was associated with shorter sleep and delayed sleep
  • shorter sleep was associated with more rumination (repetitive thinking)
  • delayed time getting to sleep was associated with more obsessive-compulsive symptoms

On average, the students:

  • went to bed at 1am and got to sleep within 22 minutes
  • slept for about seven hours
  • were mostly “evening” types
  • did not score highly overall for the symptoms on any of the questionnaires

 

How did the researchers interpret the results?

The conclusion reached by the researchers was that repetitive negative thinking “may be uniquely related to both sleep duration and timing”.

 

Conclusion

This study has found an association between shorter sleep and increased reported RNT.

However, there are a few points to bear in mind when considering how applicable the results of this study would be to the general population, people who have a mental illness or are particularly affected by RNT:

  • due to the cross-sectional measure of sleep patterns at one point in time, we cannot tell whether lack of sleep, or delayed sleep, causes RNT or whether RNT causes sleep disturbance – both directions of effect are plausible
  • none of the participants in the study were reported to be suffering from any mental illness or other conditions that may affect the level of RNT
  • they were all young, adult students
  • it could be argued that they may have been of a certain personality type to have been willing to complete seven extensive questionnaires
  • sleep patterns of people in this particular age group who are at university are unlikely to be representative of the sleep patterns they will have at other times of their life

However, commonsense tells us that a lack of sleep is likely to make any negative thoughts or mood worse. Tips on how to get a better night’s sleep can be found here.

If you are suffering from unwanted, repetitive thoughts that are causing you distress, talk to a healthcare professional. There are a range of simple techniques that can help, in addition to more formal methods such as cognitive behavioural therapy.

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

Links To The Headlines

Feeling anxious? Go to bed earlier: Getting more sleep really can calm the mind. Mail Online, December 5 2014

Links To Science

Nota JA, Coles ME. Duration and Timing of Sleep are Associated with Repetitive Negative Thinking. Cognitive Therapy and Research. Published online January 4 2014

Categories: Medical News