"WHO warns that a deadly novel coronavirus could be passed from person to person," The Independent reports.

The news – featured in much of the media – is based on the latest ‘state of play’ advice from the World Health Organization (WHO) on the novel coronavirus (nCV). However, public health officials in the UK have stated that there is no evidence of 'sustained' transmission (ie. no-one who has been infected by another person, has gone one to infect more people).

nCV, which is genetically similar to the SARS virus, was first reported in the autumn of 2012 and appears to have originated in the Middle East.

Initial symptoms of nCV are similar to a severe case of the flu and include:

• fever
• cough
• shortness of breath
• breathing difficulties

Unlike flu, nCV is thought to have a high risk of causing serious, life-threatening complications such as pneumonia and kidney failure.

What have the WHO said about nCV?

The WHO has confirmed that as of May 12 2013 there have been 34 confirmed cases – the majority of which occurred in Saudi Arabia.

The current thinking is that the virus mainly affects people who are already ill and have a weakened immune system.

How does nCV compare to SARS?

Despite nCV being similar to SARS (both come from the coronavirus ‘family’ of viruses) there are important differences between the two.

The bad news is that nCV appears to be much more deadly than SARS. Of the 34 people who have contracted it, 18 have died. Resulting in a death rate (or in medical terms, a case fatality rate) of around 52%. However, it is not clear whether there are cases of mild illness that have not been reported or confirmed. This means the real case mortality rate is far lower.

And the good news is that nCV seems to be far less contagious than SARS.

From the available evidence, it seems that nCV can only spread from person to person if prolonged close physical contact takes place. In other words, you may catch it if you share a home with an infected person, but not if you share a bus or an aeroplane.

While remaining vigilant to any potential threat, the WHO does not consider nCV to pose the same kind of potential threat as SARS or swine flu.

What is being done to counter the threat of nCV?

Global research efforts into nCV are being lead by the Kingdom of Saudi Arabia. It is currently in the process of establishing surveillance systems to track any further spread of infection.

Saudi health officials are also trying to establish the source of the virus and how it spreads.

Is there any treatment for nCV?

A recent study found that two anti-viral drugs, ribavirin and interferon-alpha 2b, can help slow the replication of the virus in human cells. This may potentially help reduce the risk of complications such as kidney failure.

However, there is currently no effective vaccine for nCV.

Is there any threat to people in the UK?

Based on the current evidence, the threat to people living in the UK is thought to be minimal.

One issue of concern is that visitors to Saudi Arabia during the Hajj in October could contract the infection.

This risk should be reduced if you take some common-sense precautions, such as:

• washing your hands frequently
• cover your mouth and nose when you sneeze or cough
• avoid sharing food, drink and utensils
• regularly clean surfaces with disinfectant

For more information, read the Public Health England advice on the novel coronavirus.

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

Links To The Headlines

New coronavirus can spread between humans, says WHO official. The Guardian, May 13 2013

WHO says new coronavirus may be passed person to person. BBC News. May 12 2013

WHO warns that deadly novel coronavirus could be passed from person to person. The Independent, May 13 2013

Coronavirus: Infection 'Spreads Between People'. Sky News, May 13 2013

Second French coronavirus case. ITV News, May 13 2013 

The Daily Mail claims a study has found a ‘Vampire treatment that rejuvenates ageing hearts’.

But before you go to grab your cloak and false pointy teeth, the research it reports on was actually in mice.

The study looked at possible ways to treat age-related cardiac hypertrophy – when the muscles of the heart become thickened, leading to a corresponding decrease in functioning ability.

Researchers joined the blood circulation of pairs of young and old mice. And one month later they looked at the resulting effects on the animal’s heart muscle.

They found that old mice who shared blood with young mice had reduced levels of cardiac hypertrophy compared to similar mice not treated with ‘young blood’.

The researchers suggest that this could be due to a chemical called growth differentiation factor 11 (GDF-11), which is high in the blood of young mice, and could help repair tissue damage.

An obvious limitation of the study is that results in mice do not always apply to humans. In humans, heart failure is where the heart cannot pump enough blood to meet the body’s needs, and this can have many different causes.

Thickening of the heart muscle is just one type of heart failure, which can be caused by high blood pressure, but can also be an inherited condition.

It is difficult to know to what extent the same growth factor could be responsible for heart muscle thickening in people with this type of heart failure. Also, its relevance – if any – to other types of heart failure (for example due to muscle damage following heart attack, due to an abnormal heart rhythm, or due to heart valve disease) is even less clear.

The findings are of scientific interest but are not going to miraculously reverse the entire disease process of heart failure in humans.

Where did the story come from?

The study was carried out by researchers from the Harvard Stem Institute and other research institutes in the US, and was funded by the American Heart Association, Glenn Foundation and National Institute of Health.

The study was published in the peer-reviewed scientific journal: Cell.

The Mail over-interprets the findings from this animal research. It is also unclear where the sub-headline ‘could be ready for use in clinical trials within 4 years’ has come from.

What kind of research was this?

The researchers say that loss of normal heart function leading to heart failure is one of the most debilitating diseases of ageing.

In particular, they discuss the type of heart failure that is often caused by high blood pressure, where the heart muscle becomes thickened and stiff (cardiac hypertrophy) so the heart chambers cannot dilate so well and fill with blood. This is known as ‘diastolic’ heart failure, as it relates to a problem when the heart is trying to refill with blood (diastolic), rather than contract (systolic).

The researchers suggest that animal studies have previously shown that chemicals circulating in the body of a young animal have been shown to restore function to the skeletal muscle of an old animal.

This process was done by what is called ‘parabiosis’ where two animals are surgically joined and so share their blood circulation.

The current animal study aimed to use a parabiosis model to try and reverse the thickening of heart muscle.

What did the research involve?

For their experiments the researchers used old mice (aged about two years) and young mice (aged two months). They used parabiosis to surgically join the blood circulation of pairs of old and young mice.

After they had been joined for one month, the researchers analysed samples from the heart muscle of the mouse pairs.

For comparison they also looked at the effect of shared blood circulation between young-young and old-old mice pairs.

They also compared with a ‘sham’ parabiosis where they surgically joined the tissue of pairs of young and old mice (at the knee joint), but without sharing their circulation.

To look into what could be the cause of any observed effects upon heart muscle, they also intensively monitored the blood pressure of mice while they were joined, and looking at levels of different chemicals in the blood of young and old mice.

What were the basic results?

The researchers found that the effect of surgically combining the circulation of the young and old mice pairs was clearly visible. The hearts of old mice that had their circulation joined to a young mouse looked much smaller and were less heavy than those of old mice who had been joined to old mice.

When they looked at the heart muscle cells under the microscope they found that the cells of old mice joined to young mice had a significantly smaller cross-sectional area than those of old mice joined to old mice, or those in the ‘sham’ parabiosis condition where their circulation hadn’t been joined to the young mice.

The effect of parabiosis on heart muscle cells was similar in both male and female old mice.

Meanwhile, the heart muscle cells of the young mice were no different in any of their three combinations (young-young, young-old or sham parabiosis).

They also carried out a number of experiments into what could be having the observed effects.

They ruled out that the smaller heart muscle cells of the old mice could have been caused by a reduction in their blood pressure. This was because all of the joined mice actually showed increases in their blood pressure compared to before they were joined. 

They also considered the possibility that the changes could be due to behavioural change from the physical constraint of being joined to another mouse, rather than any effect of the shared blood.

However, if this was the case then it would be expected the heart muscles of old mice in the sham parabiosis would also have decreased in size, and they had not.

Overall, the researchers considered the effects could be due to some chemical in the shared circulation. Separately analysing the blood from young and old mice they found that several components of their blood are different. In particular, levels of a molecule called growth differentiation factor 11 (GDF-11) are found to be lower in the blood of older mice.

When they went on to treat the heart muscle cells from rats with GDF-11 in the laboratory, they found that GDF-11 prevents the thickening of the heart cells. In a further experiment involving older female mice, the hearts of a group injected with GDF-11 were significantly lighter and the cells were significantly smaller than those of a group injected with a placebo.

How did the researchers interpret the results?

The researchers’ animal experiments suggest that the thickening of heart muscle can be influenced at least in part by certain chemicals circulating in the blood. They suggest that GDF-11 could reverse thickening of heart muscle, and so conclude that ‘at least one component of age-related diastolic heart failure is hormonal in nature and reversible’.

Conclusion

This study finds that sharing the circulation of young and old mice appears to reverse the age-related thickening of heart muscle cells in the older animal, and it seems this could be due to a certain growth factor in the blood of the young animal. The findings will be of scientific interest, and further our understanding of the processes of heart ageing in animals.

However, the findings have very limited direct relevance to humans, and do not suggest a new treatment for heart failure.

It is also certainly unknown at this point whether increasing levels of this factor in the blood of people with this type of heart failure would somehow reverse the entire disease process. Its relevance to other types of heart failure not associated with thickened heart muscle is even less clear.

Even if further research were to demonstrate that this growth factor could have a potential role in heart failure treatments in humans; joining the circulation of young people with those with heart failure in the manner used in this study is clearly not a possibility.

If the chemical were to be extracted from donor blood, or synthetically produced, there would still be many safety issues to considered, even if the treatment were found to have an effect.

Overall the research does not suggest a new treatment for heart failure in humans, though it may represent the first step towards a possible treatment at some point at the future.

However, due to the uncertainties discussed above it is impossible to estimate the likelihood of this prediction becoming fact.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

The vampire treatment that 'rejuvenates' ageing hearts: Dose of young blood can reverse life-threatening thickening of organ. Daily Mail, May 10 2013

Links To Science

Loffredo FS, Steinhauser ML, Jay SM, et al. Growth Differentiation Factor 11 Is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy. Cell. Published online May 9 2013

"Smoking just a few cigarettes a day more than doubles a woman's risk of developing rheumatoid arthritis," the Mail Online website reveals. The website reports on a Swedish study that found women who only smoke a small number of cigarettes a day significantly increase their risk of developing the condition.

This large study followed more than 30,000 women over a seven-year period to look at whether smoking increased their risk of developing rheumatoid arthritis. Smoking is already recognised as a possible risk factor for developing the condition. 

But this study showed that the risk increased even at relatively low levels of smoking. It found that even smoking as many as between one and seven cigarettes per day more than doubled a woman's chance (2.31 times) of developing rheumatoid arthritis compared with a woman who had never smoked.

Although this study provides further evidence about the dangers of smoking, it does have a number of limitations. For example, it is not clear how many women dropped out of the study, which could have biased the results. It is also unclear whether similar risk patterns would be seen in men (the condition is more common in women) or a more ethnically diverse group.

Nonetheless, this study provides evidence of yet another disease that smokers may be at significantly increased risk of developing, even if they are considered to be 'light' smokers.

Where did the story come from?

The study was carried out by researchers from the Karolinska Institutet in Sweden and was funded by research grants from the Swedish Research Council's Committee for Medicine, Committee for Research Infrastructure for maintenance of the Swedish Mammography Cohort, and the Swedish COMBINE inflammation research consortium.

It was published in the peer-reviewed science journal Arthritis Research and Therapy.

The Mail Online's coverage of the study was generally accurate, and included information about the study sample size and an idea of the prevalence of the condition.

What kind of research was this?

This was a cohort study that aimed to discover how much a woman needs to smoke in order to increase her risk of developing rheumatoid arthritis.

The authors pointed out that previous studies have shown that cigarette smoking was directly associated with a higher risk of developing rheumatoid arthritis. What was unclear was whether this risk was associated with so-called 'light' smoking and whether quitting smoking reduced the risk.

The focus of this study was therefore on examining how much the risk of developing rheumatoid arthritis increased depending on how much a woman smoked and how long they had smoked for, and whether it was possible to reduce this risk if a woman quit smoking.

Rheumatoid arthritis is what is known as an autoimmune condition, where the body's own immune system starts to attack the cells that line the joints, causing pain and swelling. Hands, feet and wrists are commonly affected, but it can also damage other parts of the body.

The condition is estimated to affect more than 580,000 people in England and Wales, and occurs more frequently in women than men. It is most common between the ages of 40 and 70, but can affect people of any age.

Exactly how smoking can increase the risk of a person developing rheumatoid arthritis is still uncertain. One theory is that that it can disrupt the normal workings of the immune system, leading to the type of abnormal immune response associated with the condition.

What did the research involve?

The researchers used an existing cohort of women called the Swedish Mammography Cohort, which included 34,101 women aged 54 to 89 years. For the current study, the group were followed from January 1 2003 to December 31 2010, in which time 219 cases of rheumatoid arthritis occurred.

Women were asked about various aspects of their diet and lifestyle via questionnaire, as well as additional questions about their smoking habits and history, physical activity, and their use of some medications and dietary supplements.

The current study population of 34,101 excluded women from the mammography cohort who had missing data on their smoking status (797), as well as women with non-rheumatoid arthritis joint conditions (2,052). Women already diagnosed with rheumatoid arthritis were also excluded.

Cases of rheumatoid arthritis were identified by linking the records of women in the cohort to medical databases. The researchers also had access to a national rheumatology register so they would be notified if a diagnosis of rheumatoid arthritis was made.

The analysis estimated the relative risk (RR) between various aspects of smoking behaviour – such as intensity, duration and time since quitting – and the risk of developing rheumatoid arthritis. The analysis took into account a variety of potentially modifying factors (confounders), including alcohol consumption, menopausal status, educational level and body mass index.

What were the basic results?

Over the seven-year study period, 219 cases of rheumatoid arthritis occurred from within the group of 34,101 (0.6% of the cohort). There was a statistically significant association between smoking intensity and the risk of developing rheumatoid arthritis.

Women who smoked between one and seven cigarettes per day were 2.31 times more likely to develop the condition compared with never smokers (RR 2.31 95% confidence interval (CI) 1.59 to 3.36) over the course of the seven-year study.

There was also a statistically significant association between how long a woman had smoked for and the risk of developing rheumatoid arthritis. Women who had been smoking for between one and 25 years were 1.60 times more likely to develop the condition compared with never smokers (RR 1.60, 95% CI 1.07 to 2.38).

Compared with never smokers, the risk for these smokers was still significantly elevated (to about twice the risk of never smokers) 15 years after the women had quit smoking (RR 1.99, 95% CI 1.23 to 3.20).

Among former smokers, there was a suggested trend that the risk of rheumatoid arthritis decreased over time since stopping smoking. For example, women who stopped smoking 15 years before the start of the study had a non-significant 30% lower risk of rheumatoid arthritis compared with those who had stopped only a year before the start of the study (RR 0.7, 95% CI 0.24 to 2.02).

How did the researchers interpret the results?

The researchers concluded that, "even light smoking is associated with increased risk of rheumatoid arthritis in women and that smoking cessation [stopping smoking] may reduce, though not remove, this risk".

Conclusion

This research indicates that a relatively low level of smoking (one to seven cigarettes per day) is associated with an increased risk of developing rheumatoid arthritis compared with women who had never smoked. This adds further knowledge to previous research that has suggested that cigarette smoking is directly linked to a higher risk of developing rheumatoid arthritis.

While this study is relatively robust and its results believable, it does have limitations that should be considered. It was not clear how many women dropped out of the study. If this was a large proportion of the women who started, it could significantly bias the results of the study.

The study also only recruited women. The same risk pattern may not have been seen if the study had recruited men, who are at lower risk of developing the condition than women. Similarly, the size of the risk differences between different smoking behaviours may be slightly different in men than women. Further research is needed to establish whether this is the case.

Another drawback is that women were recruited from just two Swedish counties. While no ethnicity data was reported, it is likely they were fairly similar ethnically, and it could be that different ethnicities may have different risk profiles for developing rheumatoid arthritis. This means that the results may differ if the study was repeated in a more ethnically diverse population.

This relatively robust study suggests that smoking can significantly increase a woman's risk of developing rheumatoid arthritis compared with women who never smoked, even if a woman only smokes relatively low levels of between one and seven cigarettes per day.

It adds to a growing body of evidence that there is no such thing as a safe level of smoking. Aside from the risk of rheumatoid arthritis, 'light' smoking can significantly increase your risk of developing lung cancer, heart disease and stroke.

Read more about how the NHS can help you quit smoking.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Smoking just a few cigarettes a day can double a woman's risk of arthritis. Mail Online, April 22 2013

Links To Science

Giusueppe DD, Orsini N, Alfredsson L, et al. Cigarette smoking and smoking cessation in relation to risk of rheumatoid arthritis in women. Arthritis Research and Therapy. Published online April 22 2013

Scientists have discovered a gene that "could rejuvenate old hearts" according to The Daily Telegraph. The newspaper goes on to say that "damaged hearts could be regenerated simply by switching off a gene which prevents cells from dividing".

Some parts of our body, such as our skin, are made up of cells that divide and reproduce throughout our lives to produce new tissue. This is known as mitosis. Other parts, such as the heart, are thought to lose this ability shortly after birth.

The Telegraph story is based on new research in mice that has identified a specific gene – dubbed the ‘heartbreak gene’ by the Mail Online – called Meis1 that appears to block the heart tissue’s ability to regenerate.

The researchers found that using various techniques to ‘switch off’ the Meis1 gene did lead to the production of new heart cells in mice.

The hope is that similar techniques could be used in humans to repair damage to the heart that can occur in cases of heart failure.

But switching off a gene to treat a progressive disease like heart failure is unlikely to be quite as simple as the Telegraph suggests. Much more research is needed before we may see a groundbreaking new treatment capable of healing ‘broken hearts’.

Where did the story come from?

The study was carried out by researchers from the University of Texas Southwestern Medical Center in the US, Ain Shams University in Egypt and the University of Queensland in Australia. The research was funded by the American Heart Association, the Gilead Sciences Research Scholars Program in Cardiovascular Disease, the Foundation for Heart Failure research and the US National Institutes of Health.

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

The media reporting of this research was generally accurate, despite some confusion from Mail Online about a "rogue gene" that stops "heart cells dividing uncontrollably".

Most importantly, the media headlines should not be interpreted to mean that “revolutionary new treatments” are on the horizon. The idea of using genes to treat disease – gene therapy – has been around since the 1970s. But, currently, there is only one licensed medication on the market that makes use of gene therapy techniques.

What kind of research was this?

This was animal and laboratory research that aimed to identify and describe the process that controls the generation of new heart cells in newborns. Newborns are able to produce new heart cells to replace injured cells. However, this ability is lost early in life (generally by seven days after birth), and the adult heart lacks this regenerative capacity.

Previous research has suggested that a gene called Meis1 is involved in the development of the foetal heart, and may be involved in regulating the regeneration of newborn heart cells. The researchers thought that this gene may also play a role in the loss of this regenerative capability.

Several heart conditions lead to damage or death of heart cells and to heart failure, where the organ is unable to pump enough blood around the body.

The adult heart is not able to generate new cells to repair such injury and heart failure is considered to be a progressive disease (gets worse over time). So any technique that could reverse this progressive decline would be welcome.

But as an animal study, any results should not be assumed to apply directly to people. Significant further research is needed to determine whether the mechanisms identified in this study provide a suitable target for addressing human heart failure or other causes of heart damage.

What did the research involve?

The researchers carried out a series of experiments to define the role of Meis1 in regulating the generation of new heart cells.

They first measured expression levels of the gene to determine how these levels changed during the first seven days of life (after which the heart is no longer able to produce new cells). Gene expression is the process through which the information encoded in our genes is used to produce proteins. Measuring the level of gene expression shows how active the gene is.

They next investigated the effect on heart cell generation of removing the Meis1 gene, using both rat heart cells as well as mice models.

The mice lacking a copy of the Meis1 gene were compared to control mice (which had copies of the gene) on several factors, including:

• changes in the production of new heart cells
• characteristics of the heart cells
• the size and function of the heart

These comparisons were made for newborn as well as adult mice.

Next, the researchers increased the expression of Meis1 to determine whether doing so produced an effect on the generation of new heart cells in mice.

Finally, they carried out a series of tests to determine how the Meis1 interacted with other parts of the system to identify the mechanism by which the gene controls heart cell generation.

What were the basic results?

The researchers found that there was an increase in Meis1 expression over the course of the first week of life, and that this expression continued into adulthood.

When Meis1 was removed, the researchers found that rat heart cells were able to produce new cells. Mice lacking the Meis1 gene exhibited a similar increase in the production of new heart cells.

Fourteen days after birth (which corresponds to one week after the heart typically stops producing new cells) these mice had hearts of similar size and function to control mice that retained the Meis1 gene. The researchers found that the hearts of mice lacking the Meis1 gene had significantly more cells that those of the control mice, and that these heart cells were smaller in size compared with controls.

When investigating the effect of the Meis1 gene of the adult mouse heart, the researchers found that heart size and function were normal in these mice at both four weeks old and at seven months old. There was also no difference in the size of the heart cells.

The mice lacking the Meis1 gene continued to produce new heart cells into adulthood, but the rate at which they produced these cells slowed as they aged.

The researchers found that newborn mice engineered to overexpress Meis1 did not generate new heart cells in response to injury, while control mice hearts regenerated normally.

Finally, the study authors identified several interactions between Meis1 and other genes in the system that controls the production of new heart cells. They found that when Meis1 is deleted, there is increased activity among some genes that promote the generation of new heart cells. There was also a corresponding decrease in the activity of genes that normally inhibit the production of these new cells.

How did the researchers interpret the results?

The researchers conclude that Meis1 is a critical component of the system that regulates the production of new heart cells. They say their research suggests that cell cycle arrest in the adult human heart (whereby the heart no longer generates new cells) may, theoretically, be reversed.

Conclusion

This research identifies a possible mechanism that leads to the inability of the adult heart to repair itself. It is premature to suggest that the study heralds a new era in treating heart failure.

As with much early stage cell and animal research, this study is probably most useful for scientists and suggests future research paths that may be helpful in the quest to treat heart conditions. It is too early to tell, however, whether the Meis1 gene will prove to be a useful target for future therapies, let alone whether treatments targeting the gene or its products will be safe and effective enough for treating heart failure patients.

Current treatments for heart failure, while a lot better than they used to be, are only of limited effectiveness. So the message is still that prevention is better than cure.

Effective ways you can reduce your risk of heart failure include:

• quit smoking if you smoke
• maintain a healthy weight
• eat a healthy diet
• take plenty of exercise

Read more about reducing your heart failure risk.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Gene could rejuvenate old hearts. The Daily Telegraph, April 17 2013

'Heartbreak gene' which stops organ recovering after injury discovered by scientists: Breakthrough could lead to revolutionary new treatments. Mail Online, April 18 2013

Links To Science

Mahmoud AI, Kocabas F, Muralidhar SA. Meis1 regulates postnatal cardiomyocyte cell cycle arrest. Nature. Published online April 17 2013

"Beetroot 'can lower blood pressure'," BBC News confidently reports. But the truth about whether beetroot can really lower your blood pressure is a little more unclear than the headlines suggest. The news comes from a study looking at the effect of nitrates on blood pressure in rats and a very small trial in people with high blood pressure.

Nitrates are molecules that occur in some foods, particularly in beetroot. Previous studies have suggested that nitrates can widen the blood vessels, which can lead to a drop in blood pressure. This study found that people who drank about one glass of beetroot juice (or rats given a dose of nitrate) had a short-term reduction in blood pressure.

The researchers argue that the use of beetroot juice, or other nitrate-rich foods, could be a useful extra treatment option for people with high blood pressure.

Despite the interesting findings, the study has some significant limitations:

• only 15 people were involved
• it did not look at whether regular consumption of beetroot juice reduced the long-term complications of high blood pressure, such as heart disease

Larger studies assessing the long-term effects of beetroot juice on high blood pressure and its complications are needed before it can be recommended as a way of lowering blood pressure.

Where did the story come from?

The study was carried out by researchers from the William Harvey Research Institute at Barts and The London School of Medicine and Dentistry, Queen Mary University of London, the University of Exeter Medical School, and Kings College London, all in the UK.

It was funded by the British Heart Foundation and was published in the peer-reviewed medical journal Hypertension.

Two of the study's authors disclose a potential conflict of interest as directors of HeartBeet Limited, which appears to be a company that sells beetroot juice and is listed at the same address as the firm that supplied the beetroot juice used in the study.

The headlines in the UK media proclaiming that beetroot "can lower blood pressure" are premature. It would be more accurate, if less sexy, to qualify this by adding "in the very short term". This research did not look at the effect of nitrate on blood pressure for longer than a 24-hour period and we don't know enough about its lasting effects.

What kind of research was this?

The researchers carried out two types of investigations. They first investigated the effect of ingested nitrate on blood pressure among rats. The researchers then carried out a randomised crossover trial on just 15 people. This second investigation aimed to see if dietary nitrate – in the form of beetroot juice – had an effect on blood pressure among people with known high blood pressure.

A randomised crossover trial is a type of study where people receive all of the treatments and are tested in a random order. This is an appropriate study design for looking at this type of research question. It means that people receive one treatment, the effect is measured, and they then 'cross over' into the other treatment group, where the effect of the second treatment (or control) is also measured.

What did the research involve?

For the first part of their study, the researchers investigated the effects of giving different doses of nitrate to healthy rats and rats that had artificially raised blood pressure. The researchers looked at the effect this had on the rats' blood pressure.

For the second part of their investigations, the researchers recruited eight women and seven men who were identified as having high blood pressure (hypertension) at a screening procedure a month before the study began. These participants were not taking any blood pressure medication.

The average age of participants was 52.9 years and they were all considered to have grade 1 hypertension, with readings of:

• systolic blood pressure (the pressure of the blood when the heart beats to pump blood out) between 140 and 159mmHg
• diastolic blood pressure (the pressure of the blood when the heart rests between beats) between 90 and 99mmHg

The agreed definition of high blood pressure is a systolic pressure reading of 140mmHg and a diastolic pressure reading of 90mmHg (140/90mmHg).

Participants were randomly assigned to drink either 250ml of beetroot juice (supplied by a firm at the same address as the company that two of the authors are directors of), considered the experimental group, or 250ml of water (containing a small amount of nitrate), which acted as the control group. In order to elevate levels of nitrite, the participants having the beetroot juice were said to have received a dose of 3.5mmol nitrate that caused a 1.5-fold increase of plasma [nitrate].
 
The participants then had their blood pressure monitored over a 24-hour period: every 15 minutes for the first three hours, then hourly for a further three hours, and again at the 24 hour mark. Participants also had their blood pressure recorded prior to the study to provide a pre-intervention blood pressure reading. After seven days, participants 'crossed over' to receive the alternative drink.

The researchers said that beetroot juice was well tolerated by the people who were given it in terms of side effects.

What were the basic results?

The main results of this study were:

Animal findings

• nitrate was found to significantly lower blood pressure among rats that had high blood pressure compared with the healthy rats
• the results was found to be dose-dependent – the higher the nitrate dose given to the rat, the bigger effect on reducing blood pressure

Human findings

• consumption of the relatively low dose of dietary nitrate caused a significant decrease in blood pressure (systolic and diastolic) compared with participants who drank water (p<0.001)
• the peak average reduction in blood pressure was 11.2 (±2.6) mmHg in the group that received nitrate compared with 0.7 (±1.9) mmHg in the water group
• after 24 hours, systolic blood pressure remained significantly lower in the group that received nitrate compared with the group that received water, and remained significantly different from values taken at baseline
• diastolic blood pressure remained lower in the group given nitrate up to measurements taken at six hours compared with those given water, but returned to values taken at baseline at the 24-hour mark
• no significant difference in heart rate was seen between the groups of human participants

Links To The Headlines

Beetroot 'can lower blood pressure'. BBC News, April 16 2013

Beetroot juice 'helps lower blood pressure': A glass a day can reduce it by 7%, say researchers. Daily Mail, April 16 2013

One vegetable a day can 'cut blood pressure'. Daily Express, April 16 2013

Links To Science

Ghosh SM, Kapil V, Fuentes-Calvo I, et al. Enhanced Vasodilator Activity of Nitrite in Hypertension - Critical Role for Erythrocytic Xanthine Oxidoreductase and Translational Potential. Hypertension. Published online April 15 2013

“Today's adults are so unhealthy they are 15 years 'older' than their parents and grandparents at the same age,” reports The Daily Telegraph. This gloomy message is based on a study that found that despite a continuing trend of increasing life expectancy, overall, the adult population is less healthy than it used to be in the past.

Researchers drew these conclusions after comparing the prevalence of risk factors for stroke, heart disease and diabetes within different generations.

It found that more recently born generations had at a similar age a higher prevalence of obesity and high blood pressure than those born 10 years earlier. Diabetes was also more prevalent among younger men, at the same age.

The good news is that the prevalence of high cholesterol did not change – possibly thanks to the development of successful treatments, such as statins.

Researchers remain unclear why the number of deaths from heart disease is falling despite poorer health. Important factors could include a reduction in smoking, as well as improved treatments.

The message from this study is undeniable: it is never too soon to take up a healthy lifestyle, including a balanced diet and plenty of exercise.

Where did the story come from?

The study was carried out by researchers from the National Institute for Public Health and the Environment, and University Medical Center Utrecht, both in the Netherlands. It was funded by the Ministry of Health, Welfare and Sport of the Netherlands and the National Institute for Public Health and the Environment.

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

It was reported fairly in the media, although both the Telegraph’s and the Daily Mail’s claim that today’s adults are ‘older’ than previous generations is not a particularly sensible, useful or accurate comparison.

There is currently no direct linear association between age and health, and people in their seventies can be as healthy as those in their thirties.

What kind of research was this?

This was a cohort study that followed more than 6,000 adults, who were between the ages of 20 and 59 years at baseline, over a period of 16 years.

It aimed to find out if there were any ‘generational shifts’ in the prevalence of ‘metabolic risk factors’ that increase the chance of developing heart disease, stroke, diabetes and some other health problems.

They include:

• being overweight or obese
• high cholesterol and/or having low levels of ‘good’ HDL cholesterol
• high blood pressure
• high blood sugar, which can increase the risk of developing diabetes

The authors point out that the health of elderly people in the future is partly determined by their exposure to such risk factors over their lifetime. But little attention has been paid to whether or not there are differences in levels of risk factors between the younger and older adult generations.

What did the research involve?

The researchers used data from a cohort study that began in 1987-1991 and followed up participants after six, 11 and 16 years.

Participants were randomly selected from civil registries of Doetinchem, a small town in the Netherlands, and were aged 20 to 59 years. After the initial visit (wave one) they were invited back in three further ‘waves’ - six, 11 and 16 years later. This resulted in:

• a total of 6,308 people in wave one
• 6,070 in wave two
• 4,898 in wave three 
• 4,517 in wave four

The researchers categorised people by ‘generations’ (10-year age groups) of 20-29 year olds, 30-39 year olds, 40-49 year olds and 50-59 year olds.

At each visit trained staff measured each participant for the metabolic risk factors mentioned above (with the exception of blood sugar levels). They also completed questionnaires on medical history, use of medication and lifestyle. Body weight and height were also measured and used to calculate body mass index (BMI).

Type 2 diabetes was self reported but usually supported by professional verification. Socioeconomic status was determined by highest level of completed education.

Researchers then analysed their results to find out if one generation had a different risk profile from one born 10 years earlier.

What were the basic results?

The results showed that the prevalence of overweight, obesity and high blood pressure increased with age in all generations, as to be expected. But in general, more recently born generations had, at a similar age, a higher prevalence of these risk factors than generations born 10 years earlier.

‘Unfavourable generation shifts’ were most pronounced for overweight or obesity, and were present in men between every generation. For example, 40% of men in their 30s at baseline were overweight. 11 years later (wave three), 52% of men in their 30s were overweight.

In women, these unfavourable changes in weight were only evident between the most recently born generations, in which the prevalence of obesity doubled in just 10 years.

Other findings from the study included:

• Unfavourable generation shifts in high blood pressure between every consecutive generation (except for the two most recently born generations of men).
• Unfavourable generation shifts in diabetes between three of the four generations of men, but not of women.
• No generation shifts for high cholesterol. Favourable shifts in ‘good’ HDL cholesterol were only observed between the oldest two generations.

In general, the pattern of generation shifts did not differ according to socioeconomic status, as they all worsened over time. The proportion of people in poorer socioeconomic groups with risk factors was, however, greater than the proportion with risk factors in the higher groups.

How did the researchers interpret the results?

The authors say that overall, based on increases in the prevalence of unhealthy weight and high blood pressure at younger age, "the more recently born adult generations are doing worse than their predecessors". Evidence to explain the changes is not clear, they add, but they note studies reporting an increase in physical inactivity.

In an accompanying press release, the lead author, Gerben Hulsegge, said that in terms of the findings on obesity: "The prevalence of obesity in our youngest generation of men and women at the mean age of 40 is similar to that of our oldest generation at the mean age of 55. This means that this younger generation is '15 years ahead' of the older generation and will be exposed to their obesity for a longer time."

He also argued that while reduction in smoking and improved healthcare have led to greater life expectancy, the current trends in obesity mean that "the rate of increase in life expectancy may well slow down".

Conclusion

This cohort study’s strength was its long follow-up period, with four measurements of risk factors taken over a period of 16 years. By following up people over time a cohort study such as this is able to track risk factors in the same people over extended periods. As long as people return for the follow-up checks, it is the best study design for tracking this sort of data and drawing the sorts of conclusions these authors make.

Another advantage is that the same group of trained workers objectively measured data on body weight, height, blood pressure and cholesterol, using standardised protocols, which reduced the chances of measurement errors.

However, it had some limitations:

• The study was based on data from people living in one town in the Netherlands and the results may not be generalisable to other populations.
• Although response rates during follow-up were good, those who dropped out before the end were more often lower educated and smokers, and were more likely to have certain risk factors, which could affect reliability of the results.
• The researchers recorded smoking at baseline (ranging from 25 to 40% among the men and women recruited) but did not report if this was measured at follow-up visits or how this has changed over the years. This appears to be an opportunity missed as it is well understood in existing research that these risk factors are often seen together.

Still, the study’s results support an important health message about establishing the need for a healthy body weight at a young age, although increased physical activity and a balanced diet should be encouraged at all ages.

Read more about exercise and healthy eating.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Today's adults 15 years 'older' than parents. The Daily Telegraph, April 10 2013

Why 30 is really 45: We're so unhealthy that we're 15 years older than our parents were at the same age. Mail Online, April 10 2013

Old before their time: Britons now ageing quicker than their parents. The Independent, April 11 2013

Links To Science

Hulsegge G, Susan H, Picavet J , et al. Today's adult generations are less healthy than their predecessors: generation shifts in metabolic risk factors: the Doetinchem Cohort Study. European Journal of Preventive Cardiology. Published online April 10 2013

"The Cuban diet – eat less, exercise more – and preventable deaths are halved," is the advice in The Independent.

This is not a new Latin diet and dance fad, but news based on research into how Cuba’s rollercoaster economic history has affected the health of the Cuban people.

During the early 1990s, Cuba suffered an economic downturn due to a tight US embargo on imports and the collapse of the Soviet Union, which had been supporting the country.

This led to a drop in the number of calories consumed in the average Cuban diet. Due to the embargo, petrol became virtually unobtainable, and more than 1 million bicycles were distributed by the government, leading to an increase in physical activity.

These factors contributed to an average weight reduction per citizen of 5.5kg over the course of the five-year economic crisis. During this time there was a significant drop in prevalence of, and deaths due to, cardiovascular diseases, type 2 diabetes and cancers.

But once the crisis was over and people started to eat more and exercise less, these trends began to reverse.

The study suggests that population-wide health initiatives that encourage people to eat less and exercise more could achieve significant positive health outcomes. The question is – how, in an affluent Western democracy, do you encourage people to eat less and exercise more if they are not forced to do so?

Where did the story come from?

The study was carried out by researchers from academic centres in Spain, Cuba and the US. There is no information about external funding.

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

It was reported accurately in the papers, although headlines like the Daily Mail’s “Lose weight the CUBAN way” and The Independent’s “The Cuban diet” trivialise the hardship that Cuban people underwent during the time in question. While they did enjoy a drop in cardiovascular disease and diabetes deaths during this period, they also experienced a sharp rise in malnutrition-associated disorders, such as neuropathies (nerve damage).

What kind of research was this?

The paper used data from regular cross-sectional health surveys of the Cuban population and drew on cardiovascular studies, chronic disease registries and vital statistics over three decades, from 1980 to 2010.

Its aim was to evaluate the associations between weight change across the whole Cuban population and the incidence, prevalence and death rates from diabetes and death rates from cardiovascular disease and cancer.

The authors say that the health effects of population-wide changes in body weight on a well-nourished population are unknown.

In Cuba, they point out, marked and rapid reductions in mortality from diabetes and coronary heart disease were observed after the economic crisis of the early 1990s when, in the aftermath of the dissolution of the USSR and during the US embargo on imports, there were severe shortages of both food and fuel.

These led to people eating less, and walking and cycling more (the government distributed more than 1 million bicycles during the crisis).

Since this time, the Cuban economy has shown a modest but constant recovery, especially since 2000.

What did the research involve?

The researchers used a variety of sources including national and regional surveys, to track changes in body weight, physical activity, smoking and daily energy intake between 1980 and 2010.

In particular, the authors drew on four cross-sectional surveys of adults aged 15 to 74, in the city of Cienfuegos, a relatively large city on the south of the island.

The surveys, of between 1,300 and 1,600 adults each, took place in 1991, 1995, 2001 and 2010 and included measurements of height and weight, which were used to assess body mass index.

The researchers also drew on national surveys of 14,304 people in 1995, 22,851 people in 2001, and 8,031 people in 2010, which assessed risk factors for chronic disease. They obtained data on diabetes rates from Cuban health registries spanning the period 1980–2009. They obtained information on mortality from diabetes, coronary heart disease, stroke, cancer and all causes for the period 1980–2010 from the Cuban Ministry of Public Health.

They analysed trends of change in disease prevalence and mortality over time and examined how this was related to changes in body weight.

What were the basic results?

Overall, between 1991 and 1995, the era of the economic crisis, the Cuban population experienced an average 5.5kg reduction in body weight. This was accompanied by rapid declines in death rates from diabetes and heart disease.

Between 1996 and 2002 (that is, with a lag of about five years after the crisis) there was an associated reduction in diabetes and cardiovascular disease mortality:

• diabetes death rates fell by 50% (13.95% annually)
• coronary heart disease (CHD) death rates fell by 34.4% (6.5% annually)
• deaths from all causes fell by 10.5%

After the crisis had passed, there was an average population-wide increase in weight of 9kg per person. In 1995, 33.5% of the population were overweight or obese and this increased to 52.9% by 2010.

This weight regain was followed by an increase in diabetes incidence and mortality:

• From 2006 to 2009, there was a 140% increase in diabetes incidence (new cases) and a 116% increase in diabetes prevalence (total number in the population with the condition).
• From 2002 onwards diabetes mortality increased by 49% (from 9.3 deaths per 10,000 people in 2002 to 13.9 deaths per 10,000 people in 2010).
• A slowing in the rate of decline in mortality from coronary heart disease was also observed.

How did the researchers interpret the results?

The researchers say that an average population-wide weight loss of 5.5kg per person was accompanied by diabetes mortality falling by half and mortality from coronary heart disease falling by a third. Increased body weight following the crisis was associated with an increase in diabetes incidence and mortality and a slowing down in the decline in mortality from CHD.

The authors suggest that a modest reduction in calorie consumption would “reverse the global obesity epidemic” and reduce deaths from diabetes by half and CHD by a third.

Conclusion

This is an interesting study that appears to show that modest weight loss within a relatively short period across the whole population is associated with a downward trend in diabetes and reductions in death rates from both diabetes and heart disease.

Similarly, weight regain was associated with an increase in diabetes incidence, prevalence and mortality as well as a slowing down in the decline of cardiovascular deaths.

This type of study draws on many different data sources and, as such, there is a possibility of error. Also, as the authors point out, data was missing on diabetes incidence during the crisis years and diabetes incidence showed wide fluctuations in subsequent years.

It is also difficult to conclude that changes in weight are solely responsible for changes in disease rates as other factors may also have a role. For example, smoking slowly decreased in Cuba during the 1990s.

It is not clear if the findings from the paper can be generalised to other countries. Cuba had, and continues to have, a highly centralised system of government where individual autonomy is limited.

To attempt to enforce a nationwide average reduction in body weight in the UK of 5.5kg per person would probably require a degree of social engineering that most people in this country would find intolerable. As the authors point out, an enforced situation of food and fuel shortages is not something anyone would wish to repeat.

While the study reinforces current health messages about the importance of diet and physical activity and a healthy weight, the best way for governments to attempt to reduce global obesity rates remains unclear.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

The Cuban diet: eat less, exercise more - and preventable deaths are halved. The Independent, April 10 2013

Hard times behind fall in heart disease and diabetes in 90s Cuba, says study. The Guardian, April 9 2013

Lose weight the Cuban way: Economic crisis triggered an average weight loss of 11lb and slashed the risk of heart disease and diabetes. Mail Online, April 9 2013

Losing just 8lb can be a lifesaver. Daily Express, April 10 2013

Links To Science

Franco M, Bilal U, Orduñez P, et al. Population-wide weight loss and regain in relation to diabetes burden and cardiovascular mortality in Cuba 1980-2010: repeated cross sectional surveys and ecological comparison of secular trends. BMJ. Published online April 9 2013

“A nutrient abundant in red meat… could raise the risk of heart disease,” the Mail Online website warns.

Its story is based on a study of the nutrient L-carnitine, which is found in red meat, dairy products and some dietary supplements.

A diet high in red meat has been thought to increase heart disease risk, although a very recent study has cast doubt on this, suggesting that only processed meat increases heart disease risk. The study looked at one of the supposed factors in any possible heart disease-related risk from red or processed meat.

In a series of experiments, researchers found evidence that naturally occurring gut bacteria broke down L-carnitine into a product called trimethylamine-N-oxide (TMAO). TMAO is known to contribute towards the hardening of the arteries (atherosclerosis) – a major risk factor for heart disease.

Overall, this study provides some evidence of an association between L-carnitine and heart disease, not a direct cause and effect.

Even if L-carnitine does have this effect, sticking to current UK recommendations (no more than 70g of red or processed meat daily) would mean you were consuming only minimal levels of L-carnitine and therefore not at the level of risk seen by this research, which looked at much higher levels of L-carnitine consumption.

Where did the story come from?

The study was carried out by researchers from Cleveland Clinic in Ohio, US and was funded by various grants from the US National Institutes of Health. The study was published in the peer-reviewed journal, Nature Medicine.

The headline somewhat exaggerated the findings and implications of the research, but overall this story was covered appropriately in the media and coverage reported correctly that part of the study was carried out in mice.

The Mail Online deserves praise for providing a comprehensive and detailed, yet easy to understand, summary of what was a complex series of related experiments.

What kind of research was this?

This was a series of experimental studies looking at the effect of a nutrient called L-carnitine (found in red meat and dairy products) on heart disease risk.

The researchers wanted to assess (as previous research had suggested) whether naturally occurring bacteria converted L-carnitine into a waste product called TMAO (trimethylamine-N-oxide).

TMAO is thought to speed up the build-up of plaque in the arteries (known as atherosclerosis), which is a risk factor for heart disease.

Although the researchers carried out part of their investigations in humans, some testing was performed in mice. It is often difficult to interpret the results of animal research, and caution should be exercised when trying to generalise the findings to humans.

What did the research involve?

In this study. the researchers carried out a series of investigative tests on both humans and mice.

For the human tests, researchers gave the nutrient L-carnitine (found in red meat and dairy products) in the form of a supplement to 77 healthy volunteers, including 26 who were vegans or vegetarians. Some of the meat-eating volunteers were given an extra eight-ounce sirloin steak (equivalent to 180mg of L-carnitine).

The participants were then given antibiotics for one week to supress bacteria in the gut from converting L-carnitine into TMAO. They were then given L-carnitine again. Their blood and urine were tested at the start of the experiment and up to three weeks after ingestion of L-carnitine. Some people also had their faeces tested.

As part of their investigations, the researchers separately checked the levels of L-carnitine in the blood of 2,595 people who were having heart check-ups. They did this to see if there was an association between L-carnitine levels and known cardiovascular disease, or risk of a cardiovascular event (such as a heart attack).

Finally, the researchers looked at the build-up of plaque in the mice’s arteries by comparing a group of mice fed L-cartinine for 10 weeks with normally fed mice. Some of these mice were pre-treated with antibiotics.

What were the basic results?

The main results from this study include:

• Meat-eating volunteers produced more TMAO than vegans or vegetarians following ingestion of L-carnitine
• There was a significant association between L-carnitine concentrations and risk of cardiovascular event among people undergoing heart check-ups, but only in those that had high TMAO concentrations. The researchers noted that this result suggests that TMAO rather than L-carnitine is the main driver of this association.
• Faecal analysis showed significant associations of L-carnitine with levels of TMAO in the blood.
• Feeding L-carnitine to mice doubled the risk of the animal developing plaque build-up in the arterial walls, but only when they had their usual gut bacteria. When the animals were treated with gut-clearing antibiotics, L-carnitine in the diet did not lead to arterial wall build-up.

How did the researchers interpret the results?

One of the lead researchers, Dr Stanley Hazen from the Cleveland Clinic in Ohio, is reported as saying “discovery of a link between L-carnitine ingestion, gut microbiota metabolism and cardiovascular disease risk has broad health-related implications. Carnitine metabolism suggests a new way to help explain why a diet rich in red meat promotes atherosclerosis”.

He goes on to say that “a diet high in carnitine actually shifts our gut microbe composition to those that like carnitine, making meat eaters even more susceptible to forming TMAO and its artery-clogging effects. Meanwhile, vegans and vegetarians have a significantly reduced capacity to synthesize TMAO from carnitine, which may explain the cardiovascular health benefits of these diets”.

The study concludes that there is ‘public health relevance, as L-carnitine is a common over-the-counter dietary supplement’. In an accompanying press release, Dr Hazen recommends that people not use L-carnitine supplements unless advised to for medical reasons.

Conclusion

Links To The Headlines

Red meat nutrient used in weight-loss and muscle-building supplements could cause heart disease. Mail Online, April 7 2013

Red meat chemical 'damages heart', say US scientists. BBC News, April 8 2013

Eating a lot of red meat can cause heart disease. Daily Express, April 8 2013

Links To Science

Koeth RA, Wang Z, Levison BS, et al. Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis. Nature Medicine. Published online April 7 2013

A brisk walk is "healthier than running", The Guardian reports, while the Daily Mail more accurately claims that walking "is as good as a run for cutting the risk of heart disease".

This news was based on a large and long-term study of runners and walkers, which found that when the same total energy was used, both activities were associated with largely similar reductions in the risk of:

• high blood pressure
• high cholesterol
• diabetes
• possibly coronary heart disease (CHD)

The study does have limitations but, generally, it seems to confirm that moderate intensity exercise (such as brisk walking) has important health benefits.

For anyone now thinking that a stroll to the shops is as good as running the marathon, there is a catch. The study compared the reductions in risk associated with the same amount of energy expenditure, whether from walking or running. Running is a vigorous intensity exercise, meaning runners use more energy than walkers over the same period. Using up the equivalent energy in walking is always going to mean you’ll have to cover more ground.

Where did the story come from?

The study was carried out by researchers from the Lawrence Berkeley National Laboratory and Hartford Hospital, both in the US. It was funded by the US National Heart, Lung and Blood Institute.

The study was published in the peer-reviewed journal Arteriosclerosis, Thrombosis and Vascular Biology.

Generally, the science was reported accurately in the media, with the Mail correctly pointing out that those walking would have to spend the same amount of energy as those running to achieve the same benefits. The Mail also included a comment from an independent UK expert. The Guardian’s claim that walking is associated with greater health benefits than running was misleading. There was no significant difference between the benefits of running and those of walking.

What kind of research was this?

The research was based on two national cohort studies. It set out to examine whether equivalent energy expended on walking (a moderate intensity exercise) and running (a vigorous intensity exercise) was associated with equivalent reductions in risk of:

• high blood pressure
• high cholesterol
• diabetes
• coronary heart disease

The researchers say that while both moderate and vigorous physical intensity is recommended in national guidelines, it remains uncertain whether the same “dose” of both types has the same long-term health benefits.

What did the research involve?

Participants for national runners’ and national walkers’ health studies were originally recruited in 1998 and 1999, respectively, and they comprised more than 63,000 runners and 42,000 walkers. For the current research, 33,060 runners (21% men) and 15,945 walkers (51.4% men) participated. This was about half of the original runners and about a third of the original walkers. The participants were 18 to 80 years old and they completed baseline and regular follow-up questionnaires on their height, weight, medical history, lifestyle and education.

The participants were also asked how many miles they walked or ran each week and how many hours a week on average they spent on running, walking and other exercises. They were also asked for their usual pace (minutes per mile) during walking or running.

Researchers calculated from this their estimated energy expenditure, called the metabolic equivalent hours per day (or MET h/d). A MET is the measure of energy expended at rest, with 3-6 METs being the energy expended in moderate exercise. In this study the runners used up the equivalent of about 5.3 METs in an hour each day and the walkers 4.7.

During 6.2 years of follow-up, participants also self-reported any new diagnoses of high blood pressure, high cholesterol, diabetes and coronary heart disease (including heart attack and angina) or surgical treatment for CHD (including coronary artery bypass and coronary angioplasty). They also reported whether they had started medications for any of these conditions since the beginning of the study.

Researchers compared energy expenditure in both groups with the risks of these cardiovascular conditions occurring during follow-up. They analysed the data using standard statistical methods and adjusted their results for confounders such as age, sex, race, education and smoking.

What were the basic results?

For each MET h/d, running was associated with:

• a 4.2% reduction in the risk of high blood pressure
• a 4.3% reduction in the risk of high cholesterol  
• a 12.1% reduction in the risk of diabetes 
• a 4.5% reduction in the risk of CHD

The corresponding reductions for walking were:

• a 7.2% reduction in the risk of high blood pressure
• a 7.0% reduction in the risk of high cholesterol  
• a 12.3% reduction in the risk of diabetes
• a 9.3% reduction in the risk of CHD

Researchers also found that the more energy used the greater the reduction in risk of these conditions.

How did the researchers interpret the results?

The researchers say that the equivalent energy expenditure from walking and running exercise produced similar risk reductions for high blood pressure, high cholesterol, diabetes and possibly CHD.

They also point out that there were additional benefits associated with exceeding current US guidelines for exercise levels.

Conclusion

This large study appears to show that moderate exercise such as brisk walking is as beneficial for health as vigorous exercise such as running, when the same energy is expended.

This study had several limitations, including its dependence on people self-reporting both their exercise levels and whether they had been diagnosed with the conditions being studied. However, this may be unavoidable in cohort studies of this type.

As the comparison was made between the results of two separate cohort studies combined as one (an indirect comparison), it is possible that the populations differed by some factor other than the intensity of exercise and particularly in how the participants were selected for study. The researchers explain that both cohorts were recruited over the same time interval, using the same questionnaire (modified slightly for the different activities). They say that both studies used subscription lists to running and walking publications and running and walking events for recruitment and the same people carried out the surveys, all funded by the same grant. This negates some of the concerns about whether the studies can be compared.

If the results of this study hold true there are a few things to bear in mind. First, in order to get the health benefits, walking needs to be faster than a stroll. To achieve ‘moderate intensity exercise’ your heart rate needs to be raised and you should experience a mild sweat.

Adults need to do around 150 minutes of moderate intensity physical activity a week. The current advice for people trying to stay fit through walking is to try to walk 10,000 steps a day.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Brisk walk healthier than running – Scientists. The Guardian, April 5 2013

Walking IS as good for your health as running - but you'll need to do it for longer. Daily Mail, April 5 2013

Walking as good as jogging for your heart. The Times, April 5 2013

Links To Science

Williams PT, Thompson PD. Walking Versus Running for Hypertension, Cholesterol, and Diabetes Mellitus Risk Reduction. Arteriosclerosis, Thrombosis, and Vascular Biology. Published online April 4 2013

‘More bananas and fewer crisps can help ward off strokes’, the Daily Mail reports, saying a study has found that people with high potassium intake have a 24% reduced risk of stroke. Researchers are also reported to say that lowering salt intake could increase benefits further.

Advice to switch from eating crisps to eating bananas is sound, but do we really need to boost our potassium intake?

The headlines stem from a well-conducted systematic review of global evidence on the effects of higher potassium concentration on cardiovascular health in healthy adults.

Good quality evidence suggests that boosting potassium intake to the recommended daily levels is associated with a decrease in blood pressure (by a few mmHg) compared to lower intakes. However, this effect was only found for people with high blood pressure.

Other evidence suggested that higher potassium intake could reduce stroke risk by 24%. However, it’s unwise to draw firm conclusions from these studies about how people’s health is affected by increased potassium intake.

A balanced diet featuring lots of fruit, vegetables and protein should give you all the potassium you need, without the need for supplements. In fact, too much potassium can be harmful, particularly for people with kidney disease or those already on certain blood pressure drugs.

Before you start scoffing bananas or popping potassium pills, it may be wise to talk about your blood pressure with your GP.

Where did the story come from?

The focus of this appraisal is on a study into potassium, carried out by researchers from the World Health Organization’s (WHO) Department of Nutrition for Health and Development, Geneva, Switzerland and other institutions in the UK. Funding was provided by various sources, including WHO funds, the Kidney Evaluation Association Japan, and the governments of Japan and the Republic of Korea. The study was published in the peer-reviewed, British Medical Journal.

The news reports are generally representative of this research.

What kind of research was this?

This was a systematic review that aimed to examine the global literature looking at the effects of potassium intake on health.

The researchers claim that historically, humans tended to have a much higher intake of potassium – above 200mmol/day. Now our intake is much less, due to diets high in processed foods and low in fresh fruit and vegetables, they say, with intake in many countries below the WHO-recommended daily intake of 70 to 80mmol/day.

Because previous studies have linked lower potassium intake to increased risk of high blood pressure and stroke, the researchers consider that increasing potassium intake may help to reduce people’s risk of such chronic conditions.

The researchers say that previous reviews have had inconsistent findings. The WHO initiated the current review to systematically gather the results of studies in healthy adults and children without illnesses that could compromise the body’s potassium balance. The WHO did this to inform future guidelines. The researchers wanted to identify randomised controlled trials (RCTs) looking at:

• how increased potassium intake affected blood pressure, death from any cause and cardiovascular disease in apparently healthy adults
• how increased potassium intake affected blood pressure in apparently healthy children
• how increased potassium intake affected blood lipid (fat) concentrations, kidney function and hormones released from the adrenal glands (such as adrenaline) in apparently healthy adults and children
• what level of potassium intake would result in the maximum benefit for reducing blood pressure, and risk of death and cardiovascular diseases
• whether the effects of increased potassium are affected by factors such as people’s health, diet, or by the type of intervention used to help them increase their potassium intake

If insufficient RCTs were identified, the researchers planned to include less robust study designs, including non-randomised trials and observational studies.

What did the research involve?

The researchers used systematic review methods recommended by the Cochrane Collaboration. They searched numerous electronic databases and manually searched reference lists of studies and reviews. They identified randomised and non-randomised trials which had allocated at least one group of participants to increased potassium intake (intervention) and one group to lower potassium intake (control) for at least four weeks. To be included in the analyses, trials had to have measured potassium from urine samples collected every 24-hours (which can be used to estimate potassium intake). The researchers excluded studies involving:

• acutely ill people
• HIV-positive people
• people admitted to hospital
• people whose urinary potassium excretion was impaired due to a medical condition or drug treatment

Researchers were looking for outcomes related to blood pressure, all-cause mortality, all cardiovascular disease, and specifically stroke and coronary heart disease. They also looked at potential adverse effects of changes in concentrations of blood fat (cholesterol and triglycerides), concentrations of catecholamine (hormones such as adrenaline produced by the adrenal glands at the top of the kidneys) and kidney function. In children, the researchers wanted to find out about blood pressure, blood fats or catecholamine concentrations.

The researchers assessed studies for quality and risk of bias. Where possible, they pooled the results in meta-analyses to estimate the effects of higher potassium intake compared to lower.

What were the basic results?

The researchers identified 37 relevant studies, 35 of which were included in the meta-analysis. Of these, 22 were RCTs of adults, 11 were cohort studies of adults, and one was an RCT of children and one a cohort study of children. Due to the limited search results for children, the researchers broadened their inclusion criteria and identified a further RCT, one non-randomised study, and one additional cohort study in children. The two randomised trials in children included a total of 250 boys and girls aged 13-15 years.

Results for adults

The 22 RCTs in adults included 1,606 participants (individual study size 12 to 353 people) and were conducted across countries worldwide. In 20 studies, participants were given potassium supplements (as the intervention), in one study, participants were given potassium supplements and dietary advice or education, and in two studies the intervention was dietary advice or education alone. The cohort studies in adults included 127,038 people.

Links To The Headlines

Halve our salt intake and save millions of lives, says new report. The Independent, 5 April 2013

More bananas and fewer crisps can help ward off strokes, say scientists. Daily Mail, 5 April 2013

Cutting back on salt key to saving lives. Daily Express, 5 April 2013

Increase potassium and cut salt to reduce stroke risk. BBC News, 5 April 2013

Eat more bananas to reduce risk of stroke, say scientists. The Times, 5 April 2013

Links To Science

Anurto NJ, Hanson S, Gutierrez H, et al. Effect of increased potassium intake on cardiovascular risk factors and disease: systematic review and meta-analyses. BMJ. Published online 5 April 2013

He FJ, Li J, MacGregor GA. Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials. BMJ. Published online 5 April 2013