No, a standing desk isn’t as unhealthy as smoking

Does a new study really claim that standing at work is as unhealthy as a cigarette a day? Closer inspection suggests probably not

A headline in the Independent today has proclaimed that standing at work is as unhealthy as a cigarette a day, citing a new study published in the American Journal of Epidemiology. Illustrated with a picture of a woman bent over her standing desk clutching at her back, were instructed to sit back down.

But a closer look at the research in question reveals very little to do with standing desks. In fact, the study did not look at standing desks at all. The research was conducted on a sample of 7,320 residents of Ontario, Canada, followed up for over a decade. And its findings are striking people whose job requires them to stand for long periods of time were twice as likely to contract heart disease compared to those who do jobs that predominantly involve being seated.

So should we all lower our standing desks and recover our office chairs from wherever weve stashed them? I am not going to rush to do so (at this point I should fess up and say I have used a standing desk for the past three years and I love it).

Firstly, did the researchers ask people whether they stood or sat at work? No, they did not. People were categorised by the job they did. This immediately means that if youre an office worker with a standing desk, youll be categorised as a sitter, because thats predominantly what office workers do. The supplementary table of the paper lists a number of common jobs and how they were categorised for the study. Seated jobs included truck drivers, administrative officers, secretaries, professional occupations in business services and accounting clerks. Standing jobs on the other hand included retail salespersons, cooks, food and beverage servers and machine or tool operators.

Now here we get on to the classic problem with observational epidemiology. People who work different types of jobs are going to be different in loads of ways other than their jobs, all of which might also impact on risk of heart disease. This is called confounding. The authors of the study take a number of these in to account, for example pre-existing health conditions, whether the person smokes, whether they were obese, and various others. But its very hard to be sure that youve taken all of the potential confounding factors like these in to account. There could very easily be other differences rather than just whether a person is more likely to be standing or sitting. For example how much they exercise could have a big impact. Perhaps, as one person on Twitter suggested to me, after a day on your feet youre less inclined to go for a run of an evening.

Also, as can be seen from the list of jobs theyve included in each group, there might be socio-economic differences between people who do jobs that require standing at work and those who are more likely to sit and these might be related to how good your diet is, how much disposable income you have, all things that sadly are associated with ill health. Even if you attempt to take these factors in to account in a statistical model, if youre relying on self-reported or large scale data its almost impossible to be sure youve really accounted for all the variability.

So while this study is really interesting, and might indicate that jobs where youre more likely to stand are linked to an increased risk of heart disease, personally I think theres a little more going on than simply that we should all sit down at work if we want to protect our hearts. Not to mention that this study has absolutely nothing to do with standing desks, and didnt actually ask the individuals included whether they did stand or sit at work, but inferred it from the type of job they did. Im not lowering my standing desk just yet.

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New heart treatment is biggest breakthrough since statins, scientists say

US researchers find heart attack survivors given anti-inflammatory injections have fewer future episodes and lower cancer risk

Anti-inflammatory injections could lower the risk of heart attacks and may slow the progression of cancer, a study has found, in what researchers say is the biggest breakthrough since the discovery of statins.

Heart attack survivors given injections of a targeted anti-inflammatory drug called canakinumab had fewer attacks in the future, scientists found. Cancer deaths were also halved in those treated with the drug, which is normally used only for rare inflammatory conditions.

Statins are the mainstay drugs for heart attack prevention and work primarily by lowering cholesterol levels. But a quarter of people who have one heart attack will suffer another within five years despite taking statins regularly. It is believed this is because of unchecked inflammation within the hearts arteries.

The research team, led from Brigham and Womens hospital in Boston, tested whether targeting the inflammation with a potent anti-inflammatory agent would provide an extra benefit over statin treatment.

The researchers enrolled more than 10,000 patients who had had a heart attack and had a positive blood test for inflammation into the trial, known as the Cantos study. All patients received high doses of statins as well as either canakinumab or a placebo, both administered by injection every three months. The trial lasted for four years.

For patients who received the canakinumab injections the team reported a 15% reduction in the risk of a cardiovascular event, including fatal and non-fatal heart attacks and strokes. Also, the need for expensive interventional procedures, such as bypass surgery and inserting stents, was cut by more than 30%. There was no overall difference in death rates between patients on canakinumab and those given placebo injections, and the drug did not change cholesterol levels.

Dr Paul Ridker, who led the research team, said the study ushers in a new era of therapeutics.

For the first time, weve been able to definitively show that lowering inflammation independent of cholesterol reduces cardiovascular risk, he said.

This has far-reaching implications. It tells us that by leveraging an entirely new way to treat patients targeting inflammation we may be able to significantly improve outcomes for certain very high-risk populations.

The hospital said the reductions in risk were above and beyond those seen in patients who only took statins.

Ridker said the study showed that the use of anti-inflammatories was the next big breakthrough following the linkage of lifestyle issues and then statins.

In my lifetime, Ive gotten to see three broad eras of preventative cardiology, he said. In the first, we recognised the importance of diet, exercise and smoking cessation. In the second, we saw the tremendous value of lipid-lowering drugs such as statins. Now, were cracking the door open on the third era. This is very exciting.

But there were some downsides to the treatment. The researchers reported an increase in the chances of dying from a severe infection of about one for every 1,000 people treated, although this was offset by an unexpected halving of cancer deaths across all cancer types. In particular, the odds of succumbing to lung cancer were cut by over 75%, for reasons the team do not yet understand. The researchers are planning further trials to investigate canakinumabs potentially protective effect against cancer.

Prof Martin Bennett, a cardiologist from Cambridge who was not involved in the study, said the trial results were an important advance in understanding why heart attacks happen. But, he said, he had concerns about the side effects, the high cost of the drug and the fact that death rates were not better in those given the drug.

Treatment of UK patients is unlikely to change very much as a result of this trial, but the results do support investigation of other drugs that inhibit inflammation for cardiovascular disease, and the use of this drug in cancer, he said.

Prof Jeremy Pearson, associate medical director at the British Heart Foundation, was optimistic about the trial opening the door to new types of treatment for heart attacks.

Nearly 200,000 people are hospitalised due to heart attacks every year in the UK, Pearson said. Cholesterol-lowering drugs like statins are given to these people to reduce their risk of another heart attack and this undoubtedly saves lives. But we know that lowering cholesterol alone is not always enough.

These exciting and long-awaited trial results finally confirm that ongoing inflammation contributes to risk of heart disease, and [lowering it] could help save lives.

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6 million middle-aged people take no exercise

Public Health Englands research suggests large numbers of adults do not walk for 10 minutes at a time once a month

About 6 million middle-aged people in England are endangering their health by not taking so much as a brisk walk once a month, government advisers have said.

Clinicians said such a lack of exercise increases an individuals risk of prematurely developing serious health conditions including type 2 diabetes, heart disease, dementia and cancer.

Public Health England (PHE) said 41% of the 15.3 million English adults aged 40 to 60 walk less than 10 minutes continuously each month at a brisk pace of at least 3mph.

PHE has launched a health campaign targeting the sedentary middle-aged by encouraging them to walk to the shop instead of using a car and to take up walking on lunch breaks to add many healthy years to their lives.

Health leaders believe that 10 minutes walking a day is likely to be seen as achievable by people who are chronically inactive and that the health benefits include increased fitness, improved mood, a healthier body weight and a 15% reduction in the risk of dying prematurely.

PHE said walking required no skill, facilities or equipment and was more accessible and acceptable than other forms of physical activity for most people. Guidance issued by the UKs four chief medical officers in 2011 instructed the British population on how much exercise they should be participating in each week.

They said that adults should do at least two and a half hours of moderately intensive activity a week.

The PHE report said a quarter of the English population are inactive, doing less than 30 minutes of exercise a week. For some of these individuals 150 minutes may seem an unrealistic aim, according to the PHE report.

PHEs One You campaign is urging those people to take up the challenge of walking briskly for 10 minutes a day. As part of the drive it has released the Active 10 app which will help users achieve the goal and GPs will be recommending it to their patients to help build up their activity levels.

Dr Jenny Harries, the deputy medical director of PHE, said: I know first hand that juggling the priorities of everyday life often means exercise takes a back seat.
Walking to the shops instead of driving or going for a brisk 10-minute walk on your lunch break each day can add many healthy years to your life. The Active 10 app is a free and easy way to help anyone build more brisk walking into their daily routine.

Prof Sir Muir Gray, a clinical adviser for the Active 10 app and the One You campaign, added: We all know physical activity is good for your health but for the first time were seeing the effects that easily achievable changes can make. By walking just 10 continuous minutes at a brisk pace every day, an individual can reduce their risk of early death by 15%.

They can also prevent or delay the onset of disability and further reduce their risk of serious health conditions, such as type 2 diabetes, heart disease, dementia and some cancers.

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Forget five a day, eat 10 portions of fruit and veg to cut risk of early death

Scientists say even just 2.5 portions daily can lower chance of heart disease, stroke, cancer and premature death

Five portions of fruit and veg a day is good for you, but 10 is much better and could prevent up to 7.8 million premature deaths worldwide every year, say scientists.

The findings of the study led by Imperial College London may dismay the two in three adults who struggle to manage three or four portions perhaps some tomatoes in a sandwich at lunchtime, an apple and a few spoonfuls of peas at dinner.

All of that is good because a daily intake of even 200g, or two and a half standard 80g portions, is associated with a 16% reduced risk of heart disease, an 18% reduced risk of stroke, a 13% reduced risk of cardiovascular disease, 4% reduced risk of cancer and a 15% reduction in the risk of premature death.

But the study suggests we should be piling up platefuls of vegetables and raiding the fruit bowl every day if we want the best chance of avoiding chronic diseases or an early death.

We wanted to investigate how much fruit and vegetables you need to eat to gain the maximum protection against disease, and premature death. Our results suggest that although five portions of fruit and vegetables is good, 10 a day is even better, said Dr Dagfinn Aune, lead author of the research from the School of Public Health at Imperial.

Eating up to 800g of fruit and vegetables equivalent to 10 portions and double the recommended amount in the UK was associated with a 24% reduced risk of heart disease, a 33% reduced risk of stroke, a 28% reduced risk of cardiovascular disease, a 13% reduced risk of total cancer, and a 31% reduction in premature deaths.

What does 800g look like?

And not all fruit and veg are created equal. Apples and pears, citrus fruits, salads and green leafy vegetables such as spinach, lettuce and chicory, and cruciferous vegetables such as broccoli, cabbage and cauliflower were found to be best at preventing heart disease and stroke.

To reduce the risk of cancer, however, the menu should include green vegetables, such as green beans; yellow and orange vegetables such as peppers and carrots; and cruciferous vegetables.

The researchers did not find any difference between the protective effects of cooked and raw fruit and vegetables.

Fruit and vegetables have been shown to reduce cholesterol levels, blood pressure, and to boost the health of our blood vessels and immune system, said Aune. This may be due to the complex network of nutrients they hold. For instance they contain many antioxidants, which may reduce DNA damage, and lead to a reduction in cancer risk.

Compounds called glucosinolates in cruciferous vegetables, such as broccoli, activate enzymes that may help prevent cancer. Fruit and vegetables may also have a beneficial effect on the naturally occurring bacteria in our gut, he said.

Most people struggle to eat three or four portions a day, the study shows. Photograph: Simon Masters/Getty Images/Vetta

And it will not be possible to bottle the effects of fruit and vegetables or put them in a pill, he said. Forget the supplements. Most likely it is the whole package of beneficial nutrients you obtain by eating fruits and vegetables that is crucial to health, he said. This is why it is important to eat whole plant foods to get the benefit, instead of taking antioxidant or vitamin supplements (which have not been shown to reduce disease risk).

The analysis in the International Journal of Epidemiology pooled the results from 95 different studies involving a total of approximately 2 million people. They assessed up to 43,000 cases of heart disease, 47,000 cases of stroke, 81,000 cases of cardiovascular disease, 112,000 cancer cases and 94,000 deaths.

Aune said more research was needed, but it is clear from this work that a high intake of fruit and vegetables hold tremendous health benefits, and we should try to increase their intake in our diet.

Sarah Toule, from the World Cancer Research Fund, said: This interesting research shows just how incredibly important vegetables and fruit are as part of a healthy diet. In fact, theyre essential for maintaining a healthy weight, which our own evidence has shown reduces the risk of 11 common cancers.

People should aim to eat at least five portions of vegetables and fruit a day but the more the better. If people find this hard, why not start by adding an extra portion of fruit or veg a day to your lunch or try swapping one of your naughty snacks for a piece of fruit?

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Eating cheese does not raise risk of heart attack or stroke, study finds

Consumption of even full-fat dairy products does not increase risk, international team of experts says

Consuming cheese, milk and yoghurt even full-fat versions does not increase the risk of a heart attack or stroke, according to research that challenges the widely held belief that dairy products can damage health.

The findings, from an international team of experts, contradict the view that dairy products can be harmful because of their high saturated fat content. The experts dismiss that fear as a misconception [and] mistaken belief.

The results come from a new meta-analysis of 29 previous studies of whether dairy products increase the risk of death from any cause and from either serious heart problems or cardiovascular disease. The study concluded that such foodstuffs did not raise the risk of any of those events and had a neutral impact on human health.

This meta-analysis showed there were no associations between total dairy, high- and low-fat dairy, milk and the health outcomes including all-cause mortality, coronary heart disease or cardiovascular disease, says the report, published in the European Journal of Epidemiology.

Ian Givens, a professor of food chain nutrition at Reading University, who was one of the researchers, said: Theres quite a widespread but mistaken belief among the public that dairy products in general can be bad for you, but thats a misconception. While it is a widely held belief, our research shows that thats wrong.

Theres been a lot of publicity over the last five to 10 years about how saturated fats increase the risk of cardiovascular disease and a belief has grown up that they must increase the risk, but they dont.

However, the governments health advisers urged consumers to continue to exercise caution about eating too many products high in saturated fat and to stick to low-fat versions instead.

Dairy products form an important part of a healthy balanced diet; however, many are high in saturated fat and salt. Were all consuming too much of both, increasing our risk of heart disease, said a spokesman for Public Health England. We recommend choosing lower-fat varieties of milk and dairy products or eating smaller amounts to reduce saturated fat and salt in the diet.

Givens and colleagues from Reading, Copenhagen University in Denmark and Wageningen University in the Netherlands analysed 29 studies involving 938,465 participants from around the world undertaken over the last 35 years, including five done in the UK.

No associations were found for total (high-fat/low-fat) dairy and milk with the health outcomes of mortality, CHD or CVD, they said. In fact, they added, fermented dairy products may potentially slightly lower the risk of having a heart attack or stroke.

Doctors, public health experts and official healthy eating guidelines have for many years identified saturated fats as potentially harmful for heart and cardiovascular health and advised consumers to minimise their intake.

That has led to consumers increasingly buying lower-fat versions of dairy products. For example, 85% of all milk sold in the UK is now semi-skimmed or skimmed.

Givens said consumers were shunning full-fat versions of cheese, milk or yoghurt in the mistaken view that they could harm their health. Young people, especially young women, were now often drinking too little milk as a result of that concern, which could damage the development of their bones and lead to conditions in later life including osteoporosis, or brittle bones, he said. Consuming too little milk can deprive young people of calcium.

Pregnant women who drank too little milk could be increasing the risk of their child having neuro-developmental difficulties, which could affect their cognitive abilities and stunt their growth, Givens added.

The most recent National Diet and Nutrition Survey, the governments occasional snapshot of eating habits, found that dairy products, including butter, accounted for the highest proportion of saturated fat consumption in British diets 27%, compared with meats 24%. But if butter was not counted then dairy products together were the second largest source of saturated fat, at 22%.

Saturated fat is a vital part of diet. The NDNS found that adults typically got 34.6% of their total energy from fats as a whole, just below the 35% the government recommends. However, while total fat consumption was just within target, saturated fats still made up an unhealthily large proportion of total food energy 12.6%, against the recommended maximum of 11%.

Givens said: Our meta-analysis included an unusually large number of participants. We are confident that our results are robust and accurate.

The research was part-funded by the three pro-dairy groups Global Dairy Platform, Dairy Research Institute and Dairy Australia but they had no influence over it, the paper said. Givens is an adviser to the Food Standards Agency.

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A danger to public health? Uproar as scientist urges us to eat more salt

Exclusive: In a new book a US scientist claims eating more salt will make us healthier. But UK experts have condemned the advice as potentially dangerous

Public health experts in the UK have spoken out against a new book that claims many of us should be eating more salt, not less claiming the advice could endanger peoples health.

New York scientist James DiNicolantonio says in his book The Salt Fix that the World Health Organisation and the US and UK advisory bodies on diet have got it wrong with their advice to cut down on salt.

Salt is necessary and good for us, he says. Eating more salt will reduce the amount of sugar in our diet and help us lose weight, he says. Indeed low-salt diets may be causing brittle bones and memory loss and more salt could fix diabetes, he claims.

Instead of ignoring your salt cravings, you should give in to them they are guiding you to better health, he argues in his book, which has won attention for his ideas in the UK media. Most of us dont need to eat low-salt diets. In fact, for most of us, more salt would be better for our health rather than less.

Meanwhile, the white crystal weve demonized all these years has been taking the fall for another, one so sweet that we refused to believe it wasnt benign. A white crystal that, consumed in excess, can lead to high blood pressure, cardiovascular disease, and chronic kidney disease: not salt, but sugar.

But Public Health England (PHE), speaking out as promotion of DiNicolantonios book gathered pace in the UK, said his advice was not only wrong but dangerous. Prof Louis Levy, head of nutrition science at PHE, said: Diet is now the leading cause of ill health. By advocating a high-salt diet this book is putting the health of many at risk and it undermines internationally recognised evidence that shows a diet high in salt is linked to high blood pressure, a known risk for heart disease.

Our work with the food industry to cut the salt in food has already seen consumption in the UK reduce by 11% and is seen as the model to aspire to globally.

The row follows other diet controversies, such as the renewed debate over saturated fat and cholesterol. But the evidence on salt is incontrovertible, according to Graham MacGregor, a professor of cardiovascular medicine, who led the campaign for action on salt and health (CASH). That succeeded in persuading the government to take action by putting pressure on fast food companies to reduce the salt levels in their ready-meals, the biggest source of salt in our diets.

He is entitled to his views but it is all based on a few studies and they are misplaced, said MacGregor. It you look at the totality of the evidence on salt, it is much stronger than for sugar or saturated fat or fruit and vegetables in a positive way. Its overwhelming because weve got all the epidemiology, migration studies [where people have gone to live in another country and changed their diet], treatment trials, mortality trials and now outcome trials in countries.

Finland has reduced salt. The UK has and there have been big drops in heart deaths. You cant really argue against the importance of salt but you always get one or two people who deny it.

MacGregor, who now also runs Action on Sugar, says DiNicolantonio is probably quite well-meaning but is one of those who think every death on the world is because of sugar.

But DiNicolantonio, who is an associate editor of the journal BMJ Open Heart and a cardiovascular research scientist at Saint Lukes Mid America Heart Institute, says the evidence does not stack up, whatever bodies such as PHE and the American Heart Association (AHA) say. The AHA recommends no more than a teaspoon of salt a day equating to 2,300 milligrams of sodium and says most Americans should cut down to not much more than half of that.

Because the average Americans sodium intake is so excessive, even cutting back to no more than 2,400 milligrams a day will significantly improve blood pressure and heart health, it says, noting that 75% of intake comes from processed, packaged or restaurant food.

DiNicolantonio says there is no evidence that a low-salt diet will reduce blood pressure in the majority of people. Evidence in the medical literature suggests that approximately 80% of people with normal blood pressure (less than 120/80 mmHg) are not sensitive to the blood-pressure-raising effects of salt at all. Among those with prehypertension (a precursor to high blood pressure), roughly 75% are not sensitive to salt. And even among those with full-blown hypertension, about 55% are totally immune to salts effects on blood pressure, he writes.

The governments scientific advisory committee on nutrition (SACN), which backed a reduction to 6g of salt a day in the UK diet from around 9g, lists a large number of trials in animals and humans that suggest high salt levels do lead to higher blood pressure in its 2003 report. However, it could not come to conclusions on the numbers of cases of heart disease and deaths that might be caused, because the data was hard to collect.

But the National Institute for Health and Care Excellence, which looked at the impact of salt reduction for the population in 2013, said the governments strategy could lead to 20,000 fewer heart deaths each year.

DiNicolantonio also claims that we lose too much salt when we exercise or sweat in heatwaves. MacGregor says that is not so. There was a very good experiment with the SAS, parachuted into a desert, which found they needed quite a low salt intake. If you have a higher salt intake it is more dangerous. They had to carry more water with them because of thirst, he said.

Speaking to the Guardian, DiNicolantonio rejected the criticism from PHE that his book would make people risk their health, saying he was advocating for a normal salt intake, which he claims is between 3,000 and 6,000 mg of sodium per day. As sodium accounts for 40% of salt, that would equate to 7.5g to 15g of salt a day. But he says that is not a high salt diet. Moreover, if a high salt diet really put peoples health at risk then why are the highest salt-eating populations (Japan, South Korea, and France) living the longest with the lowest rates of coronary heart disease in the world? he said.

Low-salt diets are putting the population at risk as there are literally millions of people who are at risk of salt deficiency, with over six million people in the US alone diagnosed with low sodium levels in the blood every year.

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Deadly gene mutations removed from human embryos in landmark study

Groundbreaking project corrects faulty DNA linked to fatal heart condition and raises hopes for parents who risk passing on genetic diseases

Scientists have modified human embryos to remove genetic mutations that cause heart failure in otherwise healthy young people in a landmark demonstration of the controversial procedure.

It is the first time that human embryos have had their genomes edited outside China, where researchers have performed a handful of small studies to see whether the approach could prevent inherited diseases from being passed on from one generation to the next.

Crispr atom

While none of the research so far has created babies from modified embryos, a move that would be illegal in many countries, the work represents a milestone in scientists efforts to master the technique and brings the prospect of human clinical trials one step closer.

The work focused on an inherited form of heart disease, but scientists believe the same approach could work for other conditions caused by single gene mutations, such as cystic fibrosis and certain kinds of breast cancer.

This embryo gene correction method, if proven safe, can potentially be used to prevent transmission of genetic disease to future generations, said Paula Amato, a fertility specialist involved in the US-Korean study at Oregon Health and Science University.

The scientists used a powerful gene editing tool called Crispr-Cas9 to fix mutations in embryos made with the sperm of a man who inherited a heart condition known as hypertrophic cardiomyopathy, or HCM. The disease, which leads to a thickening of the hearts muscular wall, affects one in 500 people and is a common cause of sudden cardiac arrest in young people.

Humans have two copies of every gene, but some diseases are caused by a mutation in only one of the copies. For the study, the scientists recruited a man who carried a single mutant copy of a gene called MYBPC3 which causes HCM.

This sequence of images shows the development of embryos after injection of a gene-correcting enzyme and sperm from a donor with a genetic mutation known to cause hypertrophic cardiomyopathy. Photograph: (OHSU)/OHSY

When the scientists made embryos with the mans sperm and healthy eggs from donors, they found that, as expected, about half of the embryos carried the mutant gene. If the affected embryos were implanted into women and carried to term, the resulting children would inherit the heart condition.

Writing in the journal Nature, the researchers describe how gene editing dramatically reduced the number of embryos that carried the dangerous mutation. When performed early enough, at the same time as fertilisation, 42 out of 58 embryos, or 72%, were found to be free of the disease-causing mutation.

The work has impressed other scientists in the field because in previous experiments, gene editing has worked only partially, mending harmful mutations in some cells, but not others. Another problem happens when the wrong genes are modified by mistake, but in the latest work the scientists found no evidence of these so-called off target effects

Theyve got remarkably good results, its a big advance. said Richard Hynes, a geneticist at MIT who this year co-chaired a major report on human genome editing for the US National Academy of Sciences (NAS). This brings it closer to clinic, but theres still a lot of work to do.

Today, people who carry certain genetic diseases can opt for IVF and have their embryos screened for harmful mutations. The procedure can only help if there is a chance that some embryos will be healthy. According to Shoukhrat Mitalipov, who led the latest research, gene editing could bolster the number of healthy embryos available for doctors to implant.

More work is needed to prove that gene editing would be safe to do in people, but even if it seems safe, scientists face major regulatory hurdles before clinical trials could start. In the US, Congress has barred the Food and Drug Administration from even considering human trials with edited embryos, while in the UK it is illegal to implant genetically modified embryos in women. The procedure is controversial because genetic modifications made to an embryo affect not only the child it becomes but future generations too. Its still a long road ahead, said Mitalipov. Its unclear when wed be allowed to move on.

In the latest study, the mutation was corrected by a route that scientists have not seen before, with the cell copying healthy DNA from the mothers egg instead of the template. One question scientists need to explore now is whether mutations carried by eggs can be corrected as easily as those carried by sperm.

If all of this holds up for different genes and is also true when the mutation is inherited from the mother, it will be a major step forward, said Janet Rossant, senior scientist and chief of research emeritus at the Hospital for Sick Children in Toronto.

Asked about the potential for gene editing to produce designer babies, Rossant, a co-author of the NAS report on gene editing, said it was a distant prospect. We are still a long way from serious consideration of using gene editing to enhance traits in babies, she said. We dont understand the genetic basis of many of the human traits that might be targets for enhancement. Even if we did, a genetic alteration that enhanced one trait could have unexpected negative consequences on other traits, and this would be an inherited feature for the next generation.

The NAS report came out strongly against any form of gene editing designed to simply enhance human potential, she added.

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Robot hearts: medicines new frontier

The long read: From bovine valves to electrical motors and 3-D printed hearts, cardiologists are forging ahead with technologies once dismissed as crazy ideas

On a cold, bright January morning I walked south across Westminster Bridge to St Thomas Hospital, an institution with a proud tradition of innovation: I was there to observe a procedure generally regarded as the greatest advance in cardiac surgery since the turn of the millennium and one that can be performed without a surgeon.

The patient was a man in his 80s with aortic stenosis, a narrowed valve which was restricting outflow from the left ventricle into the aorta. His heart struggled to pump sufficient blood through the reduced aperture, and the muscle of the affected ventricle had thickened as the organ tried to compensate. If left unchecked, this would eventually lead to heart failure. For a healthier patient the solution would be simple: an operation to remove the diseased valve and replace it with a prosthesis. But the mans age and a long list of other medical conditions made open-heart surgery out of the question. Happily, for the last few years, another option has been available for such high-risk patients: transcatheter aortic valve implantation, known as TAVI for short.

This is a non-invasive procedure, and takes place not in an operating theatre but in the catheterisation laboratory, known as the cath lab. When I got there, wearing a heavy lead gown to protect me from X-rays, the patient was already lying on the table. He would remain awake throughout the procedure, receiving only a sedative and a powerful analgesic. I was shown the valve to be implanted, three leaflets fashioned from bovine pericardium (a tough membrane from around the heart of a cow), fixed inside a collapsible metal stent. After being soaked in saline it was crimped on to a balloon catheter and squeezed, from the size and shape of a lipstick, into a long, thin object like a pencil.

The consultant cardiologist, Bernard Prendergast, had already threaded a guidewire through an incision in the patients groin, entering the femoral artery and then the aorta, until the tip of the wire had arrived at the diseased aortic valve. The catheter, with its precious cargo, was then placed over the guidewire and pushed gently up the aorta. When it reached the upper part of the vessel we could track its progress on one of the large X-ray screens above the table. We watched intently as the metal stent described a slow curve around the aortic arch before coming to rest just above the heart.

There was a pause as the team checked everything was ready, while on the screen the silhouette of the furled valve oscillated gently as it was buffeted by pulses of high-pressure arterial blood. When Prendergast was satisfied that the catheter was precisely aligned with the aortic valve, he pressed a button to inflate the tiny balloon. As it expanded it forced the metal stent outwards and back to its normal diameter, and on the X-ray monitor it suddenly snapped into position, firmly anchored at the top of the ventricle. For a second or two the patient became agitated as the balloon obstructed the aorta and stopped the flow of blood to his brain; but as soon as it was deflated he became calm again.

Prendergast and his colleagues peered at the monitors to check the positioning of the device. In a conventional operation the diseased valve would be excised before the prosthesis was sewn in; during a TAVI procedure the old valve is left untouched and the new one simply placed inside it. This makes correct placement vital, since unless the device fits snugly there may be a leak around its edge. The X-ray picture showed that the new valve was securely anchored and moving in unison with the heart. Satisfied that everything had gone according to plan, Prendergast removed the catheter and announced the good news in a voice that was probably audible on the other side of the river. Just minutes after being given a new heart valve, the patient raised an arm from under the drapes and shook the cardiologists hand warmly. The entire procedure had taken less than an hour.

According to many experts, this is what the future will look like. Though available for little more than a decade, TAVI is already having a dramatic impact on surgical practice: in Germany the majority of aortic valve replacements, more than 10,000 a year, are now performed using the catheter rather than the scalpel.

In the UK, the figure is much lower, since the procedure is still significantly more expensive than surgery this is largely down to the cost of the valve itself, which can be as much as 20,000 for a single device. But as the manufacturers recoup their initial outlay on research and development, it is likely to become more affordable and its advantages are numerous. Early results suggest that it is every bit as effective as open-heart surgery, without many of surgerys undesirable aspects: the large chest incision, the heart-lung machine, the long period of post-operative recovery.

The essential idea of TAVI was first suggested more than half a century ago. In 1965, Hywel Davies, a cardiologist at Guys Hospital in London, was mulling over the problem of aortic regurgitation, in which blood flows backwards from the aorta into the heart. He was looking for a short-term therapy for patients too sick for immediate surgery something that would allow them to recover for a few days or weeks, until they were strong enough to undergo an operation. He hit upon the idea of a temporary device that could be inserted through a blood vessel, and designed a simple artificial valve resembling a conical parachute. Because it was made from fabric, it could be collapsed and mounted on to a catheter. It was inserted with the top of the parachute uppermost, so that any backwards flow would be caught by its inside surface like air hitting the underside of a real parachute canopy. As the fabric filled with blood it would balloon outwards, sealing the vessel and stopping most of the anomalous blood flow.

This was a truly imaginative suggestion, made at a time when catheter therapies had barely been conceived of, let alone tested. But, in tests on dogs, Davies found that his prototype tended to provoke blood clots and he was never able to use it on a patient.

Doctors perform minimally invasive heart surgery on a patient. Photograph: Steve Russell/Toronto Star via Getty Images

Another two decades passed before anybody considered anything similar. That moment came in 1988, when a trainee cardiologist from Denmark, Henning Rud Andersen, was at a conference in Arizona, attending a lecture about coronary artery stenting. It was the first he had heard of the technique, which at the time had been used in only a few dozen patients, and as he sat in the auditorium he had a thought, which at first he dismissed as ridiculous: why not make a bigger stent, put a valve in the middle of it, and implant it into the heart via a catheter? On reflection, he realised that this was not such an absurd idea, and when he returned home to Denmark he visited a local butcher to buy a supply of pig hearts. Working in a pokey room in the basement of his hospital with basic tools obtained from a local DIY warehouse, Andersen constructed his first experimental prototypes. He began by cutting out the aortic valves from the pig hearts, mounted each inside a home-made metal lattice then compressed the whole contraption around a balloon.

Within a few months Andersen was ready to test the device in animals, and on 1 May 1989 he implanted the first in a pig. It thrived with its prosthesis, and Andersen assumed that his colleagues would be excited by his works obvious clinical potential. But nobody was prepared to take the concept seriously folding up a valve and then unfurling it inside the heart seemed wilfully eccentric and it took him several years to find a journal willing to publish his research.

When his paper was finally published in 1992, none of the major biotechnology firms showed any interest in developing the device. Andersens crazy idea worked, but still it sank without trace.

Andersen sold his patent and moved on to other things. But at the turn of the century there was a sudden explosion of interest in the idea of valve implantation via catheter. In 2000, a heart specialist in London, Philipp Bonhoeffer, replaced the diseased pulmonary valve of a 12-year-old boy, using a valve taken from a cows jugular vein, which had been mounted in a stent and put in position using a balloon catheter.

In France, another cardiologist was already working on doing the same for the aortic valve. Alain Cribier had been developing novel catheter therapies for years; it was his company that bought Andersens patent in 1995, and Cribier had persisted with the idea even after one potential investor told him that TAVI was the most stupid project ever heard of.

Eventually, Cribier managed to raise the necessary funds for development and long-term testing, and by 2000 had a working prototype. Rather than use an entire valve cut from a dead heart, as Andersen had, Cribier built one from bovine pericardium, mounted in a collapsible stainless-steel stent. Prototypes were implanted in sheep to test their durability: after two-and-a-half years, during which they opened and closed more than 100m times, the valves still worked perfectly.

Cribier was ready to test the device in humans, but his first patient could not be eligible for conventional surgical valve replacement, which is safe and highly effective: to test an unproven new procedure on such a patient would be to expose them to unnecessary risk.

In early 2002, he was introduced to a 57-year-old man who was, in surgical terms, a hopeless case. He had catastrophic aortic stenosis which had so weakened his heart that with each stroke it could pump less than a quarter of the normal volume of blood; in addition, the blood vessels of his extremities were ravaged by atherosclerosis, and he had chronic pancreatitis and lung cancer. Several surgeons had declined to operate on him, and his referral to Cribiers clinic in Rouen was a final roll of the dice. An initial attempt to open the stenotic valve using a simple balloon catheter failed, and a week after this treatment Cribier recorded in his notes that his patient was near death, with his heart barely functioning. The mans family agreed that an experimental treatment was preferable to none at all, and on 16 April he became the first person to receive a new aortic valve without open-heart surgery.

Over the next couple of days the patients condition improved dramatically: he was able to get out of bed, and the signs of heart failure began to retreat. But shortly afterwards complications arose, most seriously a deterioration in the condition of the blood vessels in his right leg, which had to be amputated 10 weeks later. Infection set in, and four months after the operation, he died.

He had not lived long nobody expected him to but the episode had proved the feasibility of the approach, with clear short-term benefit to the patient. When Cribier presented a video of the operation to colleagues they sat in stupefied silence, realising that they were watching something that would change the nature of heart surgery.

When surgeons and cardiologists overcame their initial scepticism about TAVI they quickly realised that it opened up a vista of exciting new surgical possibilities. As well as replacing diseased valves it is now also possible to repair them, using clever imitations of the techniques used by surgeons. The technology is still in its infancy, but many experts believe that this will eventually become the default option for valvular disease, making surgery increasingly rare.

While TAVI is impressive, there is one even more spectacular example of the capabilities of the catheter. Paediatric cardiologists at a few specialist centres have recently started using it to break the last taboo of heart surgery operating on an unborn child. Nowhere is the progress of cardiac surgery more stunning than in the field of congenital heart disease. Malformations of the heart are the most common form of birth defect, with as many as 5% of all babies born with some sort of cardiac anomaly though most of these will cause no serious, lasting problems. The heart is especially prone to abnormal development in the womb, with a myriad of possible ways in which its structures can be distorted or transposed. Over several decades, specialists have managed to find ways of taming most; but one that remains a significant challenge to even the best surgeon is hypoplastic left heart syndrome (HLHS), in which the entire left side of the heart fails to develop properly. The ventricle and aorta are much smaller than they should be, and the mitral valve is either absent or undersized. Until the early 1980s this was a defect that killed babies within days of birth, but a sequence of complex palliative operations now makes it possible for many to live into adulthood.

Because their left ventricle is incapable of propelling oxygenated blood into the body, babies born with HLHS can only survive if there is some communication between the pulmonary and systemic circulations, allowing the right ventricle to pump blood both to the lungs and to the rest of the body. Some children with HLHS also have an atrial septal defect (ASD), a persistent hole in the tissue between the atria of the heart which improves their chances of survival by increasing the amount of oxygenated blood that reaches the sole functioning pumping chamber. When surgeons realised that this defect conferred a survival benefit in babies with HLHS, they began to create one artificially in those with an intact septum, usually a few hours after birth. But it was already too late: elevated blood pressure was causing permanent damage to the delicate vessels of the lungs while these babies still in the womb.

A prototype of a fully implantable artificial heart, as presented by the French heart specialist Alain Carpentier. Photograph: Jacques Brinon/AP

The logical albeit risky response was to intervene even earlier. In 2000, a team at Boston Childrens Hospital adopted a new procedure to create an ASD during the final trimester of pregnancy: they would deliberately create one heart defect in order to treat another. A needle was passed through the wall of the uterus and into the babys heart, and a balloon catheter used to create a hole between the left and right atria. This reduced the pressures in the pulmonary circulation and hence limited the damage to the lungs; but the tissues of a growing foetus have a remarkable ability to repair themselves, and the artificially created hole would often heal within a few weeks. Cardiologists needed to find a way of keeping it open until birth, when surgeons would be able to perform a more comprehensive repair.

In September 2005 a couple from Virginia, Angela and Jay VanDerwerken, visited their local hospital for a routine antenatal scan. They were devastated to learn that their unborn child had HLHS, and the prognosis was poor. The ultrasound pictures revealed an intact septum, making it likely that even before birth her lungs would be damaged beyond repair. They were told that they could either terminate the pregnancy or accept that their daughter would have to undergo open-heart surgery within hours of her birth, with only a 20% chance that she would survive.

Devastated, the VanDerwerkens returned home, where Angela researched the condition online. Although few hospitals offered any treatment for HLHS, she found several references to the Boston foetal cardiac intervention programme, the team of doctors that had pioneered the use of the balloon catheter during pregnancy.

They arranged an appointment with Wayne Tworetzky, the director of foetal cardiology at Boston Childrens Hospital, who performed a scan and confirmed that their unborn childs condition was treatable. A greying, softly spoken South African, Tworetzky explained that his team had recently developed a new procedure, but that it had never been tested on a patient. It would mean not just making a hole in the septum, but also inserting a device to prevent it from closing. The VanDerwerkens had few qualms about accepting the opportunity: the alternatives gave their daughter a negligible chance of life.

The procedure took place at Brigham and Womens Hospital in Boston on 7 November 2005, 30 weeks into the pregnancy, in a crowded operating theatre. Sixteen doctors, with a range of specialisms, took part: cardiologists, surgeons, and four anaesthetists two to look after the mother, two for her unborn child. Mother and child needed to be completely immobilised during a delicate procedure lasting several hours, so both were given a general anaesthetic. The team watched on the screen of an ultrasound scanner as a thin needle was guided through the wall of the uterus, then the foetuss chest and finally into her heart an object the size of a grape.

A guidewire was placed in the cardiac chambers, then a tiny balloon catheter was inserted and used to create an opening in the atrial septum. This had all been done before; but now the cardiologists added a refinement. The balloon was withdrawn, then returned to the heart, this time loaded with a 2.5 millimetre stent that was set in the opening between the left and right atria. There was a charged silence as the balloon was inflated to expand the stent; then, as the team saw on the monitor that blood was flowing freely through the aperture, the room erupted in cheers.

Grace VanDerwerken was born in early January after a normal labour, and shortly afterwards underwent open-heart surgery. After a fortnight she was allowed home, her healthy pink complexion proving that the interventions had succeeded in producing a functional circulation.

But just when she seemed to be out of danger, Grace died suddenly at the age of 36 days not as a consequence of the surgery, but from a rare arrhythmia, a complication of HLHS that occurs in just 5%. This was the cruellest luck, when she had seemingly overcome the grim odds against her. Her death was a tragic loss, but her parents courage had brought about a new era in foetal surgery.

Much of the most exciting contemporary research focuses on the greatest, most fundamental cardiac question of all: what can the surgeon do about the failing heart? Half a century after Christiaan Barnard performed the first human heart transplant, transplantation remains the gold standard of care for patients in irreversible heart failure once drugs have ceased to be effective. It is an excellent operation, too, with patients surviving an average of 15 years. But it will never be the panacea that many predicted, because there just arent enough donor hearts to go round.

With too few organs available, surgeons have had to think laterally. As a result, a new generation of artificial hearts is now in development. Several companies are now working on artificial hearts with tiny rotary electrical motors. In addition to being much smaller and more efficient than pneumatic pumps, these devices are far more durable, since the rotors that impel the blood are suspended magnetically and are not subject to the wear and tear caused by friction. Animal trials have shown promising results, but, as yet, none of these have been implanted in a patient.

Another type of total artificial heart, as such devices are known, has, however, recently been tested in humans. Alain Carpentier, an eminent French surgeon still active in his ninth decade, has collaborated with engineers from the French aeronautical firm Airbus to design a pulsatile, hydraulically powered device whose unique feature is the use of bioprosthetic materials both organic and synthetic matter. Unlike earlier artificial hearts, its design mimics the shape of the natural organ; the internal surfaces are lined with preserved bovine pericardial tissue, a biological surface far kinder to the red blood cells than the polymers previously used. Carpentiers artificial heart was first implanted in December 2013. Although the first four patients have since died two following component failures the results were encouraging, and a larger clinical trial is now under way.

Christiaan Barnard having dinner in Monte Carlo with Princess Grace of Monaco. Photograph: AP

One drawback to the artificial heart still leads many surgeons to dismiss the entire concept out of hand: the price tag. These high-precision devices cost in excess of 100,000 each, and no healthcare service in the world, publicly or privately funded, could afford to provide them to everybody in need of one. And there is one still more tantalising notion: that we will one day be able to engineer spare parts for the heart, or even an entire organ, in the laboratory.

In the 1980s, surgeons began to fabricate artificial skin for burns patients, seeding sheets of collagen or polymer with specialised cells in the hope that they would multiply and form a skin-like protective layer. But researchers had loftier ambitions, and a new field tissue engineering began to emerge.

High on the list of priorities for tissue engineers was the creation of artificial blood vessels, which would have applications across the full range of surgical specialisms. In 1999 surgeons in Tokyo performed a remarkable operation in which they gave a four-year-old girl a new artery grown from cells taken from elsewhere in her body. She had been born with a rare congenital defect which had completely obliterated the right branch of her pulmonary artery, the vessel conveying blood to the right lung. A short section of vein was excised from her leg, and cells from its inside wall were removed in the laboratory. They were then left to multiply in a bioreactor, a vessel that bathed them in a warm nutrient broth, simulating conditions inside the body.

After eight weeks, they had increased in number to more than 12m, and were used to seed the inside of a polymer tube which functioned as a scaffold for the new vessel. The tissue was allowed to continue growing for 10 days, and then the graft was transplanted. Two months later the polymer scaffold around the tissue, designed to break down inside the body, had completely dissolved, leaving only new tissue that would it was hoped grow with the patient.

At the turn of the millennium, a new world of possibility opened up when researchers gained a powerful new tool: stem cell technology. Stem cells are not specialised to one function but have the potential to develop into many different tissue types. One type of stem cell is found in growing embryos, and another in parts of the adult body, including the bone marrow (where they generate the cells of the blood and immune system) and skin. In 1998 James Thomson, a biologist at the University of Wisconsin, succeeded in isolating stem cells from human embryos and growing them in the laboratory.

But an arguably even more important breakthrough came nine years later, when Shinya Yamanaka, a researcher at Kyoto University, showed that it was possible to genetically reprogram skin cells and convert them into stem cells. The implications were enormous. In theory, it would now be possible to harvest mature, specialised cells from a patient, reprogram them as stem cells, then choose which type of tissue they would become.

Sanjay Sinha, a cardiologist at the University of Cambridge, is attempting to grow a patch of artificial myocardium (heart muscle tissue) in the laboratory for later implantation in the operating theatre. His technique starts with undifferentiated stem cells, which are then encouraged to develop into several types of specialised cell. These are then seeded on to a scaffold made from collagen, a tough protein found in connective tissue. The presence of several different cell types means that when they have had time to proliferate, the new tissue will develop its own blood supply.

Clinical trials are still some years away, but Sinha hopes that one day it will be possible to repair a damaged heart by sewing one of these patches over areas of muscle scarred by a heart attack.

Using advanced tissue-engineering techniques, researchers have already succeeded in creating replacement valves from the patients own tissue. This can be done by harvesting cells from elsewhere in the body (usually the blood vessels) and breeding them in a bioreactor, before seeding them on to a biodegradable polymer scaffold designed in the shape of a valve. Once the cells are in place they are allowed to proliferate before implantation, after which the scaffold melts away, leaving nothing but new tissue. The one major disadvantage of this approach is that each valve has to be tailor-made for a specific patient, a process that takes weeks. In the last couple of years, a group in Berlin has refined the process by tissue-engineering a valve and then stripping it of cellular material, leaving behind just the extracellular matrix the structure that holds the cells in position.

The end result is therefore not quite a valve, but a skeleton on which the body lays down new tissue. Valves manufactured in this way can be implanted, via catheter, in anybody; moreover, unlike conventional prosthetic devices, if the recipient is a child the new valve should grow with them.

If it is possible to tissue-engineer a valve, then why not an entire heart? For many researchers this has come to be the ultimate prize, and the idea is not necessarily as fanciful as it first appears.

In 2008, a team led by Doris Taylor, a scientist at the University of Minnesota, announced the creation of the worlds first bioartificial heart composed of both living and manufactured parts. They began by pumping detergents through hearts excised from rats. This removed all the cellular tissue from them, leaving a ghostly heart-shaped skeleton of extracellular matrix and connective fibre, which was used as a scaffold onto which cardiac or blood-vessel cells were seeded. The organ was then cultured in a bioreactor to encourage cell multiplication, with blood constantly perfused through the coronary arteries. After four days, it was possible to see the new tissue contracting, and after a week the heart was even capable of pumping blood though only 2% of its normal volume.

This was a brilliant achievement, but scaling the procedure up to generate a human-sized heart is made far more difficult by the much greater number of cells required. Surgeons in Heidelberg have since applied similar techniques to generate a human-sized cardiac scaffold covered in living tissue. The original heart came from a pig, and after it had been decellularised it was populated with human vascular cells and cardiac cells harvested from a newborn rat. After 10 days the walls of the organ had become lined with new myocardium which even showed signs of electrical activity. As a proof of concept, the experiment was a success, though after three weeks of culture the organ could neither contract nor pump blood.

A surgeon using a catheter during an operation. Photograph: Kent Nishimura/Denver Post via Getty Images

Growing tissues and organs in a bioreactor is a laborious business, but recent improvements in 3D printing offer the tantalising possibility of manufacturing a new heart rapidly and to order. 3D printers work by breaking down a three-dimensional object into a series of thin, two-dimensional slices, which are laid down one on top of another. The technology has already been employed to manufacture complex engineering components out of metal or plastic, but it is now being used to generate tissues in the laboratory. To make an aortic valve, researchers at Cornell University took a pigs valve and X-rayed it in a high-resolution CT scanner. This gave them a precise map of its internal structure which could be used as a template. Using the data from the scan, the printer extruded thin jets of a hydrogel, a water-absorbent polymer that mimics natural tissue, gradually building up a duplicate of the pig valve layer by layer. This scaffold could then be seeded with living cells and incubated in the normal way.

Pushing the technology further, Adam Feinberg, a materials scientist at Carnegie Mellon University in Pittsburgh, recently succeeded in fabricating the first anatomically accurate 3D-printed heart. This facsimile was made of hydrogel and contained no tissue, but it did show a remarkable fidelity to the original organ. Since then, Feinberg has used natural proteins such as fibrin and collagen to 3D-print hearts. For many researchers in this field, a fully tissue-engineered heart is the ultimate prize.

We are left with several competing visions of the future. Within a few decades it is possible that we will be breeding transgenic pigs in vast sterile farms and harvesting their hearts to implant in sick patients. Or that new organs will be 3D-printed to order in factories, before being dispatched in drones to wherever they are needed. Or maybe an unexpected breakthrough in energy technology will make it possible to develop a fully implantable, permanent mechanical heart.

Whatever the future holds, it is worth reflecting on how much has been achieved in so little time. Speaking in 1902, six years after Ludwig Rehn became the first person to perform cardiac surgery, Harry Sherman remarked that the road to the heart is only two or three centimetres in a direct line, but it has taken surgery nearly 2,400 years to travel it. Overcoming centuries of cultural and medical prejudice required a degree of courage and vision still difficult to appreciate today. Even after that first step had been taken, another 50 years elapsed before surgeons began to make any real progress. Then, in a dizzying period of three decades, they learned how to open the heart, repair and even replace it. In most fields, an era of such fundamental discoveries happens only once if at all and it is unlikely that cardiac surgeons will ever again captivate the world as Christiaan Barnard and his colleagues did in 1967. But the history of heart surgery is littered with breakthroughs nobody saw coming, and as long as there are surgeons of talent and imagination, and a determination to do better for their patients, there is every chance that they will continue to surprise us.

Main photograph: Getty Images

This is an adapted extract from The Matter of the Heart by Thomas Morris, published by the Bodley Head

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No such thing as ‘fat but fit’, major study finds

Metabolically healthy obese are 50% more likely to suffer heart disease than those of normal weight, finds University of Birmingham study

People who are obese run an increased risk of heart failure and stroke even if they appear healthy, without the obvious warning signs such as high blood pressure or diabetes, according to a major new study.

The findings, presented at the European Congress on Obesity in Porto, Portugal, may be the final death knell for the claim that it is possible to be obese but still metabolically healthy or fat but fit say scientists.

Several studies in the past have suggested that the idea of metabolically healthy obese individuals is an illusion, but they have been smaller than this one. The new study, from the University of Birmingham, involved 3.5 million people, approximately 61,000 of whom developed coronary heart disease.

The issue has been controversial. Obesity is usually measured by body mass index (BMI) a ratio of weight against height. It is generally agreed to be imperfect because athletes and very fit people with dense muscle can have the same BMI as somebody who is obese.

The scientists examined electronic health records from 1995 to 2015 in the Health Improvement Network a large UK general practice database. They found records for 3.5 million people who were free of coronary heart disease at the starting point of the study and divided them into groups according to their BMI and whether they had diabetes, high blood pressure [hypertension], and abnormal blood fats [hyperlipidemia], which are all classed as metabolic abnormalities. Anyone who had none of those was classed as metabolically healthy obese.

The study found that those obese individuals who appeared healthy in fact had a 50% higher risk of coronary heart disease than people who were of normal weight. They had a 7% increased risk of cerebrovascular disease problems affecting the blood supply to the brain which can cause a stroke, and double the risk of heart failure.

Dr Rishi Caleyachetty, who led the study, said it was true that weightlifters could be healthy and yet have a BMI that suggested they were obese. I understand that argument. BMI is crude but it is the only measure we have in the clinic to get a proxy for body fat. It is not realistic [to use anything else] in a GP setting or in the normal hospital clinic. We have to rely on BMI measurements, however crude they may be, he said.

While BMI results for particular individuals could be misleading, the study showed that on a population level, the idea that large numbers of people can be obese and yet metabolically healthy and at no risk of heart disease was wrong.

Caleyachetty said: The priority of health professionals should be to promote and facilitate weight loss among obese persons, regardless of the presence or absence of metabolic abnormalities.

At the population level, so-called metabolically healthy obesity is not a harmless condition and perhaps it is better not to use this term to describe an obese person, regardless of how many metabolic complications they have.

Last August a study from Sweden, which followed 1.3 million men over 30 years, found that those who were the fittest when they were 18 years old were 51% less likely to die prematurely than those who were the least fit. But if the men were obese, that cancelled out the advantage they had from their fitness in their youth.

Professor Peter Nordstrom, who led the study published in the International Journal of Epidemiology, said at the time: These results suggest low BMI early in life is more important than high physical fitness with regard to reducing the risk of early death.

Professor Timothy Gill from the Boden Institute of Obesity, Nutrition, Exercise and Eating Disorders at the University of Sydney, Australia, said that there would always be some people who remain healthy in spite of obesity, just as there are some lifetime smokers who do not get lung cancer.

I think you can argue that there are still likely to be some people who are not going to suffer the ill-health consequences as much as other people just because of the distribution of risk, he said.

The World Obesity Federation has this month officially recognised obesity as a disease because of the wide variety of health problems associated with it.

Susannah Brown, senior scientist at World Cancer Research Fund, said the studys finding, emphasise the urgent need to take the obesity epidemic seriously.

As well as increasing your risk of cardiovascular disease, being overweight or obese can increase your risk of 11 common cancers, including prostate and liver. If everyone were a healthy weight, around 25,000 cases of cancer could be prevented in the UK each year.

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L Arginine Benefits Erectile Dysfunction Blood Pressure Weight Loss Bodybuilding Vestige Hindi Best

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L-arginine is a chemical building block called "an amino acid." It is obtained from the diet and is necessary for the body to make proteins. L-arginine is found in red meat, poultry, fish, and dairy products. It can also be made in a laboratory and used as medicine.


L-arginine is used for heart and blood vessel conditions including congestive heart failure (CHF), chest pain, high blood pressure, and coronary artery disease. L-arginine is also used for recurrent pain in the legs due to blocked arteries (intermittent claudication), decreased mental capacity in the elderly (senile dementia), erectile dysfunction (ED), and male infertility.


Some people use L-arginine for preventing the common cold, improving kidney function after a kidney transplant, high blood pressure during pregnancy (pre-eclampsia), improving athletic performance, boosting the immune system, and preventing inflammation of the digestive tract in premature infants.

L-arginine is used in combination with a number of over-the-counter and prescription medications for various conditions. For example, L-arginine is used along with ibuprofen for migraine headaches; with conventional chemotherapy drugs for treating breast cancer; with other amino acids for treating weight loss in people with AIDS; and with fish oil and other supplements for reducing infections, improving wound healing, and shortening recovery time after surgery.

Some people apply L-arginine to the skin to speed wound healing and for increasing blood flow to cold hands and feet, especially in people with diabetes. It is also used as a cream for sexual problems in both men and women.

How does it work?

L-arginine is converted in the body into a chemical called nitric oxide. Nitric oxide causes blood vessels to open wider for improved blood flow. L-arginine also stimulates the release of growth hormone, insulin, and other substances in the body.


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