Published29 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy James GallagherHealth and science correspondentAn unprecedented analysis of how cancers grow has revealed an “almost infinite” ability of tumours to evolve and survive, say scientists. The results of tracking lung cancers for nine years left the research team “surprised” and “in awe” at the formidable force they were up against.They have concluded we need more focus on prevention, with a “universal” cure unlikely any time soon.Cancer Research said the study showed the importance of early detection.The study – entitled TracerX – provides the most in-depth analysis of how cancers evolve and what causes them to spread.Cancers change and evolve over time – they are not fixed and immutable. They can become more aggressive: better at evading the immune system and able to spread around the body. A tumour starts as a single, corrupted cell, but becomes a mixture of millions of cells that have all mutated in slightly different ways. TracerX tracked that diversity and how it changes over time inside lung cancer patients.”That has never been done before at this scale,” said Prof Charles Swanton, from the Francis Crick Institute and University College London.More than 400 people – treated at 13 hospitals in the UK – had biopsies taken from different parts of their lung cancer as the disease progressed.”It has surprised me how adaptable tumours can be,” Prof Swanton told me. “I don’t want to sound too depressing about this, but I think – given the almost infinite possibilities in which a tumour can evolve, and the very large number of cells in a late-stage tumour, which could be several hundred billion cells – then achieving cures in all patients with late-stage disease is a formidable task.” Image source, Michael BowlesProf Swanton said: “I don’t think we’re going to be able to come up with universal cures.”If we want to make the biggest impact we need to focus on prevention, early detection and early detection of relapse.” Obesity, smoking, alcohol and poor diet all increase the risk of some cancers. Tackling inflammation in the body is also being seen as a way of preventing cancer. Inflammation is the likely explanation for air pollution causing lung cancers and inflammatory bowel disease increasing the risk of colon cancer. Cancer rules rewritten by air-pollution discoveryThe evolutionary analysis has been published across seven separate studies in the journals Nature and Nature Medicine.The research showed:Highly aggressive cells in the initial tumour are the ones that ultimately end up spreading around the body Tumours showing higher levels of genetic “chaos” were more likely to relapse after surgery to other parts of the bodyAnalysing blood for fragments of tumour DNA meant signs of it returning could be spotted up to 200 days before appearing on a CT scanThe cellular machinery that reads the instructions in our DNA can become corrupted in cancerous cells making them more aggressive.The researchers hope the findings could, in the future, help them predict how a patient’s tumour will spread and to tailor treatment. Dr David Crosby, the head of prevention and early detection at Cancer Research UK, said: “The exciting results emerging from TracerX improve our understanding that cancer is a disease which evolves as it progresses, meaning that late-stage cancers can become very hard to treat successfully. “This underscores the crucial importance of further research to help us to detect cancers at the earliest stages of their development or even better, to prevent them from happening at all.” Follow James on Twitter.

Published19 March 2023Shareclose panelShare pageCopy linkAbout sharingBy James GallagherInside Health presenter, BBC Radio 4You cannot escape the hype around weight-loss injections. Social media is full of before-and-after pictures. They are the source of wild gossip about Hollywood stars, and now the UK’s National Health Service is going to pay for them. You can understand the appeal. Excess weight affects our health and leads to stigma – and the mantra of “diet and exercise” has simply failed for most people.But should we be calling semaglutide, the drug in question, a “miracle” or “skinny jab” when some doctors think it is as controversial as treatments get? Does the hype match the reality? Or are we failing to tackle the causes of obesity and just consigning people to a lifetime of medication?Jan, from Kent, was one of the first people in the world to take part in the trials of semaglutide. It is sold as Wegovy for weight-loss and as Ozempic for diabetes, although some people have been buying this version to lose weight. We all know somebody like Jan, who has tried every diet, and she has been battling her waistline her whole life.Semaglutide mimics a hormone that is released when we eat. It tricks the brain into thinking we are full and dials down appetite so we eat less. Once Jan started having the injections, her relationship with food was so transformational that she told me it was either down to the drug or “I’ve been abducted by aliens”.For the first time she could go into a cafe, see some millionaire’s shortbread and not have her body screaming, “I need one”. Instead it was, “I don’t feel hungry… my body was saying you don’t want it, it wasn’t me using willpower,” she says.The results of semaglutide are undeniable – at least for a while.On average, people who were obese lost about 15% of their body weight when taking semaglutide alongside healthy lifestyle advice in a trial. Note this is not a “skinny jab” – 15% takes you from 20 stone down to 17. That study showed the weight came off over the first year and then stabilised for the remaining three months of the trial. We do not know what happens when people take the drug for years.Jan lost 28kg (more than four stone). It meant she could finally enjoy her 60th birthday present – a flight in a Tiger Moth aeroplane, having been over the maximum weight limit before. “I was flying in more ways than one, and boy did I enjoy it.”The results seem more compelling than your typical diet, which often starts well but then your depleted fat stores signal to the brain to seek food. That is why diets ultimately fail.”More than 90% of people tend to end up back at the weight they were before they started on their dietary journey,” says Prof Sir Stephen O’Rahilly, the director of the Medical Research Council’s Metabolic Diseases Unit.He sees these drugs as the “beginning of an exciting era” where drugs can help people who have “struggled for a long time” with weight that is damaging their health. Jan’s trial concluded, and she was no longer able to take semaglutide. Without the drug her brain was no longer being tricked into thinking she was full.”I was quite upset because the weight was going back on,” she told me – and she was “promising the world” to anybody who could give her the drug. She tried other weight-loss injections, but ultimately chose to have major surgery and a gastric sleeve to reduce the size of her stomach, so she would feel full faster. Jan has “no regrets” and still describes the drug as the “best thing that ever happened to me”. The weight comes backHowever, her experience is far from unique and the weight gain after coming off semaglutide is swift. The best long-term data we have shows people regain two-thirds of their lost weight within two years of stopping. “It’s a drug that seems to need to be kept taken in order to ensure that weight doesn’t return and that’s, for me, a big problem,” says Dr Margaret McCartney, a GP and champion of evidence in medicine. The NHS is offering semaglutide for only two years, which is how long people can access weight loss clinics. Given the weight gain after coming off the drug, it is fair to ask – what is the point?”It’s really pretty awful for many people who are wanting to lose weight, and have struggled usually for years. If you get something that ends up working for you, and then for the NHS to go and withdraw that again, it does seem to me to be a bit unfair,” says Dr McCartney. There are, of course, circumstances where temporarily losing weight may be beneficial. Some surgeries and treatments are only offered to people below a set threshold, for example.It is a new drug and the long-term safety is unknown. Side effects include vomiting, fatigue and an inflamed pancreas. Medical victory or societal failure?Personally, I cannot figure out whether we should celebrate that medicine has produced such a drug, or if it is actually the opposite – that we have failed so badly to tackle obesity throughout society that we now need drugs.”Many of us have been wrestling with that,” says Naveed Sattar, professor of metabolic medicine at the University of Glasgow.He comes down on the side of pragmatism. Half the planet is projected to be overweight or obese by 2035, and excess weight is linked to type 2 diabetes, heart disease and some cancers. Cheap calories have “fed into human biology of being tempted by food and overeating”, he says.And many NHS patients “have four or five conditions as a result of their excess weight, and at the moment we pay lip service to it”, he says.Meanwhile government obesity policies in the UK – 14 of them in the past three decades – have not turned the tide and that has largely been felt by the poorest people in the country. There is a clear link between deprivation and obesity. Dr McCartney argues we need to tackle how the world we live in fuels obesity rather than “expecting” people to put on weight “and then accept a medical intervention to treat it”.Listen to Inside Health on BBC Sounds: Is this a new era in tackling obesity?Semaglutide is changing the landscape of obesity – and alternatives are on the way.Prof O’Rahilly says that even if we solve the societal causes of obesity “there will be obese people and they will become ill”, so he thinks the drugs will move us to a world of treating obesity “properly as a medical condition”.But these drugs remain controversial – and we have only discussed their use for improving health. Further concerns are being raised about the impact on people, often young women, who are pressured to look a certain way when “beautiful” is often equated to “thin”. The role of celebrity culture, the availability of semaglutide privately through online-only consultations, and the impact on eating disorders are also fuelling questions.Whatever you think about semaglutide, the debate around this drug, and the hype, is clearly not going away.Follow James on Twitter. Inside Health was produced by Erika Wright. More from Inside HealthCold: What does an unheated room do to your body?Exercise: What’s the least we can get away with?Covid: Have I dodged it and what does it mean?Multiple sclerosis: Is a virus we all have causing MS?Long Covid: ‘I’ve had long Covid for two years now’More on this storyAppetite drug could mark ‘new era’ in obesityPublished11 February 2021

Published1 day agoShareclose panelShare pageCopy linkAbout sharingBy James GallagherInside Health presenter, BBC Radio 4You cannot escape the hype around weight-loss injections. Social media is full of before-and-after pictures. They are the source of wild gossip about Hollywood stars, and now the UK’s National Health Service is going to pay for them. You can understand the appeal. Excess weight affects our health and leads to stigma – and the mantra of “diet and exercise” has simply failed for most people.But should we be calling semaglutide, the drug in question, a “miracle” or “skinny jab” when some doctors think it is as controversial as treatments get? Does the hype match the reality? Or are we failing to tackle the causes of obesity and just consigning people to a lifetime of medication?Jan, from Kent, was one of the first people in the world to take part in the trials of semaglutide. It is sold as Wegovy for weight-loss and as Ozempic for diabetes, although some people have been buying this version to lose weight. We all know somebody like Jan, who has tried every diet, and she has been battling her waistline her whole life.Semaglutide mimics a hormone that is released when we eat. It tricks the brain into thinking we are full and dials down appetite so we eat less. Once Jan started having the injections, her relationship with food was so transformational that she told me it was either down to the drug or “I’ve been abducted by aliens”.For the first time she could go into a cafe, see some millionaire’s shortbread and not have her body screaming, “I need one”. Instead it was, “I don’t feel hungry… my body was saying you don’t want it, it wasn’t me using willpower,” she says.The results of semaglutide are undeniable – at least for a while.On average, people who were obese lost about 15% of their body weight when taking semaglutide alongside healthy lifestyle advice in a trial. Note this is not a “skinny jab” – 15% takes you from 20 stone down to 17. That study showed the weight came off over the first year and then stabilised for the remaining three months of the trial. We do not know what happens when people take the drug for years.Jan lost 28kg (more than four stone). It meant she could finally enjoy her 60th birthday present – a flight in a Tiger Moth aeroplane, having been over the maximum weight limit before. “I was flying in more ways than one, and boy did I enjoy it.”The results seem more compelling than your typical diet, which often starts well but then your depleted fat stores signal to the brain to seek food. That is why diets ultimately fail.”More than 90% of people tend to end up back at the weight they were before they started on their dietary journey,” says Prof Sir Stephen O’Rahilly, the director of the Medical Research Council’s Metabolic Diseases Unit.He sees these drugs as the “beginning of an exciting era” where drugs can help people who have “struggled for a long time” with weight that is damaging their health. Jan’s trial concluded, and she was no longer able to take semaglutide. Without the drug her brain was no longer being tricked into thinking she was full.”I was quite upset because the weight was going back on,” she told me – and she was “promising the world” to anybody who could give her the drug. She tried other weight-loss injections, but ultimately chose to have major surgery and a gastric sleeve to reduce the size of her stomach, so she would feel full faster. Jan has “no regrets” and still describes the drug as the “best thing that ever happened to me”. The weight comes backHowever, her experience is far from unique and the weight gain after coming off semaglutide is swift. The best long-term data we have shows people regain two-thirds of their lost weight within two years of stopping. “It’s a drug that seems to need to be kept taken in order to ensure that weight doesn’t return and that’s, for me, a big problem,” says Dr Margaret McCartney, a GP and champion of evidence in medicine. The NHS is offering semaglutide for only two years, which is how long people can access weight loss clinics. Given the weight gain after coming off the drug, it is fair to ask – what is the point?”It’s really pretty awful for many people who are wanting to lose weight, and have struggled usually for years. If you get something that ends up working for you, and then for the NHS to go and withdraw that again, it does seem to me to be a bit unfair,” says Dr McCartney. There are, of course, circumstances where temporarily losing weight may be beneficial. Some surgeries and treatments are only offered to people below a set threshold, for example.It is a new drug and the long-term safety is unknown. Side effects include vomiting, fatigue and an inflamed pancreas. Medical victory or societal failure?Personally, I cannot figure out whether we should celebrate that medicine has produced such a drug, or if it is actually the opposite – that we have failed so badly to tackle obesity throughout society that we now need drugs.”Many of us have been wrestling with that,” says Naveed Sattar, professor of metabolic medicine at the University of Glasgow.He comes down on the side of pragmatism. Half the planet is projected to be overweight or obese by 2035, and excess weight is linked to type 2 diabetes, heart disease and some cancers. Cheap calories have “fed into human biology of being tempted by food and overeating”, he says.And many NHS patients “have four or five conditions as a result of their excess weight, and at the moment we pay lip service to it”, he says.Meanwhile government obesity policies in the UK – 14 of them in the past three decades – have not turned the tide and that has largely been felt by the poorest people in the country. There is a clear link between deprivation and obesity. Dr McCartney argues we need to tackle how the world we live in fuels obesity rather than “expecting” people to put on weight “and then accept a medical intervention to treat it”.Listen to Inside Health on BBC Sounds: Is this a new era in tackling obesity?Semaglutide is changing the landscape of obesity – and alternatives are on the way.Prof O’Rahilly says that even if we solve the societal causes of obesity “there will be obese people and they will become ill”, so he thinks the drugs will move us to a world of treating obesity “properly as a medical condition”.But these drugs remain controversial – and we have only discussed their use for improving health. Further concerns are being raised about the impact on people, often young women, who are pressured to look a certain way when “beautiful” is often equated to “thin”. The role of celebrity culture, the availability of semaglutide privately through online-only consultations, and the impact on eating disorders are also fuelling questions.Whatever you think about semaglutide, the debate around this drug, and the hype, is clearly not going away.Follow James on Twitter. Inside Health was produced by Erika Wright. More from Inside HealthCold: What does an unheated room do to your body?Exercise: What’s the least we can get away with?Covid: Have I dodged it and what does it mean?Multiple sclerosis: Is a virus we all have causing MS?Long Covid: ‘I’ve had long Covid for two years now’More on this storyAppetite drug could mark ‘new era’ in obesity11 February 2021

Published24 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy James GallagherHealth and science correspondentGiving young babies – between four and six months old – tiny tastes of smooth peanut butter could dramatically cut peanut allergies, say scientists. Research shows there is a crucial opportunity during weaning to cut allergy cases by 77%. They say the government’s advice on weaning – which says no solids until around six months – needs to change. Experts warn whole or chopped nuts and peanuts are a choking risk and should not be given to children under five.The current NHS guidance does say peanut (crushed, ground or butter) can be introduced from around six months old.A baby is ready for their first solid food if:they can stay in a sitting position, holding their head steadyco-ordinate their eyes, hands and mouth so they can look at their food, pick it up and put it in their mouthswallow food, rather than spit it back outWhy do food allergies happen?Peanut allergy has been rising in the UK with an estimated one-in-50 children now affected.Food allergies are the result of our immune system mistaking something harmless for a severe threat. For some, even a small amount of peanut can lead to such an overwhelming immune reaction that it becomes life-threatening. Peanut allergy has become so common that some schools ban the ingredient.There had been long-standing advice to avoid foods that can trigger allergies during early childhood. At one point, families were once told to avoid peanut until their child was three years old. However, evidence over the last 15 years has turned that on its head. Instead, eating peanut while the immune system is still developing – and learning to recognise friend from foe – can reduce allergic reactions, experts say. It also means the body’s first experience of peanut is in the tummy where it is more likely to be recognised as food rather than on the skin, where it may be more likely to be treated as a threat. Israel, where peanut snacks are common in early life, has much lower rates of allergy.Other studies have suggested introducing other foods linked to allergies – such as egg, milk and wheat – early also reduced allergy.Image source, Getty ImagesThe latest research, published in the Journal of Allergy and Clinical Immunology, calculated when is the best time to start introducing foods containing peanut.The analysis was conducted by the University of Southampton, King’s College London and the research arm of the NHS – the National Institute for Health and Care Research.They found the critical period to start was between four and six months, during which the allergy could be cut by 77%.That is the equivalent of preventing 10,000 out of the roughly 13,000 cases of peanut allergy each year.Delaying the introduction of peanut-based foods until the child was one-year-old would only cut allergy cases by 33%, according to the research.For babies with eczema, which is a risk factor for allergy, the investigators recommend starting at four months – as long as the baby is ready. They say parents should start by offering small amounts of fruit or vegetables. Then when the baby is comfortable, around three tablespoons of peanut butter a week should be introduced and maintained for years. Peanut butter, which can be quite dry, can be given with breastmilk.Prof Graham Roberts, from the University of Southampton, said decades of advice to avoid peanut had “understandably led to parental fear” of giving children peanut and shifting rules led to large amounts of confusion from both within medicine and from parents.However, he said this was a “simple, low-cost, safe intervention” that would “deliver vast benefits for future generations”.Official advice is to start offering solid foods alongside milk at around six months old, and the government has launched a campaign on the correct time to wean due to parents starting earlier.More on this storyParents worry after peanut allergy drug sales flop2 December 2022’If this works, I won’t worry about peanuts’28 June 2022Give peanut to babies early – advice5 January 2017Related Internet LinksJournal of Allergy and Clinical ImmunologyUS Guidance – Peanut allergy early exposureFood allergies in babies and young children – NHSAllergy UKThe BBC is not responsible for the content of external sites.

Published11 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Tim Betler, University of PittsburghBy James GallagherHealth and science correspondentElectrically stimulating the spinal cord instantly restores some ability to control the arm and hands in people who have had a stroke, US researchers say.Heather Rendulic, from Pittsburgh, was able to cut and eat a steak by herself for the first time in nine years. She said the technology was “nothing short of amazing”.The University of Pittsburgh team say more research is needed to see who can benefit, as the spinal implants have been tested in only two people.Strokes disrupt the blood supply in the brain and lead to brain cells dying. This often leaves those that survive with long-term health problems.People can retain the desire and intent to move but the instructions from the brain become so weak nothing happens.Never recoveredWhen Heather was in her early 20s, she was diagnosed with a cluster of abnormal blood vessels in her brain – a cavernous angioma. It bled multiple times and led to a large stroke. One morning, she woke up unable to move the left side of her body. In the nine years that followed, Heather learned to walk again but control of her left arm and hand never recovered – “something I struggle with every day”. Even the simplest tasks, such as putting on shoes, became a challenge. Before having the procedure, Heather’s goal was “to be able to cut a piece of steak”, as she relied on her husband to do it. Image source, Tim Betler, University of Pittsburgh Heather had electrodes implanted in her neck so parts of her spinal cord could be stimulated. The nervous system communicates with electricity – but after Heather’s stroke, the electrical signals travelling from her brain were too weak to activate the nerves controlling her arm and hand movements. Stimulation excites the nerves so they are already itching to respond – and now, those weak messages are enough to trigger movement. It worked on the first day and Heather was able to open and close her hand for the first time in nine years.’Started crying'”Nobody was expecting it would work that fast,” Dr Marco Capogrosso, from the University of Pittsburgh, told me.”She started crying, the family was there and they started crying and then all of us started crying, so it was a very, very emotional moment.”Heather was “moving my arm and hand in ways I haven’t for almost a decade”.And she got her steak. Image source, Tim Betler, University of PittsburghImage source, Tim Betler, University of PittsburghThe details, published in the journal Nature Medicine, showed the device worked in Heather and one other volunteer. However, the experiment was designed to last for only a month – after which, the electrodes were removed and the beneficial stimulation was gone. But the researchers say the results give a glimpse into the future, where implants could make meaningful differences to people’s lives. Dr Marco Capogrosso told me: “Our patients recover but they don’t become completely normal.”They can recover a lot of independence and a lot of quality of life, just because they can use their arm and hand now, even though they probably cannot play the piano.”The team believe the field could advance quickly as they are using technologies already approved for managing severe pain. But for now, it will take more clinical trials to work out who benefits and how to move the equipment from the laboratory to the home. Dr Rubina Ahmed from the Stroke Association said: “The research is still in the early stages and surgical implants may not be suitable for everyone. Non-invasive stimulation methods are also being tested which could be used by a wider range of people.” Follow James on Twitter.

Published13 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy James GallagherHealth and science correspondentA rapid test that can help preserve the hearing of newborn babies is set to be used by NHS hospitals. For some babies, commonly used antibiotics can become toxic. The drugs damage sensory cells inside the ear leading to permanent hearing loss. The test – which analyses babies’ DNA – can quickly spot those who are vulnerable.It means they can be given a different type of antibiotic and avoid having a lifetime of damaged hearing. Gentamicin is the first-choice antibiotic if a newborn develops a serious bacterial infection. It is life-saving and safe for the majority of people. However, it has a rare side effect. About 1,250 babies in England and Wales are born with a subtle change in their genetic code that allows the antibiotic to bind more strongly to the hair cells in their ears, where it becomes toxic.These tiny hairs help convert sounds into the electrical signals that are understood by the brain. If they are damaged, it results in hearing loss. The side effect is well known, but until now there was no test that could get the results fast enough. It would be dangerous to delay treatment, and alternative antibiotics are not used as they have their own side effects and because of concerns about antibiotic resistance.The new genedrive kit analyses a sample taken from inside the baby’s cheek. Tests at two neonatal intensive care units in Manchester and Liverpool showed it could spot who was susceptible to hearing loss in 26 minutes, and using it did not delay treatment.The National Institute for Health and Care Excellence (NICE) – which decides which drugs and technologies the NHS uses – has provisionally approved the test.Mark Chapman, interim director of medical technology at NICE, said: “Hearing loss has a substantial impact on the quality of the life of the baby and their family.”Having this test available to NHS staff can avoid the risk of hearing loss in babies with the variant who need treatment with antibiotics.”He also said the costs of treating hearing loss was “high”. Fitting a pair of cochlear implants – which use a microphone to convert sounds to an electrical signal – costs about £65,000. The NICE recommendations apply directly to England and Wales, but are often adopted more widely. The test will be made available as part of an early assessment to consider how well it works in a range of hospitals, and to see what impact it has on antibiotic use, before it gets final approval.Susan Daniels, chief executive of the National Deaf Children’s Society, said: “It’s very encouraging that more evidence will be gathered on this important development. “I hope this additional evidence will support the argument for the rollout of technology which could play a pivotal role in preventing deafness in a small number of babies in the future.”Follow James on TwitterMore on this storyMatching drugs to DNA is ‘new era of medicine’29 March 2022

Published33 minutes agoSharecloseShare pageCopy linkAbout sharingBy James GallagherHealth and science correspondentA teenage girl’s incurable cancer has been cleared from her body in the first use of a revolutionary new type of medicine. All other treatments for Alyssa’s leukaemia had failed. So doctors at Great Ormond Street Hospital used “base editing” to perform a feat of biological engineering to build her a new living drug.Six months later the cancer is undetectable, but Alyssa is still being monitored in case it comes back. Alyssa, who is 13 and from Leicester, was diagnosed with T-cell acute lymphoblastic leukaemia in May last year. T-cells are supposed to be the body’s guardians – seeking out and destroying threats – but for Alyssa they had become the danger and were growing out of control. Her cancer was aggressive. Chemotherapy, and then a bone-marrow transplant, were unable to rid it from her body. Without the experimental medicine, the only option left would have been merely to make Alyssa as comfortable as possible. “Eventually I would have passed away,” said Alyssa. Her mum, Kiona, said this time last year she had been dreading Christmas, “thinking this is our last with her”. And then she “just cried” through her daughter’s 13th birthday in January. Image source, Family PhotoImage source, Family PhotoWhat happened next would have been unthinkable just a few years ago and has been made possible by incredible advances in genetics. The team at Great Ormond Street used a technology called base editing, which was invented only six years ago. Bases are the language of life. The four types of base – adenine (A), cytosine (C), guanine (G) and thymine (T) – are the building blocks of our genetic code. Just as letters in the alphabet spell out words that carry meaning, the billions of bases in our DNA spell out the instruction manual for our body. Base editing allows scientists to zoom to a precise part of the genetic code and then alter the molecular structure of just one base, converting it into another and changing the genetic instructions. The large team of doctors and scientists used this tool to engineer a new type of T-cell that was capable of hunting down and killing Alyssa’s cancerous T-cells. They started with healthy T-cells that came from a donor and set about modifying them.The first base edit disabled the T-cells targeting mechanism so they would not assault Alyssa’s body The second removed a chemical marking, called CD7, which is on all T-cellsThe third edit was an invisibility cloak that prevented the cells being killed by a chemotherapy drugThe final stage of genetic modification instructed the T-cells to go hunting for anything with the CD7 marking on it so that it would destroy every T-cell in her body – including the cancerous ones. That’s why this marking has to be removed from the therapy – otherwise it would just destroy itself. If the therapy works, Alyssa’s immune system – including T-cells – will be rebuilt with the second bone-marrow transplant.CAR-T: ‘Living drug’ offers hope to terminal blood cancer patientsDesigner cells reverse one-year-olds cancerWhen the idea was explained to the family, mum Kiona was left thinking: “You can do that?” It was Alyssa’s decision to be the first to take the experimental therapy – which contained millions of the modified cells – in May this year.Image source, Great Ormond Street Hospital”She’s the first patient to be treated with this technology,” said Prof Waseem Qasim, from UCL and Great Ormond Street. He said this genetic manipulation was a “very fast-moving area of science” with “enormous potential” across a range of diseases. Alyssa was left vulnerable to infection, as the designer cells attacked both the cancerous T-cells in her body and those that protect her from disease. After a month, Alyssa was in remission and was given a second bone-marrow transplant to regrow her immune system. Alyssa spent 16 weeks in hospital and couldn’t see her brother, who was still going to school, in case he brought germs in. There were worries after the three-month check-up found signs of the cancer again. But her two most recent investigations have been clear. “You just learn to appreciate every little thing. I’m just so grateful that I’m here now,” said Alyssa. “It’s crazy. It’s just amazing I’ve been able to have this opportunity, I’m very thankful for it and it’s going to help other children, as well, in the future.”She’s eyeing-up Christmas, being a bridesmaid at her auntie’s wedding, getting back on her bike, going back to school and “just doing normal people stuff”.The family hope the cancer will never return, but are already grateful for the time it has bought them. “To have this extra year, this last three months when she’s been home, has been a gift in itself,” said Kiona.Dad James said: “I find it quite hard to talk about how proud we are. When you see what she’s gone through and her vitality of life she’s brought to every situation, it’s outstanding.”Most children with a leukaemia respond to the main treatments, but it is thought that up to a dozen a year could benefit from this therapy.Alyssa is just the first of 10 people to be given the drug as part of a clinical trial. Dr Robert Chiesa, from the bone-marrow transplant department at Great Ormond Street Hospital, said: “It is extremely exciting. Obviously, this is a new field in medicine and it’s fascinating that we can redirect the immune system to fight cancer.”The technology, though, only scratches the surface of what base editing could achieve.Dr David Liu, one of the inventors of base editing at the Broad Institute, told me it was “a bit surreal” that people were being treated just six years after the technology was invented. In Alyssa’s therapy, each of the base edits involved breaking a section of genetic code so it no longer worked. But there are more nuanced applications where instead of switching an instruction off you can fix a defective one. Sickle-cell anaemia, for example, is caused by just one base change that could be corrected.So there are already trials of base editing under way in sickle-cell disease, as well as high cholesterol that runs in families and the blood disorder beta-thalassemia.Dr Liu said the “therapeutic applications of base editing are just beginning” and it was “humbling to be part of this era of therapeutic human gene editing”, as science was now taking “key steps towards taking control of our genomes”.Follow James on Twitter.More on this story’Designer cells’ reverse baby’s cancer5 November 2015

Published30 minutes agoSharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesBy James GallagherHealth and science correspondentThe first drug to slow the destruction of the brain in Alzheimer’s has been heralded as momentous and historic.The research breakthrough ends decades of failure and shows a new era of drugs to treat Alzheimer’s – the most common form of dementia – is possible. Yet the medicine, lecanemab, has only a small effect and its impact on people’s daily lives is debated. And the drug works in the early stages of the disease, so most would miss out without a revolution in spotting it.Lecanemab attacks the sticky gunge – called beta amyloid – that builds up in the brains of people with Alzheimer’s. For a medical field littered with duds, despair and disappointment, some see these trial results as a triumphant turning point. Alzheimer’s Research UK said the findings were “momentous”. One of the world’s leading researchers behind the whole idea of targeting amyloid 30 years ago, Prof John Hardy, said it was “historic” and was optimistic “we’re seeing the beginning of Alzheimer’s therapies”. Prof Tara Spires-Jones, from the University of Edinburgh, said the results were “a big deal because we’ve had a 100% failure rate for a long time”.Dementia: Lifestyle changes that could lower your riskFresh clue to mystery of elderly super brains’Just like that – the woman I love changed’Calls for support for young Alzheimer’s sufferersCurrently, people with Alzheimer’s are given other drugs to help manage their symptoms, but none change the course of the disease.Lecanemab is an antibody – like those the body makes to attack viruses or bacteria – that has been engineered to tell the immune system to clear amyloid from the brain.Amyloid is a protein that clumps together in the spaces between neurons in the brain and forms distinctive plaques that are one of the hallmarks of Alzheimer’s.The large-scale trial involved 1,795 volunteers with early stage Alzheimer’s. Infusions of lecanemab were given every fortnight. The results, presented at the Clinical Trials on Alzheimer’s Disease conference in San Francisco and published in the New England Journal of Medicine, are not a miracle cure. The disease continued to rob people of their brain power, but that decline was slowed by around a quarter over the course of the 18 months of treatment. The data is already being assessed by regulators in the US who will soon decide whether lecanemab can be approved for wider use. The developers – the pharmaceutical companies Eisai and Biogen – plan to begin the approval process in other countries next year. David Essam, who is 78 and from Kent in the UK, took part in the international trial. His Alzheimer’s meant he had to give up work as a joiner – he could no longer remember how to build a cabinet or use his tools. He now uses a digital watch as he can’t tell time using a clock face. “He’s not the man he was, he needs help with most things, his memory in general is almost non-existent,” said his wife Cheryl. But she said the trial had given the family hope. David said: “If somebody can slow it [Alzheimer’s] down and eventually stop it all together that would be brilliant, it’s just a horrible nasty thing.”There are more than 55 million people in the world like David and the numbers with Alzheimer’s disease are projected to exceed 139 million by 2050.Will it make a difference?There is debate among scientists and doctors about the “real world” impact of lecanemab. The slower decline with the drug was noticed using ratings of a person’s symptoms. It’s an 18-point scale, ranging from normal through to severe dementia. Those getting the drug were 0.45 points better off. Prof Spires-Jones said that was a “small effect” on the disease, but “even though it is not dramatic, I would take it”. Dr Susan Kohlhaas, from Alzheimer’s Research UK, said it was a “modest effect… but it gives us a little bit of a foothold” and the next generation of drugs would be better.There are also risks. Brain scans showed a risk of brain bleeds (17% of participants) and brain swelling (13%). Overall, 7% of people given the drug had to stop because of side effects.A crucial question is what happens after the 18 months of the trial, and the answers are still speculation. Dr Elizabeth Coulthard, who treats patients at North Bristol NHS Trust, says that people have, on average, six years of living independently once mild cognitive impairment starts.Slow that decline by a quarter and it could equate to an extra 19 months of independent life, “but we don’t know that yet”, she says.It is even scientifically plausible that the effectiveness could be greater in longer trials. “I don’t think we can assume that this is it,” says Dr Kohlhass.The emergence of drugs that do alter the course of the disease asks big questions of whether the health service is ready to use them. The drugs have to be given early in the disease before too much damage to the brain is done, whereas most people referred to memory services are in the later stages of the disease. That requires people coming forward at the earliest signs of memory problems and doctors being able to send them for amyloid tests – either brain scans or spinal fluid analysis – to a determine if they have Alzheimer’s or another form of dementia. At the moment only 1-2% of people with dementia have such tests. “There’s an enormous gulf between current service provision and what we need to do, to deliver disease modifying therapies,” said Dr Coulthard.She said that, currently, only those living near big medical centres or paying privately were likely to benefit. Scientists also stressed that amyloid was only one part of the complex picture of Alzheimer’s disease and should not become the sole focus of therapies.The immune system and inflammation are heavily involved in the disease and another toxic protein called tau is the one that’s found where brain cells are actually dying. “That’s where I would put my money,” said Prof Spires-Jones. She added: “I’m very excited we’re on the cusp of understanding enough to get a hold of the problem and we should have something that will make a bigger difference in a decade or so.”Follow James on Twitter.More on this storyAlzheimer’s-slowing drug labelled historic28 September

Published2 days agoSharecloseShare pageCopy linkAbout sharingImage source, James GallagherBy James GallagherInside Health presenter, BBC Radio 4Mention deadly cold and I think of polar explorers with icicles dangling from their beards and mountaineers tackling the heights of Everest; of fingers turning black with frostbite and the chilling clutch of hypothermia. So I was sceptical when I was asked to take part in a cold experiment that took place at just 10 degrees Celsius. Yes, 10C.To me that’s mild, nowhere near freezing and certainly no Arctic blast. Surely we’d have to go much colder before putting a strain on the body? I was wrong.”It sounds mild, but it is a real physiological challenge,” Prof Damian Bailey, from the University of South Wales, tells me. He’s invited me to his laboratory to explore the impact of cold homes on our bodies and why such seemingly mild temperatures can become deadly. “Ten degrees is the average temperature that people will be living in, if they can’t afford to heat their homes,” said Prof Bailey.And as I was about to find out, 10C has a profound impact on the heart, lungs and brain. Listen to Inside Health podcast: How can a cool homes affect your health?I’m led into the environmental chamber in the corner of the laboratory – it’s all shiny metal walls and thick, heavy doors. In this air-tight room, scientists can precisely set the temperature, humidity and oxygen levels. I’m hit with a blast of warm 21C air. The plan is to start at 21C, drop the temperature down to 10C and chart how my body responds to the chill. First, I am wired up to countless state-of-the-art gizmos for the most in-depth analysis my body has ever faced.My chest, arms and legs are dotted with monitors to track my body temperature, heart rate and blood pressure.”You will look like something out of Star Wars,” says Prof Bailey as another sensor and trailing cable is attached to my body. A headset is fitted to monitor the blood flow in my brain just as the first beads of sweat breakout on my brow; an ultrasound inspects the carotid arteries in my neck (hearing the rhythmic whoosh of blood going to my brain is oddly reassuring) and I breathe into a huge tube that analyses the air I exhale. Image source, James GallagherThe measurements are done. The scientists know how my body performs in a pleasant 21C. So the fans kick in and a cool breeze gradually lowers the temperature in the chamber. “Your brain is tasting your blood as we speak and it’s tasting the temperature and the brain is now sending signals to the rest of your body,” Prof Bailey tells me. The goal is to keep my core – that’s my major organs including my heart and liver – at around 37C.I was still unaware of the profound changes happening inside my body, but there were already clues on the outside. By the time the room has dropped to 18C I was no longer sweating and the hairs on my arms were starting to stand up to help insulate my body. “Science tells us that 18 degrees is the tipping point… the body is now working to defend that core temperature,” Prof Bailey shouts over the droning fans.Next my fingers turn white and they feel cold. The blood vessels in my hands are being closed off – known as vasoconstriction – in order to keep my warm blood for my critical organs.This would happen even more quickly if I were a different gender. “Women do tend to feel the cold more, because of hormones (oestrogen) their blood vessels in their hands and feet are more likely to constrict… and that makes us feel cold,” says Dr Clare Eglin from the University of Portsmouth.My first shiver kicks in at 11.5C as my muscles begin to shake to generate heat.At 10C the fans shut down. I’m feeling uncomfortable, but not freezing as we repeated all the bodily measurements again at the lower temperature and it soon became clear I was wrong to doubt that 10C would affect me. “The body is working jolly hard at 10 degrees,” says Prof Bailey.What shocks me is the change in blood flow to the brain and how much longer it takes me to complete a shape-sorting game.I wouldn’t want to be trying to do school homework in a cold room or to have this compound something like dementia.”You’re delivering less blood to the brain, so there’s less oxygen and less glucose [sugar] getting into the brain and the downside of that is it’s having a negative impact on your mental gymnastics,” Prof Bailey says.But my body is achieving its main goal of keeping my core body temperature stable – it’s just having to do more work. I’m pumping warm blood around my body more intensely with my heart beating faster and blood pressure also shooting up. “That increasing blood pressure is a risk factor for a stroke, it’s a risk factor for a heart attack,” Prof Bailey tells me.The blood itself is also changing “so it becomes a bit like treacle”, says Prof Bailey, and this thicker gloopier blood also adds to the risk of a dangerous blockage.It’s why heart attacks and strokes are more common in the winter. Image source, James GallagherFortunately, I started off with “fabulous vasculature”, Prof Bailey tells me, but these internal changes are a risk to those who already have poor heart health and the elderly. “The evidence clearly suggests that cold is more deadly than the heat, there are a higher number of deaths caused through cold snaps than there are through the heat snaps,” says Prof Bailey.”So I really do think that more recognition needs to be paid for the dangers associated with cold.”Cold favours viruses tooThe cold also lends a helping hand to many infections that thrive in the winter months such as flu. Pneumonia, when there is inflammation in the lungs because of an infection, is more common after cold weather. It is easier for viruses to spread because we’re more likely to meet up indoors with the windows shut and no fresh air to blow viruses away. Cold also makes it easier for viruses to survive outside the body and cold air contains less virus-trapping moisture. Dry air allows viruses to travel further distances, says Prof Akiko Iwasaki, an immunobiologist from Yale University. She has also performed experiments showing breathing in cold air affects how the immune system works in the nose.Prof Iwasaki tells me: “At these cooler temperatures, your immune response becomes less active and this can allow virus to grow better within your nose.”What can you actually do about it?In an ideal world we’d all heat the room we’re in to at least 18C. When that is not possible, Prof Bailey says “it’s like preparing for a mountaineering expedition”.His tips are:focus on clothes that provide good insulation such as those made of woolgloves and warm socks are more important than a hat (but a woolly hat will help too)switch foods to a higher carbohydrate diet generate more body heat by moving around and not just sitting in a chair and watching TV.This video can not be playedTo play this video you need to enable JavaScript in your browser.Follow James on Twitter. Inside Health was produced by Gerry Holt. More from Inside HealthCovid: Have I dodged it and what does it mean?Multiple sclerosis: Is a virus we all have causing MS?Long Covid: ‘I’ve had long Covid for two years now’

Published9 hours agoSharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesBy James GallagherHealth and science correspondentLeprosy bacteria may hold the secret to safely repairing and regenerating the body, researchers at the University of Edinburgh say. Animal experiments have uncovered the bacteria’s remarkable ability to almost double the size of livers by stimulating healthy growth. It is a sneakily selfish act that gives the bacteria more tissue to infect. But working out how they do it could lead to new age-defying therapies, the scientists say.’Biological alchemy’ Leprosy causes disability when it infects the nerves, skin and eyes. Throughout history, those infected have been shunned. But the bacterium that causes it, Mycobacterium leprae, has other, unusual properties, including the ability to perform “biological alchemy”, converting one type of bodily tissue into another, which are fascinating scientists.So the researchers turned to the only other animals to catch the disease – armadillos. Image source, Getty ImagesThe infection heads to the armoured animals’ livers, where, the researchers found, it performed a controlled hijacking of the organ to reprogram it for its own purpose. “It was a totally unexpected,” Prof Anura Rambukkana, from the University of Edinburgh’s centre for regenerative medicine, told me.The results, published in Cell Reports Medicine, showed the liver nearly doubled in size. You might expect such growth to be defective or even cancerous – but detailed analysis showed it was both healthy and functional, complete with the usual array of blood vessels and bile ducts. “It is kind of mind-blowing,” Prof Rambukkana said. “How do they do that? There is no cell therapy that can do that.” Rapidly increaseIt appears the leprosy bug is rewinding the developmental clock in the liver. Fully grown liver cells are metabolic powerhouses with hundreds of jobs in the body. But the bacteria are taking them back a stage – like becoming a teenager again – where they can rapidly increase in number before maturing back into adulthood.Interrogating the activity of different parts of the cells’ DNA revealed a picture more akin to that of a much younger animal or even a fetus, when the liver is still forming. ‘Natural process’But the precise details of how this is all happening remain elusive. Nobel Prize-winning research has shown it is possible to forcibly turn the clock all the way back to the point at which cells regain the ability to become any other type of cell in the body – but this runs the risk of turning them cancerous. “The [leprosy] bugs use alternative pathways,” Prof Rambukkana told me. “It’s a much safer way and they take a longer time to do that, so this is a natural process.” ‘Promising results’The hope is the approach can be harnessed for repairing the livers of people waiting for a transplant – or even to reverse some of the damage caused by ageing elsewhere in the body. “The dream is to use the same bacterial strategy, to use the ingenuity of bacteria to generate new medicines for regeneration and repair,” Prof Rambukkana said.”If you can harness that, you should be able to turn that mechanism into a jab you have every three months or something.”All these ideas remain untested, however.Dr Darius Widera, of the University of Reading, said: “Overall, the results could pave the way for new therapeutic approaches to the treatment of liver diseases such as cirrhosis.”However, as the research has been done using armadillos as model animals, it is unclear if and how these promising results can translate to the biology of the human liver. “Moreover, as the bacteria used in this study are disease-causing, substantial refinement of the methods would be required prior to clinical translation.”Follow James on Twitter.