Tag: health

  • Patients Are Turning to Vibrators to Relieve Their Migraines

    Patients Are Turning to Vibrators to Relieve Their Migraines

    [ad_1]

    My friend Jack suffers from the most terrible migraines. But he has an unusual solution. When his migraine starts, he lays down and gently straps a vibrator to the top of his forehead. He swears that it offers instant relief from the pain.

    Though unconventional, Jack’s idea has historic roots. In 1892, neurologist Jean-Martin Charcot observed that Parkinson’s patients showed improvements in their tremors after prolonged carriage rides. He attributed this to rhythmic vibrations and fashioned a “fauteuil trepidant”—a shaking chair, which replicated the movement. His student, Georges Gilles de la Tourette, later extended the technique to treat migraines using a vibrating helmet. Both therapies provided “a powerful sedative for the nervous system,” wrote Charcot.

    Though these early inventions fell out of favor, recent studies are revisiting the potential of vibration therapy for treating migraines, and are starting to reveal why vibration might be the breakthrough migraine sufferers have been seeking. “Some of the people using vibration as a therapy for migraine are experiencing huge benefits, it’s very exciting to see,” says Tie-Quang Li at the Karolinska Institute in Stockholm, Sweden, who has investigated the effects of vibration on migraines.

    Despite migraines affecting an estimated 1 billion people worldwide, we know very little about how they are caused or how to treat them. Migraines usually begin with an aura—visual disturbances such as flashing lights or shimmering spots—followed by pain, blurred vision, nausea, and sensitivity to light.

    While the exact causes of migraine remain unclear, focus has shifted from early theories that blamed dilated blood vessels to the role of the hypothalamus, a brain structure that is involved with pain messages, and inflammation of the meninges, the three layers of tissue that protect the brain and spinal cord. Current migraine drugs constrict blood vessels or block receptors in the pain network, but they don’t work for everyone and can cause side effects.

    This has led many to explore alternative remedies, such as vibration therapy. Online forums are full of similar anecdotes to Jack’s. “I massaged my neck with a vibrator, and it completely removed the migraine pain I had been suffering with for years,” wrote one Reddit user.

    While some research posits that vibration simply distracts from the pain, recent evidence suggests more is going on. In the first trial of its kind, Jan-Erik Juto and Rolf Hallin at the Karolinska Institute inserted a catheter with a vibrating balloon into the nostril of migraine sufferers at the start of an attack. The volunteers recorded their migraine pain before, during, and after the 15-minute treatment.

    The small pilot study showed promise: 17 out of 18 people reported at least 50 percent pain relief, compared with three of 17 people who received a placebo treatment. Moreover, half of the people who received the treatment were completely pain-free 15 minutes after it finished, compared with only two in the placebo group.

    In the paper, Juto and Hallin speculate that nasal vibration targets a collection of nerve cells called the sphenopalatine ganglion, or SPG. Located just under the nasal membrane, the SPG is connected to the hypothalamus. During a migraine attack, the hypothalamus is thought to lose control over a collection of structures in the brain called the limbic system, which affects how a person responds to pain. By stimulating the SPG and indirectly the hypothalamus, vibration may help restore control.

    [ad_2]

    Source link

  • Why Women Get Migraines More Than Men

    Why Women Get Migraines More Than Men

    [ad_1]

    Migraine attacks are no ordinary headache. They can cause intense pain and sickness, lasting hours or even days, making it impossible to do anything but rest in a dark, quiet room. And for millions of women, these debilitating attacks aren’t just an occasional experience but a recurring ordeal.

    Women suffer from migraines three times as often as men, with episodes that are more prolonged and intense. “It’s far more common than most people realize,” says Anne MacGregor, a specialist in headache and women’s health. Despite various treatment options, migraines remain the leading cause of disability-adjusted life years (DALYs)—a measure of disease burden that accounts for time lost to ill health—for women between the ages of 15 and 49. While there’s still some mystery around how migraines work, one reason for this sex difference is hormones.

    During early childhood, boys are slightly more prone to migraines than girls, but puberty tips the balance dramatically. At this time, sex hormones begin to fluctuate and trigger physical changes including the onset of menstruation. This is often when girls experience their first migraine. From puberty onwards, girls experience migraines at a higher rate than boys, with this disparity growing more pronounced as people reach their mid-thirties and persisting into late life. “It’s chaotic at the two ends of a woman’s reproductive years,” MacGregor says.

    In adulthood, many women who suffer from migraines report experiencing attacks associated with their menstrual cycle. A sudden drop in estradiol—a potent form of estrogen—is thought to play a key role. A few days before menstruation, known as the late luteal phase, estradiol levels plummet. Women who are susceptible to migraines tend to experience a faster rate of estradiol decline around the time of their period compared to women who don’t. While estrogen drops around ovulation, too, the decline is not as rapid, which might explain why migraines aren’t as common at this time. The role of estrogen has also been observed in transgender women on hormone therapy, who show similar migraine frequency to cisgender women.

    Periods of fluctuating estrogen are also tied to migraines in women. As women hit perimenopause, the transitional period leading up to menopause, hormones become especially erratic. “Those women who didn’t particularly have menstrual migraine beforehand become more likely to experience it during perimenopause,” MacGregor says. After menopause, some experience relief. “But it’s important to say that patterns are variable—not everyone gets better,” says Richard Lipton, a neurologist and epidemiologist at the Albert Einstein College of Medicine in New York.

    Estrogen’s link to migraine is well documented, but researchers don’t yet fully understand how it contributes to the onset and progression of migraine. Lipton explains that migraine is a disorder characterized by a sensitive brain. “When I say sensitive, I mean vulnerable to exogenous factors that make migraine more likely,” he says. Something like a change in hormones can trigger a reaction.

    But estrogen doesn’t act alone. Changing estrogen levels also influence other hormones such as serotonin, which typically protects against migraine by lowering pain sensitivity. When estrogen levels drop, so do serotonin levels, increasing the likelihood of migraine. Triggers also act in tandem. When enough factors align—such as the drop in estrogen, combined with a lack of sleep, irregular meals, dehydration, or stress— an attack can ensue.

    [ad_2]

    Source link

  • Adaptogenic drinks: The Race to Make Your Coffee Do More and More

    Adaptogenic drinks: The Race to Make Your Coffee Do More and More

    [ad_1]

    While Four Sigmatic smuggles its adaptogens directly into coffee grounds, many adaptogenic drinks pitch themselves as something alternative, often with a lower caffeine content. UK-based Spacegoods’ Rainbow Dust, unmissable in bright pink and purple packaging, contains 80 milligrams—less than most coffees. Its ingredients list boasts lion’s mane, cordyceps, and chaga mushrooms, alongside other plant-based adaptogens ashwagandha, maca root, and rhodiola rosea. It’s a lot to pack into a spoon of powder, which comes in flavor options of chocolate, coffee, strawberry, vanilla cinnamon, and a decaffeinated raw cocoa variety.

    A bag and scoop with brown powder

    Courtesy of Spacegoods

    Ecommerce entrepreneur Matthew Kelly launched the brand in 2022 following the failure of his previous business, an online neon sign retailer that went into administration in 2021. Kelly came across functional mushrooms while scrambling to figure out his next move.

    Kelly’s ecommerce background is clear in Spacegoods’ online presence. Like many of the direct-to-consumer functional drink brands, the company heavily promotes a subscription model, and after purchasing some Rainbow Dust I found myself chased by Instagram ads and marketing emails promising all sorts of benefits.

    Kelly admits that advertising adaptogenic drinks requires treading a delicate line. Manufacturers want to shout about their products’ potential benefits, but the UK’s Advertising Standards Authority forbids claims that food products could prevent, treat or cure human disease; various brands have had to pull ads that mention health conditions such as anxiety, dementia, or ADHD.

    I tried the original chocolate flavor of Rainbow Dust and found it to be sickly sweet. Granted, it didn’t taste like mushrooms, but it didn’t exactly put me in mind of a health drink. Kelly concedes that pitching a chocolate-flavored drink as an improvement on coffee may have confused some buyers; he prefers the coffee flavor, introduced this year.

    Those with a more grown-up palate may wish to try US brand MUD\WTR—a name founder Shane Heath says was inspired by his colleagues’ reactions to his homemade prototypes and which ended up having “natural virality.” A former caffeine junkie, Heath turned to coffee alternatives after noticing negative effects on his sleep and mood. His tagline: “I wasn’t mad at coffee, just disappointed.”

    Whisk Assessment

    The original version of MUD\WTR contains only 35 milligrams of caffeine, alongside lion’s mane, cordyceps, chaga, and reishi mushrooms, as well as a few other ingredients. Its real winning formula, however, is in its cacao and masala chai flavoring. The natural earthiness of the spices cleverly masks any unpleasant mushroom taste. Made by mixing with either hot water or milk, it’s not anything like coffee but still feels sophisticated (although I did find quite a lot of sediment settled to the bottom of the cup).

    I initially scoffed at the company’s insistence on selling its powder in a starter kit containing a mini electric frother, but as I whisked up a cup, I recalled Spector’s observation about the role of ritual in amplifying perceived benefits and wondered if this additional preparation step was in fact a shrewd decision. It forced a pause which in itself inspired focus—Right, I’m going to whisk up this drink and then sit down to write that story. I’m pretty sure my ensuing productive writing session was largely a result of the placebo effect, but I’ll take it.

    [ad_2]

    Source link

  • The Multiple Ways Climate Change Threatens to Make Migraines Worse

    The Multiple Ways Climate Change Threatens to Make Migraines Worse

    [ad_1]

    Migraines have long had an intimate relationship with the elements. Alongside stress and hormones, fluctuations in meteorological conditions are one of the most commonly cited triggers for an attack. “Patients will often say that they can predict the weather,” says Vincent Martin, director of the Headache and Facial Pain Center at University of Cincinnati and president of the US National Headache Foundation. They may foresee rainfall two or three days out, as a blossoming migraine alerts them to a drop in barometric pressure.

    Martin has researched the impact of temperature and other weather conditions on migraines, and he believes the climate crisis—which brings warming temperatures and more extreme weather events—could worsen the disease. “I think [climate change] is going to have an enormous effect on migraine,” he says.

    This summer, Martin and his colleagues presented a study that reviewed over 70,000 daily diary records of 660 migraine patients and cross-referenced them with regional weather data, such as wind speed, temperature, humidity, and barometric pressure. The researchers found that, for every daily temperature increase of 10 degrees Fahrenheit, there was a 6 percent increase in occurrence of headaches. One reason heat might trigger migraines could be due to the loss of water and electrolytes through sweat, Martin says; it could also be that the sun acts as a photic trigger, meaning its bright light could spark a migraine.

    Other research has similarly found a link between rising temperatures and migraines. A 2015 study looked at emergency department admissions due to migraine at a hospital in Turkey over a year and compared them against different weather parameters, such as temperature, humidity, and pressure. It found the number of migraine patients rose as temperatures increased and humidity decreased.

    Fred Cohen, assistant professor of medicine at Icahn School of Medicine at Mount Sinai in New York and a coauthor on the study with Martin, is concerned that the changing climate could directly impact migraine burden. He led a separate review paper published earlier this year that uncovered a peculiar trend. The review found that while the prevalence of migraines—meaning the number of people who get them—has stayed around the same in the US over the past 30 years, migraine-related disability—which is determined by how much time patients lose for work and socializing due to migraines—has mushroomed.

    Cohen and his coauthors discovered that the number of people reporting migraine-related disability had almost doubled by some measures. This could in part be because doctors have gotten better at assessing migraines, or because people have become more aware of their condition and more comfortable discussing it. But also, Cohen says, it could be because “something’s going on.” One explanation the study authors suggest is the changing environment.

    It’s not just rising temperatures that migraine sufferers should be concerned about, either. Climate change is associated with an increase in air pollutants, such as those produced by wildfires, which are another known trigger for migraines. Although the mechanism by which pollution triggers migraines is not yet understood, multiple studies have found that short-term exposure to air pollutants is accompanied by a jump in migraine-specific emergency department visits. Indeed, during the intense wildfires on the east coast of North America last summer, “calls to the headache center were skyrocketing,” says Cohen.

    [ad_2]

    Source link

  • Strange Visual Auras Could Hold the Key to Better Migraine Treatments

    Strange Visual Auras Could Hold the Key to Better Migraine Treatments

    [ad_1]

    Exactly why CSD starts, nobody knows. Similarly, plenty of mysteries remain about what activates the pain of migraines. Past studies have proposed that migraine headaches occur when something in the cerebrospinal fluid indirectly activates nerves in the nearby meninges, the layers of membrane between the brain and the skull. Rasmussen’s experiment, led by neuroscientist Maiken Nedergaard, initially set out to find evidence to support this—but they came away empty-handed. “We didn’t get anything,” he says.

    So they tried a different approach, injecting fluorescent tracer substances into the cerebrospinal fluid and imaging the mice’s skulls. The tracers concentrated at the end of the trigeminal nerve, “these big nerve bundles that lie like two sausages on the base of the skull.” It was a big surprise, he says, to find substances were able to reach this part of the peripheral nervous system, where they could activate pain receptors. “So we got excited and also very puzzled—like, how does it even get there?” This led them to the opening—the end of the trigeminal nerve that was in open contact with the cerebrospinal fluid.

    The researchers also sampled the cerebrospinal fluid and found more than 100 proteins that rose or fell in the aftermath of CSD, suggesting potential involvement in the pain of migraine. A dozen of the proteins that increased are known to act as transmitter substances capable of activating sensory nerves, including one called calcitonin gene-related peptide (CGRP), a known target for migraine drugs. Rasmussen says it was a good sign to find it among the mix. “But for us, what is most interesting is really the 11 other proteins that have not been described before,” he says—as these could open the door for new treatments.

    There are still reasons to be cautious, says Turgay Dalkara, a professor of neurology at Hacettepe University in Turkey with an interest in auras. Mouse models are useful, but the size differences in rodent and human skulls are problematic—especially when it comes to the area where the opening was found. “From the mouse to the human, the surface-volume ratio is dramatically different,” he says. The idea that Rasmussen’s team initially investigated—that CSD releases substances that activate and sensitize nerves in the meninges—remains the best supported mechanism observed in humans, he adds. Rasmussen’s finding, of this previously undiscovered spot where cerebrospinal fluid could touch nerves, should be considered a possible addition to this picture, not a replacement for it.

    Hadjikhani agrees but is nevertheless excited to find a further pathway for investigation. For doctors, the lack of understanding about how migraines work means sleuthing for the right combinations of medicines to give sufferers some relief. “You try one. You try a combination. You take one off,” she says. “You have to be Sherlock Holmes, finding what triggers things.”

    The fact that migraines vary so much means there may never be a silver bullet solution. Rasmussen hopes that, in the long term, being able to observe changes in an individual’s cerebrospinal fluid could minimize this guesswork and lead to personalized solutions.

    [ad_2]

    Source link

  • RSV Can Be a Killer. New Tools Are Identifying the Most At-Risk Kids

    RSV Can Be a Killer. New Tools Are Identifying the Most At-Risk Kids

    [ad_1]

    After 25 years as a pediatric infectious diseases specialist, Asunción Mejías is too familiar with the deadly unpredictability of respiratory syncytial virus (RSV), an infection that hospitalizes up to 80,000 children under the age of 5 every year in the US.

    “It’s a disease which can change very quickly,” says Mejías, who works at St. Jude Children’s Research Hospital in Memphis, Tennessee. “I’ve always told my colleagues that for every two children that are admitted, one can go to the ICU in the next three hours and the other one may go home the next day. It’s totally unpredictable.”

    RSV infections are very common, to the point that nearly every child will have one before they turn 2 years old. Most children experience symptoms similar to a cold, like coughing and sneezing, but some can develop severe lung disease: RSV is responsible for more than 100,000 infant deaths globally every year, nearly half of which are in babies under 6 months of age.

    The problem is, aside from a few known risk factors such as premature birth and preexisting lung conditions, it’s hard to tell which children will be worst affected. “Eighty percent of children that end up in the hospital with RSV seem totally healthy,” Mejías says. “They were born full term, and don’t have any risk factors for severe disease.”

    So around the world, different research groups are attempting to train machine learning algorithms or develop statistical models that can indicate which children are most vulnerable to RSV. Based on vast databases of electronic health records, these tools aim to identify groups of risk factors that can help predict which children are more likely to be hospitalized with an infection. Health care providers can then use this information to prioritize the most at-risk children for vaccines and other preventative measures.

    Earlier this year, respiratory epidemiologist Tina Hartert and her colleagues at Vanderbilt University developed one such tool using a statistical model to identify a set of 19 risk factors for RSV, after training it on data from more than 400,000 infants on the Tennessee Medicaid program. “It allows an individual infant’s risk to be calculated at birth,” says Hartert.

    Some of the variables used in the tool are unsurprising. Prenatal smoking, for example, is known to impair lung development in the unborn fetus, making a baby more vulnerable to viral pneumonia, while babies with a low birth weight already lack the strength to breathe normally. However, in many cases, Hartert says it is a combination of different risk factors that converge to make a child vulnerable. “Assessing just individual factors misses lots of at-risk infants,” she says.

    In 2023, regulators in the US approved a vaccine called Abrysvo that is designed to be given to mothers during weeks 32 to 36 of pregnancy, with the aim of ensuring that babies are born with protective antibodies against RSV. They also approved a drug called Beyfortus, a laboratory-made protein called a monoclonal antibody, which can be administered through a single injection to provide protection ahead of the winter RSV season.

    [ad_2]

    Source link

  • We need to start telling women how pregnancy changes their brain

    We need to start telling women how pregnancy changes their brain

    [ad_1]

    New Scientist. Science news and long reads from expert journalists, covering developments in science, technology, health and the environment on the website and the magazine.

    “There are barely any areas of the brain that go untouched by pregnancy”

    Jecapix/Getty Images

    When I was expecting my first child, I knew what to expect. An expanding belly, a bout of morning sickness, perhaps a little sciatica. I’d been to birthing classes, I knew how to change a diaper and I was fully prepared for imminent exhaustion.

    Except I wasn’t prepared. I was missing one vital piece of information: that pregnancy would change the structure and function of my brain – perhaps irreversibly.

    No doctor or midwife mentioned it. Yet evidence has been building for years to…

    [ad_2]

    Source link

  • Snoring isn’t just a nuisance, it’s dangerous. Why can’t we treat it?

    Snoring isn’t just a nuisance, it’s dangerous. Why can’t we treat it?

    [ad_1]

    Spain. Benidorm. 1997.

    Martin Parr/Magnum Photos

    It has ruined many a night’s sleep, and no doubt a lot of relationships too. Trying to sleep next to a snoring partner is exactly that: trying. Once the engines fire up, there are few countermeasures besides a shove, earplugs and the patience of a saint.

    That’s the thing about snoring: many of us consider it to be little more than an embarrassment or an annoyance and grudgingly put up with it. But accumulating findings suggest that this trivialises an important, and common, health problem.

    Snoring isn’t just associated with broken sleep, it can be a warning sign of trouble ahead and also appears to have some potentially serious impacts on the snorer’s cardiovascular system. Despite a proliferation of remedies, there is a paucity of evidence about what works. But as sleep researchers increasingly wake up to the hidden dangers of snoring, there is hope the nightmare will soon end.

    Snoring is very common, though getting a handle on exactly how common is difficult. Many snorers are blissfully unaware that they do it. “If you ask someone ‘Do you snore?’, they’ll say ‘I dunno, I’m sleeping’, ” says Danny Eckert, director of sleep health at Flinders Health and Medical Research Institute in Adelaide, Australia. “Their bed partner might tell them, but a lot of people don’t have a bed partner.” In Eckert’s experience, however, it is rampant.…

    [ad_2]

    Source link

  • The complicated role loneliness plays in 26 common health conditions

    The complicated role loneliness plays in 26 common health conditions

    [ad_1]

    Loneliness is associated with multiple health conditions

    Marc Bruxelle RF / Alamy

    The idea that loneliness leads to certain health conditions is now being called into question. Although loneliness is associated with a range of negative physical health outcomes, including an increased risk of premature death, it might just be correlated with many of the conditions it was previously assumed to cause.

    “Loneliness seems to act as more of an indicator of disease rather than a direct cause,” says Jihui Zhang at Guangzhou Medical University. “Instead, socioeconomic factors, lifestyle choices and genetic predisposition might be driving risk for diseases like diabetes and heart diseases.”

    Social connection is essential to our mental health and ability to thrive. Yet loneliness – the painful feeling that arises from social disconnection – affects a growing number of people around the world.

    To learn more about how this affects health, Zhang and his colleagues analysed data from several biomedical databases, including the medical information of 476,100 people in the UK, 16,000 in China and 14,000 in the US. They found that participants who reported feelings of loneliness were at a higher risk of 30 out of 56 individual conditions, ranging from cancers to digestive system conditions.

    Then the researchers performed a second round of statistical analysis on 26 of those 30 conditions, focusing on the subset of participants whose genetic data was available. The results revealed that most of the conditions were not, in fact, caused by loneliness. These health problems, including cardiovascular disease, obesity and type 2 diabetes, merely occurred alongside loneliness. But loneliness could still potentially play some role in causing six of the conditions: depression, hypothyroidism, asthma, sleep apnea, substance abuse and hearing loss.

    According to Yu He, also at Guangzhou Medical University, the findings have important implications for real-world interventions. “Addressing loneliness is important, but it’s not the only factor in preventing diseases,” she says. “Public health authorities should also focus on improving mental health services and promoting healthy lifestyles.”

    David Sbarra at the University of Arizona says the new study “should give us pause in how we think about the public health goals of reducing loneliness to improve human health”.

    “To be sure, loneliness itself is highly aversive and seems to be causally associated with the emergence of depressive episodes, but in terms of the connection to health, some of the most cherished findings in the field need to be reconsidered,” says Sbarra. “It is important to understand where the causal effects might exist and where the correlations seem to exist.”

    Zhang, He and their colleagues are planning to investigate the underlying biological mechanisms behind their findings, including how loneliness affects things like stress hormones and inflammation. They also hope to run studies on groups of people from other parts of the world to see if their current findings – which are predominately based on data from people in the UK – hold up.

    Sbarra adds that, to truly determine whether loneliness causes certain conditions, researchers will need to study whether having better social connection leads to health improvements. “Obviously, any intervention studies showing that you can improve health markers by reducing loneliness would be truly remarkable,” he says. “We have very few examples suggesting this is indeed possible.”

    Topics:

    [ad_2]

    Source link

  • Scientists Crack a 50-Year Mystery to Discover a New Set of Blood Groups

    Scientists Crack a 50-Year Mystery to Discover a New Set of Blood Groups

    [ad_1]

    There were many challenges in the process of confirming the role of the MAL gene, including a study by rival researchers that suggested a completely different gene could be responsible. “We suddenly thought, ‘Oh no, maybe all this work we’ve been doing has been wasted,’” recalls Tilley. “That was a real low point.” Thornton chimes in: “But we were convinced we were right.”

    In the end, the other study turned out to be wrong, and one of its authors later joined forces with Tilley, Thornton, and their colleagues. Together, the group was subsequently able to prove the significance of the MAL gene in some key experiments. First, following painstaking efforts to find antibodies that would react with it, they established that the crucial AnWj antigen (encoded by the MAL gene) was indeed present on the surface of most people’s red blood cells. Then, they took AnWj-negative blood cells, lacking said antigen, and inserted a complete MAL gene into those cells. This had the hoped-for effect of generating the antigen on the cell surface, turning the cells AnWj-positive. That was definitive proof that the researchers had found the gene responsible for this rare red blood cell variation.

    Now that they know the gene in question, it should make it much easier to find AnWj-negative people who could become blood donors so that, if people affected by this blood group ever need a transfusion, they can have one safely.

    “What they did was really clever,” says Sara Trompeter, a consultant hematologist and pediatric hematologist at University College Hospitals London. Trompeter also works for NHS Blood and Transplant but was not involved in the AnWj study. “They presented it at a conference, some of their early work. It was like watching one of those detective shows where they’re just picking up on tiny clues and testing hypotheses—things that other people might have ignored.”

    Mark Vickers, a hematologist at the University of Aberdeen, who also was not involved in the study, agrees that the results are robust. “They’ve really gone to town and done some very nice work,” he says. “As far as this blood group is concerned, this is going to be the unequivocal landmark paper.”

    There are few indications as to what factors might influence someone to have genes that make their blood AnWj-negative. One family of AnWj-negative individuals in the paper was Arab-Israeli, but the authors stress that there is no clear link to ethnicity at this stage. The vast majority of people who are AnWj-negative are not genetically predisposed to it. Rather, they have such blood because of a hematological disorder or because they have one of the cancers that can affect their MAL gene. “It’s not truly negative. It’s just suppressed,” says Thornton, referring to those cases.

    There are questions remaining though. Babies don’t actually develop the AnWj antigen on their red blood cells until they’re seven days old. The mechanisms as to why that is remain murky. Vickers suggests it could be something to do with the variety of changes that happen in a fetus’s blood around the time of birth—for example, when its dependence on nutrition and oxygen from its mother’s blood ends.

    Tilley, Thornton, and colleagues were also responsible for discovering the genetic basis for the 44th blood group system, called Er, in 2022, as well as the MAM blood group system in 2020, among others. During the past decade or so, blood researchers around the world have described roughly one new blood group system every year, on average. “We’ve got some more in the pipeline,” teases Thornton.

    There are still a handful of enigmatic blood samples—blood that reacts to other people’s blood in unexpected ways—out there, tucked away in lab storages. Scientists—mindful of the patients whose lives are affected by this, who will struggle to find matching blood donors, or who, in some cases, may suffer devastating complications during pregnancy—regularly pore over those samples, hoping to explain them one day.

    At least one more mystery has been solved. Describing how she feels upon seeing her and her colleagues’ paper published at last, and reflecting on nearly 20 years of work, Tilley just says: “It’s a huge relief.”

    [ad_2]

    Source link