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Miami Herald
9 hours ago
- Automotive
- Miami Herald
Shared mobility: Making travel easier for all
Walk around most large metropolitan cities in Europe and the United States, and you'd be forgiven for thinking that we're living in a brave new world of affordable and effortless mobility for all, with the smartphone in your pocket a portal to a cornucopia of shared e-scooters, bikes and electric cars, and an Uber or Lyft never more than five minutes away. But if you're disabled or elderly, living in a low-income area or-imagine-without a smartphone or credit card, using these shared mobility services becomes a lot more difficult. They tend to cluster in more affluent urban areas, and are often inaccessible to people with reduced mobility or those traveling with young children needing child seats. In part because of these factors, users are disproportionately younger, wealthier, able-bodied, white and male. Shared mobility could be a key part of a more sustainable transportation system. But to be most effective, it needs to include everyone. For-profit shared mobility providers have largely failed to deliver on this, but various initiatives and projects are finding creative solutions to reach underserved communities, Knowable Magazine says. The potential benefits are large. On-demand shared mobility that feeds into well-developed public transportation systems could reduce the number of vehicles in some cities by 90 percent and cut transportation emissions by 50 percent-but only if it largely replaces private car use. "The car has to be a guest, not the main actor," says Luis Martinez, lead modeler at the International Transport Forum, who coauthored a paper on shared mobility and sustainability in the 2024 Annual Review of Environment and Resources. Achieving that goal will be challenging, especially in the Global North, where people choose private cars for 61 percent of the kilometers they travel. To move more people away from private vehicles to shared ones, expanding access to a wider share of the population is an important first step, researchers say, because a lot of people are left out today. A 2019 study of 10 US cities, for example, showed that white Americans have access to almost three times as many carshare locations and two times as many bikeshare locations within a half-mile radius as African Americans. When hailing rides from their home, African Americans also wait up to 22 percent longer for the ride to arrive. But even when efforts are made to expand services to underserved areas of a city, other hurdles persist. A fifth of low-income Americans still don't have a smartphone and almost a quarter don't have a bank account-both prerequisites for using most such services. A 2017 survey in Philadelphia, Chicago and New York City's borough of Brooklyn, showed that low-income people of color are just as interested in bikesharing as other groups, but less likely to use such a system: While 10 percent of higher-income white residents and five percent of higher-income residents of color were members of a bikeshare system, only two percent of lower-income residents were. Forty-eight percent of lower-income residents of color cited cost as a big barrier. In addition, lack of familiarity with the bikeshare system was holding a third of people back. How to bridge the accessibility gap? A fundamental problem, Martinez says, is that "private businesses will always go where the money is." Unsurprisingly, then, public agencies are the ones stepping in. A handful of cities in the United States, for example, have launched subsidy programs for low-income residents, which have shown promise in increasing the use of shared mobility while decreasing the use of personal vehicles. In 2024, a survey of almost 250 bike- and e-scooter-share programs in the U.S. found that 70 percent had taken steps to reach underserved groups, with measures like cash payment and non-smartphone options being among the most popular. Nongovernmental organizations are also filling the gap. One example is a program by nonprofit Shared Mobility Inc. in Buffalo, New York. In the summer of 2020, it suddenly found itself in possession of 3,000 electric bikes, part of the fleet Uber scrapped when selling the bikesharing arm of its business earlier that year. "The E-Bike Library model was born from that," explains Shane Paul, who oversees the initiative, helping community-based organizations set up e-bike libraries for underserved populations. At their first location in a transit desert on Buffalo's East Side, 71 percent of members were first-time e-bike riders and 84 percent identified as people of color. Shared e-bikes are a particularly promising substitute for cars in urban areas, with one report estimating that a shift to e-bikes could take 8 million cars off U.S. roads. E-bike libraries address a number of barriers: The bikes are free, and the libraries are hosted by places that are already an important part of the community. In addition to maintaining the bikes, the programs also organize training, group rides and educational events to familiarize people with cycling culture and safety. "It can be something as simple as making sure you lock your bike," says Paul. "These types of programs create a space for people to learn these skills." Personal interactions and affordability are also important for Mobitwin, a social transportation service for elderly people and those with reduced mobility. Founded by the Belgian mobility nongovernmental organization Mpact, it lets elderly people request a ride from a volunteer for a nominal fee. The program, which has been running since the 1980s, currently serves around 40,000 people in Belgium. Being able to get out and about is a crucial part of participating in society, and reduced mobility in old age goes hand in hand with social isolation and loneliness, says Esen Köse, project manager at Mpact. "We want to make sure that people who are often not in the societal cycle of going to work or going to school, who are actually often left out, that they still have an option to get out of the house and do the simple daily things, like going to the grocery store, going to the hairdresser, seeing families." The booking process still primarily operates through a phone call-a recent attempt to switch to an app proved ill-suited to older users and was never implemented. A lack of digital literacy was one problem, but members also don't want to give up the social connection that comes from calling up an operator and requesting a ride, says Köse. Devising programs that work isn't just about the latest technology or trends in shared mobility options, she adds. "It's really starting from, 'OK, what are the needs of the people?'" Tim, a carsharing service run by the Austrian city of Graz, also maintains an email- and phone-based booking system in addition to its app. "Senior citizens are often also good with phones," says Katharina Mayer, head of the service. "But some are not, so we offer the necessary support." The service has also recently added a wheelchair-friendly vehicle to the fleet, and it is focused on optimizing the service for women. In 2024, only 39 percent of Tim's carsharing users were women, and customer satisfaction surveys showed that a lack of car seats for children was one of the reasons. This led Tim to include booster seats in all its cars, with seats for younger children available upon request free of charge. A survey planned for later this year will measure the impact of this change, but already, Mayer says, new customers call to inquire whether child seats are available. The mobility patterns of women also differ from those of men, in part because women tend to combine multiple short trips into one journey, for example to buy groceries and pick up children on the way home from work. "That makes their mobility a lot more complex," says Lina Mosshammer, founder and CEO of the Austrian mobility consulting company Point&. Since shared mobility solutions are usually priced by duration, distance or both, trip-chaining makes them more expensive, and most services aren't designed with small children in mind. Small tweaks like adapting the handle design on e-scooters for women's hands, which are often smaller, and offering family accounts or cheaper fares for breaks in travel can help to accommodate caregivers' needs, says Mosshammer. Free helmets and SOS buttons on bikes and e-scooters could also help address their concerns for personal safety. When mobility companies have more women in management and other positions, they also tend to have more women as users, she adds. "You tend to plan for what you know. That's why it's so important to bring in different perspectives in the development of mobility." Station-based systems-where cars are picked up and dropped off at fixed locations such as train stations, rather than left on the street as is the case with free-floating systems-can also make it easier for women to plan for their complex transportation needs. "Let's say you have to bring your kid to violin lessons every Thursday. You can book a car for every Thursday between 2 p.m. and 4 p.m. a month in advance, and you know the car will be there," says Mayer. There is another reason that the city of Graz opted for this model: A free-floating system competes with public transport, while a station-based one complements it. "Our big goal is for people in Graz to sell their cars," says Mayer. "Our vehicles must offer enough options to facilitate this shift." This story was produced by Knowable Magazine and reviewed and distributed by Stacker. © Stacker Media, LLC.
Yahoo
12-06-2025
- Health
- Yahoo
How stress shapes cancer's course
About two millennia ago, the Greek physicians Hippocrates and Galen suggested that melancholia—depression brought on by an excess of "black bile" in the body—contributed to cancer. Since then, scores of researchers have investigated the association between cancer and the mind, with some going as far as to suggest that some people have a cancer-prone or "Type C" personality. Most researchers now reject the idea of a cancer-prone personality. But they still haven't settled what influence stress and other psychological factors can have on the onset and progression of cancer, Knowable Magazine notes. More than a hundred epidemiological studies—some involving tens of thousands of people—have linked depression, low socioeconomic status and other sources of psychological stress to an increase in cancer risk, and to a worse prognosis for people who already have the disease. However, this literature is full of contradictions, especially in the first case. In recent decades, scientists have approached the problem from another angle: experiments in cells and animals. These have revealed important mechanisms by which stress can alter tumors, says Julienne Bower, a health psychologist at UCLA who coauthored a 2023 article on the connection between the brain and the immune system in diseases, including cancer, in the Annual Review of Clinical Psychology. Such studies are showing that "psychological factors can influence aspects of actual tumor biology," she says. On the flip side, studies in people and animals suggest that blocking the chemical signals of stress may improve cancer outcomes. Today, a growing number of researchers think that psychological factors can influence cancer's progression once someone has the disease. "I don't think anyone appreciated the magnitude by which even mild stress, if it's chronic, can have such a negative influence on cancer growth," says Elizabeth Repasky, a cancer immunologist at the Roswell Park Comprehensive Cancer Center in Buffalo, New York. New interest in the relationship between stress and cancer growth emerged in part from research into how stress affects the body's response to human immunodeficiency virus (HIV). In the 1990s and early 2000s, genomics researcher Steve Cole and his team at UCLA investigated why people infected with HIV who were under high stress tended to have worse outcomes, including larger viral loads and poorer responses to antiretroviral drugs. Cole's team discovered several routes through which stress could worsen HIV infections. In monkeys, they found, the lymph nodes of stressed animals had many more connections to sympathetic nerve cell fibers—which execute the body's fight-or-flight response—than the nodes of unstressed monkeys. Lymph nodes contain immune cells, and the nerve fibers reduced the antiviral function of these cells, which, in turn, led to an increase in the replication of a version of HIV that infects monkeys and apes. Lymph nodes, in addition to housing immune cells, also act as the body's drainage system, flushing away toxins through a network of tissues, organs and nodes called the lymphatic system. Importantly, cancer cells can hijack this system, using it to travel through the body. Erica Sloan, a postdoctoral trainee of Cole who was involved in the HIV work, wondered whether stress, via the sympathetic nervous system, might also affect lymph nodes in those with cancer. Sloan, now a cancer researcher at Monash University in Australia, went on to discover in mice that chronic stress increases the number of connections between the lymphatic system and breast tumors, making the cancer cells more likely to spread. Strikingly, treatment with a drug—a beta blocker that blunts the activity of key molecules of the sympathetic nervous system such as norepinephrine—prevented these effects. Research by other groups has shown that stress can lead to molecular changes, particularly within the immune system, that influence how cancer progresses. Some of this work suggests that, when stress leads to inflammation—a broad immune reaction typically brought on by injuries and infections—it can boost the growth of tumors. Stress can also impair the activity of immune cells that play an active role in fighting cancer. In the early 2000s, research by University of Iowa behavioral scientist Susan Lutgendorf and her colleagues found that in patients with ovarian cancer, depression and anxiety were associated with impaired tumor-fighting immune cells. In another study of people with ovarian cancer, the researchers found that poor social support was linked to higher levels of a growth factor that stimulates blood vessel growth around tumors. This growth, called angiogenesis, enables new blood vessels to supply nutrients to tumors and—like the lymphatic system—provide pathways through which cancer cells can spread to other parts of the body. Lutgendorf and her colleagues have since found that stressful situations have a similar effect on mice with ovarian cancer, enhancing tumor angiogenesis and cancer spread. Equally important, they've found that these effects can be reversed with beta blockers. Other groups have found similar effects of blocking stress signals on other types of cancer in rodents, including blood and prostate cancer. In addition, researchers have found that increasing levels of stress hormones such as norepinephrine and cortisol in mice can make previously dormant cancer cells more likely to divide and form new tumors. Studies like these are revealing that stress can trigger a cascade of biochemical changes and alter a cancer cell's environment in a way that may promote its spread. "Stress signaling and stress biology really have an impact on most—if not all—of these processes," says Jennifer Knight, a cancer psychiatrist at the Medical College of Wisconsin. If stress can make cancer worse, how can the process be stopped? Little by little, new treatments are emerging. For about half a century, clinicians have used beta blockers to treat hypertension. By scouring data from patient registries, researchers found that people with cancer who already had been taking certain kinds of beta blockers at the time of diagnosis often had better outcomes, including longer survival times, than those who were not on the medicines. Over the past few years, several clinical trials—most of which are small and early-stage—have directly tested whether beta blockers could benefit people with cancer. In one pair of studies, a research team led by neuroscientist Shamgar Ben-Eliyahu at Tel Aviv University, administered the beta blocker propranolol along with an anti-inflammatory drug to people with colorectal or breast cancer five days before surgery. The team chose this timing because earlier research had shown that while surgery is an opportunity to remove the tumor, it can also paradoxically provide the chance for the cancer to spread. So blocking any potential effects of stress on cancer spread, they reasoned, could be crucial to a patient's long-term prognosis. These trials, which involved dozens of patients, revealed that the tumor cells of those who received the drugs showed fewer molecular signs of being able to spread—a process known as metastasis—less inflammation, and an increase in some tumor-fighting immune cells. For colorectal cancer patients, there were also hints that the intervention could reduce cancer recurrence: Three years after the procedure, cancer returned in two of the 16 patients who received the drugs, compared to six of 18 patients who didn't receive those meds. Other studies have assessed the effect of using beta blockers alone, without anti-inflammatory drugs. In 2020, Sloan and her colleagues published a study including 60 breast cancer patients, half of whom were randomly assigned to receive propranolol a week before surgery, while the other half received a placebo. They, too, found that tumor cells from patients who received beta blockers had fewer biomarkers of metastasis. Stress-reducing beta blockers may also benefit other cancer treatments. In a 2020 study, Knight and her team looked at the effect of beta blockers in 25 patients with multiple myeloma who were receiving blood stem cell transplants. Patients who took beta blockers had fewer infections and faster blood cell recovery—although the study was too small to properly evaluate clinical outcomes. And in a small study of nine people with metastatic skin cancer, Repasky and her colleagues found hints that beta blockers might boost the effectiveness of cancer immunotherapy treatments. While studies on beta blockers are promising, it's not clear that these drugs will improve outcomes in all kinds of cancers, such as lung cancer and certain subtypes of breast cancer. Some patients can react badly to taking the medications—particularly those with asthma or heart conditions such as bradycardia, in which the heart beats unusually slowly. And, crucially, the drugs only block the endpoint of stress, not its cause, Repasky says. They will therefore likely need to be combined with mindfulness, counseling and other stress-reducing strategies that get closer to the root of the problem. Such interventions are also in the works. Bower and her team have conducted clinical trials of mind-body interventions such as yoga and mindfulness meditation with breast cancer survivors, to improve health and promote lasting remission. They've found that these therapies can decrease inflammatory activity in circulating immune cells, and they speculate that this may help to reduce tumor recurrence. Ultimately, bigger clinical trials are needed to firmly establish the benefits of beta blockers and other stress-reducing interventions on cancer survival outcomes—and determine how long such effects might last. The timing of treatment and the type of cancer being treated may play a role in how well such therapies work, researchers say. But lack of funding has been a barrier to conducting the larger follow-up studies needed to answer such questions. The work isn't yet backed by pharmaceutical companies or other organizations that support large studies in oncology, Knight says. And for now, whether stress can increase a person's risk of developing cancer in the first place, as the ancient Greeks once postulated, remains a mystery. Population studies linking stress to cancer risk are often complicated by other factors, such as smoking, poor nutrition and limited access to health care. "We have no definitive way of saying, 'If you're stressed out, you're going to develop cancer,'" says Patricia Moreno, a clinical psychologist at the University of Miami Miller School of Medicine and coauthor of an article in the 2023 Annual Review of Psychology about stress management interventions in cancer. But for people who already have a cancer diagnosis, many researchers argue that the evidence is strong enough to include stress management in clinical practice. On average, cancer patients do not receive psychological therapies that can reduce stress at the level for which they are needed, says Barbara Andersen, a clinical psychologist at Ohio State University. Although they won't be necessary for every patient, many can benefit from mind-body interventions, she says. "I'm not saying they should be a first priority, but they shouldn't be the last." This story was produced by Knowable Magazine and reviewed and distributed by Stacker.
The Wire
08-06-2025
- Health
- The Wire
Worm-Inspired Treatments Inch Toward the Clinic
Menu हिंदी తెలుగు اردو Home Politics Economy World Security Law Science Society Culture Editor's Pick Opinion Support independent journalism. Donate Now Science Worm-Inspired Treatments Inch Toward the Clinic Amber Dance, Knowable Magazine 3 hours ago Infection by certain wrigglers may reduce inflammation and fight obesity and diabetes. Scientists are at work to turn the findings into therapies. Illustration via Canva. Real journalism holds power accountable Since 2015, The Wire has done just that. But we can continue only with your support. Contribute now The experiment was a striking attempt to investigate weight control. For six weeks, a group of mice gorged on lard-enriched mouse chow, then scientists infected the mice with worms. The worms wriggled beneath the animals' skin, migrated to blood vessels that surround the intestines, and started laying eggs. Bruno Guigas, a molecular biologist at the Leiden University Center for Infectious Diseases in the Netherlands, led this study some years back and the results, he says, were 'quite spectacular.' The mice lost fat and gained less weight overall than mice not exposed to worms. Within a month or so, he recalls, the scientists barely needed their scale to see that the worm-infested mice were leaner than their worm-free counterparts. Infection with worms, it seems, reversed obesity, the researchers reported in 2015. While it's true that worms gobble up food their hosts might otherwise digest, that doesn't seem to be the only mechanism at work here. There's also some intricate biology within the emerging scientific field of immunometabolism. Over the past couple of decades, researchers have recognized that the immune system doesn't just fight infection. It's also intertwined with organs like the liver, the pancreas and fat tissue, and implicated in the progression of obesity and type 2 diabetes. These and other metabolic disorders generate a troublesome immune response — inflammation — that worsens metabolism still further. Metabolic disease, in other words, is inflammatory disease. Scientists have also observed a metabolic influence of worms in people who became naturally infected with the parasites or were purposely seeded with worms in clinical trials. While the physiology isn't fully understood, the worms seem to dampen inflammation, as discussed in the 2024 Annual Review of Nutrition. 'We're never going to cure or treat metabolic disease with worm infections,' says Guigas. They cause unpleasant side effects like nausea, and it would be impractical to dose millions of people with parasites. But worms can be valuable tools for scientists to understand the feedback between inflammation and metabolism. The findings could inspire more traditional, less ick-inducing treatments. The worms' good turns The worms we're talking about are helminths such as flukes and roundworms. While they've largely been eliminated from developed nations, an estimated 1.5 billion people worldwide carry them. They can be dangerous in high numbers, and cause symptoms such as diarrhea and malnutrition in those at high risk, including children and immunocompromised individuals, and during pregnancy. But for most people, infection with a few worms is pretty benign. 'Throughout human evolution, I think, there's been this nice sort of truce,' says Paul Giacomin, an immunologist at James Cook University in Cairns, Australia. As part of that detente, he says, helminths evolved molecules that tell the human immune system, 'I'm not here, don't worry about me.' In turn, people might have evolved to depend a bit on worms to temper inflammation. Today, metabolic disease is a massive global problem, with obesity affecting an estimated 890 million people. Another 580 million have type 2 diabetes, which arises when the hormone insulin, which controls blood sugar levels, is in short supply or the body's cells become insensitive to it. Links between metabolic disease and worm infection emerged from research on human populations. Studies in Australia, Turkey, Brazil, China, India and Indonesia showed that people with metabolic conditions such as diabetes were less likely to have helminth infections, and vice versa. 'This observation is quite strong,' says Ari Molofsky, an immunologist at the University of California, San Francisco. Going a step further, scientists observed what happened when they provided deworming treatments. 'The overwhelming majority of the studies showed that deworming worsens your metabolic health,' says Giacomin. Scientists looked to lab mice for additional clues. Molofsky and colleagues, in 2011, reported that when they infected mice on high-fat food with the gut worm Nippostrongylus brasiliensis, the infection improved blood sugar control. Similarly, in Guigas' study, published in 2015, the worms — blood flukes called Schistosoma mansoni — improved not just weight, but also blood sugar processing. And the worms needn't be alive: Even molecules collected from crushed worm eggs improved metabolism. The going hypothesis is that metabolic problems kick off a vicious immunometabolic cycle. First, Guigas says, damaged cells in metabolic organs cry for help, releasing molecular signals that call in immune cells. When the immune cells arrive, they morph into forms that promote a type of inflammation called Th1. Th1 responses are good at combating viruses, but they're the wrong choice here. Th1 can aggravate metabolic problems by impairing insulin manufacture, altering insulin signaling and amplifying insulin resistance. Thus, instead of helping, the immune cells cause further stress in the metabolic tissues. So the tissues call in more immune cells — and the cycle repeats. Worms seem to break the cycle. In great part, that's probably because their 'I'm not here' message causes a different kind of immune response, Th2, that dampens the Th1 reaction and re-normalizes the system. Other mechanisms might also be at work: Worms might reduce appetite; it's known they can alter gut microbes; and Guigas suspects they can also manipulate creatures' metabolisms via non-immune pathways. 'The parasitic worms are real masters at controlling inflammation,' says Giacomin, who coauthored an article on helminths and immunity in the 2021 Annual Review of Immunology. Thus, scientists interested in controlling immunometabolic disease might take cues from these wriggly little metabolic masterminds. In fact, researchers have already tested helminths to control inflammation in autoimmune conditions such as inflammatory bowel disease. The accumulating evidence linking worms to metabolic benefits in animals and people inspired Giacomin and colleagues to conduct a trial of their own. Commencing in 2018, they decided to try the hookworm Necator americanus in 27 obese people who had insulin resistance, putting them at risk for type 2 diabetes. The researchers applied worm larvae in patches on the subjects' arms; after passing through the skin, the worms would travel through the blood stream, to the lungs and then to the small intestine. An additional 13 participants were assigned to placebo patches with Tabasco sauce to mimic the itch of entering worms. N. americanus is a common cause of hookworm infections across much of the world. While most cases are asymptomatic, the time when the worms are attaching to the intestinal wall can cause symptoms like nausea and low iron levels, especially if there are a lot of worms. So the main goal was to determine if the treatment was safe, trying doses of 20 or 40 worms. Many subjects suffered short-term unpleasantness such as bloating or diarrhea as they adjusted to their new intestinal tagalongs, but overall, most did fine. After 12 months, the people who got hookworms had lower insulin resistance and reduced fasting blood sugar levels. After two years, those who received 20 worms had lost an average of 11 pounds — though not all individuals lost weight, and some gained. 'It was quite convincing that the worms were having some sort of beneficial effect,' says Giacomin. The subjects were convinced too: When the study was over, the researchers offered deworming, but most participants elected to keep their worms. Giacomin and Guigas hope to identify worm components or invent worm-inspired molecules to produce similar effects without whole parasites. Giacomin cofounded a company, Macrobiome Therapeutics in Cairns, to develop hookworm molecules into treatments. Such medications might be based on the wriggly parasites, but they'd be an easier pill to swallow. This article was originally published on Knowable Magazine. The Wire is now on WhatsApp. Follow our channel for sharp analysis and opinions on the latest developments. Make a contribution to Independent Journalism Related News US Supreme Court Rules $1.29 Bn Lawsuit Against ISRO-Owned Antrix to Proceed On Science and Changing Culture: A Conversation with Professor P. Balaram Indian Astronaut Shubhanshu Shukla-led Mission to International Space Station Pushed to June 10 How The Cat Got Her Spots J.V. Narlikar: Visionary Cosmologist, Tireless Science Populariser, Beloved Mentor What Jayant Narlikar Wrote on Scientific Temper a Decade Ago Still Holds True The Science Behind Growing Old A Tiny Insect is Revealing How Larger Animals Sense Electric Fields How Stress Shapes Cancer's Course About Us Contact Us Support Us © Copyright. All Rights Reserved.
Yahoo
08-05-2025
- Science
- Yahoo
Scientists raise concern as eerie phenomenon spreads across US coastlines: 'We're about 50 years behind'
The Chesapeake Bay has taken on a haunted appearance. Our overheating planet is helping turn the region into a graveyard for cedar and pine trees, per Knowable Magazine. As the world warms, driving sea levels higher, saltwater is encroaching along the world's coasts and into its estuaries. The seawater invasion can overtake the freshwater that gives life to deciduous trees. It is happening in the Chesapeake Bay, and it isn't going unnoticed. Scientists released a report on the salinization that is impacting coastal ecosystems. "The impact of saltwater intrusion on coastal forests and farmland is typically understood as sea-level-driven inundation of a static terrestrial landscape, where ecosystems neither adapt to nor influence saltwater intrusion," according to a study conducted by an international team of scientists. "Yet recent observations of tree mortality and reduced crop yields have inspired new process-based research into the hydrologic, geomorphic, biotic, and anthropogenic mechanisms involved." "When a lot of these forests die back, instead of being replaced with a native salt marsh ... what's actually taking its place is a phragmites marsh," University of Maryland Eastern Shore in Princess Anne forest ecologist, and coauthor of the Annual Review of Marine Science article, Stephanie Stotts, told Knowable Magazine. The Minnesota Aquatic Invasive Species Research Center describes phragmites, also known as common reed, as "a tall, densely growing perennial grass that can take over large areas, displacing native vegetation and reducing habitat quality for fish and wildlife." Trees die slowly; sometimes, it takes several decades for them to perish. It will take a long time for us to see the full consequences of these lifeless forests. "We're about 50 years behind," said Stotts, per Knowable Magazine. Ghost forests are the remains of a once-vibrant woodland ecosystem that has succumbed to the poisoning of encroaching saltwater. Forests have morphed into marshes during prior periods of rising sea levels. Scientists point out that marshes have some positive attributes. They are home to oysters, clams, shrimp, and certain bird species. The problem with ghost forests is that they can disrupt the carbon cycle. In other words, forests absorb more carbon pollution from the atmosphere than they release. After trees die, they can eventually contribute to the heat-trapping gases in the atmosphere, fueling even more warming. Living trees can also act as a buffer to storms. Ghost forests increase the vulnerability along coastlines to erosion and storm surge. While extreme weather events have always existed, experts have found that the human-induced climate crisis supercharges these events, putting our communities in even more danger and devastating ecosystems. The saltwater encroaching along the world's coastlines is accelerating as our overheating planet drives rising seas. Moving away from dirty energy sources to renewable options will help cool our planet and reduce the rise in sea levels. Do you think America has a plastic waste problem? Definitely Only in some areas Not really I'm not sure Click your choice to see results and speak your mind. Scientific studies can help illustrate how the buildup of heat-trapping gases in our atmosphere is impacting our planet, but getting the word out by exploring critical climate issues and talking to family and friends about them to raise awareness is important. So is supporting politicians who are fighting for the future of our planet. Join our free newsletter for good news and useful tips, and don't miss this cool list of easy ways to help yourself while helping the planet.
Yahoo
10-04-2025
- Health
- Yahoo
Everything you need to know about bird flu
In early 2024, the bird influenza that had been spreading across the globe for nearly three decades did something wholly unexpected: It showed up in dairy cows in the Texas Panhandle. A dangerous bird flu, in other words, was suddenly circulating in mammals—mammals with which people have ongoing, extensive contact. "Holy cow," says Thomas Friedrich, a virologist at the University of Wisconsin–Madison. "This is how pandemics start." This bird flu, which scientists call highly pathogenic avian influenza, or H5N1, is already at panzootic—animal pandemic—status, killing birds in every continent except for Australia, Knowable Magazine explains. Around the world, it has also affected diverse mammals including cats, goats, mink, tigers, seals and dolphins. Thus far, the United States is the only nation with H5N1 in cows; it's shown up in dairies in at least 17 states. In all of known history, "This is the largest animal disease outbreak we've ever had," says Maurice Pitesky, a veterinary researcher at the University of California, Davis. The virus, which emerged nearly three decades ago, is now creating upheaval in the poultry and dairy industries and making economic and political waves due to the fluctuating price of eggs. But there's more at risk here than grocery-store sticker shock. As it has journeyed around the world on the wings of migrating birds, the virus has infected more than 960 people since 2003, killing roughly half of them. Since the start of 2024, it's infected dozens of people in the United States—mainly farm workers—and it killed its first person stateside in January of 2025. So far, H5N1 flu hasn't acquired the key trick of passing with ease from person to person, which is what could enable a human pandemic. For now, both the U.S. Centers for Disease Control and Prevention and the World Health Organization rate the public health risk as low. But the situation could change. "The thing about this virus is, every time we think we know what's going to happen, it does something totally unexpected," says Michelle Wille, a virus ecologist at the WHO Collaborating Centre for Reference and Research on Influenza in Melbourne, Australia. "And that's the only consistent thing I can say about it." Biologically, H5N1 isn't so different from any other influenza A virus—the type that resides mainly in wild birds, as well as bats, and has occasionally jumped into human populations. It contains eight pieces of genetic material encoding 11 known proteins. Two proteins, the "H" and the "N" ones, stud the virus's exterior. H stands for hemagglutinin: It sticks to a cell's sugars so the virus can gain entry. N is for neuraminidase: It allows newborn viral particles to exit the cell. But there's lots of possible variety. The influenza A virus has at least 19 options for the H protein and 11 for the N protein, most of which are present in the various flu strains infecting wild waterfowl. H5N1 flu has version 5 of the H protein and version 1 of the N protein. There are also variants for the other genes. If two different flu viruses meet in a cell that they've both infected, they can swap genes back and forth, creating new kinds of flu offspring. Thus, all sorts of influenza A viruses infect the guts of wild waterfowl, usually without harm to the birds. But the viruses can cause trouble if they move into other creatures. A few decades ago, scientists thought they had a handle on what would happen if some bird influenza A virus spilled over into other species. In domestic poultry, it could turn nasty, but it was generally a "one-and-done" situation, says Bryan Richards, emerging disease coordinator at the U.S. Geological Survey's National Wildlife Health Center in Madison, Wisconsin. What happened in past instances was that all the farm birds would die, the virus would run out of hosts—the end. And the leap from birds to humans is not easily made. Scientists had long assumed that to infect people, an avian influenza A virus would have to trade genes with another virus in an intermediate species, like a pig, to adapt to mammalian biology. So back in 1996, when domestic geese in Guangdong province, China, came down with H5N1, it was hardly cause for worldwide alarm. But a year later, in Hong Kong, a 3-year-old boy died after suffering high fever and pneumonia. It took experts from around the world three months to identify the virus. At first, no one believed it was H5N1, says Robert Webster, a virologist and emeritus professor at St. Jude Children's Research Hospital in Memphis, Tennessee, who led one of the teams that made the ID. A virus with an H5 was supposed to be a chicken virus. But this H5N1 infected 18 people and killed six of them. "This was a nasty bastard," says Webster. Webster and other experts descended on Hong Kong, where they protected themselves by inhaling inactivated H5N1 virus obtained from that first case, as Webster recounts in the Annual Review of Virology. They learned that the boy's family had visited a live bird market, and testing identified more H5N1-infected birds in those markets and on farms. It had apparently arrived in ducks from China. "What blew everyone's mind, in 1997, was that humans clearly got infected with the avian virus, skipping the pig step," says Friedrich. Hong Kong killed all the poultry. That particular viral lineage was snuffed out. But its parent, back in mainland China, remained. And the vast viral lineage it spawned would continue to defy scientists' expectations. "This wasn't the one-and-done," says Richards. "The virus keeps throwing curveballs." H5N1 spread from farm to farm. It continued to infect people, usually those in very close contact with their domestic birds. Then, in 2005, the virus lobbed another curveball: It spilled back into wild birds, by now in a form altered enough to be deadly to them—killing thousands of bar-headed geese, gulls and great cormorants in China's Qinghai Lake Nature Reserve. "That," says Richards, "set the stage for where we are today." More birds, likely both wild and domestic, brought H5N1 into Europe and Africa. Through genetic mixing and matching, H5 hooked up with other partners, like N8, for a time. In late 2014, migratory birds brought H5N8 from Asia to the Pacific Coast of North America, where H5 also hooked up with an N2, and the outbreak spread across several states before fizzling out. The virus continued to spread in Asia, Europe and Africa, usually as H5N8, with a bit of H5N6. In 2020, reports of H5-containing virus infections in wild and domestic birds started to rise. A new variant of the H5 gene, called 2.3.4.4b, was first spotted in the Netherlands. Viruses carrying this H5 seem to have a particular ability to cross over and infect mammals, says Friedrich. By 2021, the 2.3.4.4b variety of H5 was back with a form of N1. "From there, we started seeing this mass spread event," says Wille. The virus arrived in North America in late 2021, this time to stay. The panzootic had begun. As birds migrate south for the winter, they bring H5N1 to poultry farms. Most infected chickens will die, and the primary defense is culling. In the U.S., more than 166 million chickens have been culled since 2022, though a lull in cases led egg prices to drop in early March 2025. To prevent spread, biosecurity has become the key watchword. For poultry farmers, that means a variety of things such as limiting human interaction with flocks, washing hands and boots, and wearing face masks. But the virus just keeps spilling over from wild birds into farmers' flocks. Part of the problem, Pitesky says, is that poultry farms are often located near water sources, like lagoons and rain ponds, where migrating birds roost overnight, putting wild and domestic animals in close proximity. It's a gut virus in wild birds, and it spreads easily through their feces. In February 2025, the U.S. Department of Agriculture announced allocation of up to $1 billion in additional funds to combat highly pathogenic avian flu, including support for biosecurity, financial relief for farmers and vaccine research. Companies have designed bird vaccines against H5-containing highly pathogenic avian influenza for a couple of decades, updating them as the virus evolved. The USDA announced in January 2025 that it would update its stockpile of vaccines for chickens, and Zoetis of Parsippany, New Jersey, recently created an updated version. It's based on a strain that was circulating in 2022 and has continued to do so, says senior vice president for global biologics research and development Mahesh Kumar, who works in Zoetis' Kalamazoo, Michigan, facility. The vaccine is effective at preventing symptoms and death, but does not prevent infection or viral transmission, Kumar says. Zoetis' past vaccines have been used in a handful of other nations for poultry and one even was used by the US Fish & Wildlife Service to protect California condors in 2023. In early 2025, the USDA granted Zoetis a conditional license for that new formula, but this preliminary licensure is just a step along the way to use, not permission to market or sell the vaccine widely. In fact, the US has never allowed widespread poultry vaccination for highly pathogenic avian flu, though poultry receive a number of other vaccines. There are concerns that vaccination could push the virus to mutate faster. But the big issue blocking vaccination is that doing so could limit international poultry trade, and the U.S. is a major exporter of live poultry. A vaccinated animal could carry the virus without symptoms, and many nations don't want birds that might be invisibly carrying H5N1. To get around that problem, Zoetis' vaccine has a twist. In preparing inactivated virus, the scientists used the N2 neuraminidase, instead of the N1 that H5 has recently buddied up with. That provides a way to check whether birds have antibodies that would indicate they've been exposed to the vaccine's N2, to the real virus's N1, or to both. Still, it is uncertain whether the U.S. would ever broadly deploy an avian flu vaccine. Pitesky says that much of the power rests with farmers who raise broiler chickens for meat and export; broilers make up about two-thirds of U.S. poultry sales. If the broiler farmers aren't on board, he believes it's unlikely the USDA would promote vaccination. The decision might end up being made at a state-by-state level, depending on regional poultry industries, suggests Rocio Crespo, a veterinary researcher at North Carolina State University in Raleigh. Kumar says Zoetis could turn stockpiled materials into ready-to-use vaccine in two months or less, depending on how close to finished form the vaccine is in storage. "We want to be ready," he says. And now the poultry industry's catastrophe has become the dairy industry's problem, too. The virus's 2024 appearance in Texas dairies was a surprise for flu experts: "The literature suggested that dairy cows don't get influenza A's," says Pitesky — but, "as the joke goes, cows don't read the literature." Dairies were caught off guard, without the guidelines and support systems that exist for poultry. And according to some reports, they've been slow to adopt biosecurity measures. Cows infected with H5N1 usually survive, though they must be taken out of the regular population and spend weeks in a hospital barn. Inflammation in their udders, or mastitis, turns their milk thick and yellowish; splashes of contaminated milk in the milking parlors create potential for the virus to move from animal to animal. (One study suggested that more widespread or respiratory infection does not occur, and there's no sign yet that beef cattle have been affected.) The USDA now requires the 48 contiguous states to test milk for H5N1. That testing identified two new spillovers of H5N1 into dairy herds, in Nevada and Arizona, reported in February of 2025. And, worryingly, that virus was a different version than the one that infected cows in 2024. That 2024 spillover featured an H5N1 with a particular collection of flu gene sequences, still H5 2.3.4.4b, called B3.13. But flu viruses evolve rapidly, and that H5 2.3.4.4b has shuffled genes with other viruses more than once, creating lots of variants and subvariants. More recently, another variant called D1.1 has been spreading in wild birds. While B3.13 still accounts for most cattle infections, it's D1.1 that hopped into dairies in early 2025. The long-term implications for cattle of D1.1, and avian flu in general, aren't yet clear. "We're really hoping this has just been a unique set of circumstances and that we don't get any more spillover events," says Jamie Jonker, chief science officer of the National Milk Producers Federation in Arlington, Virginia. But, he adds, "we'd like a vaccine to be in the toolbox and to understand how it can be used." Zoetis and other companies are working on H5N1 vaccines for cows, though it's too soon to know if and how such vaccines would be deployed. Even with vaccines, though, "we may not be able to put out this fire," says Gregory Gray, an infectious disease epidemiologist at the University of Texas Medical Branch at Galveston. "It appears, to many of us, that these viruses are going to be endemic, or we say 'enzootic,' for a long time." What kind of risk does all this pose for people? Gray has studied a number of viruses in cattle and other animals, and he says that while spillovers from one species to another are common, it's rare that a virus adapts to spread easily in the new species. As of spring 2025, there are no confirmed cases of human-to-human H5N1 transmission in the United States. "It's not like in the movies," Gray says. "It's going to take continual spillover events for it to get a foothold." But it can happen, as it did in 2009, when an H1N1 influenza A virus with a novel mix of genes jumped from pigs into people, where it then spread widely. This caused a pandemic, killing an estimated 123,000 to 203,000 people worldwide, a death toll grossly eclipsed by the more than 7 million who died of Covid-19. To become adept at infecting humans, the virus would have to change the structure of its hemagglutinin. Its current version sticks to a specific arrangement of sugars on the surface of bird cells. The birdlike sugar arrangement is found in cow udders, explaining the mastitis. Humans do have this birdlike sugar arrangement, but it's buried deep in the lungs, making the virus hard to catch and hard to spread to another person. It's also present in human eyes, which could explain why pinkeye was the most common clinical sign in people who caught bird flu in the U.S. in 2024 (many also experienced fever and respiratory symptoms). But for ongoing person-to-person transmission through coughs, sneezes and sniffles, researchers think H5N1 would have to mutate to recognize a sugar arrangement found in the human upper respiratory tract—the nose, nasal cavity, sinuses, mouth, throat and voice box. It would also have to make changes to the protein that copies its genes, the viral polymerase. This polymerase would need to switch from working well with bird proteins to working well with human ones. It has done that, to some extent: Some versions of H5N1 have acquired relevant mutations that help it replicate in mammal cells. But as of spring 2025, none of the viruses that have jumped from cows to humans have hemagglutinin mutations that are predicted to support person-to-person transmission, Friedrich says. H5N1 could either evolve on its own, or trade genes with another human-infecting flu. The latter possibility is particularly concerning at times of high rates of seasonal flu, such as during the 2024-25 winter. The more flu virus floating around, the more chances for two kinds to meet in the same cell in the same animal and exchange genes, to birth something new and potentially dangerous. Factors beyond the virus itself influence pandemic risk, too. "There are a lot of things that have to align, not only on the virus side, but also on the people side," says Valerie Le Sage, a virologist at the University of Pittsburgh who cowrote an overview of barriers to flu transmission in the 2023 Annual Review of Virology. One of them is disease history. From recent experiments with ferrets, which get and transmit the virus similarly to the way people do, Le Sage suspects that people who've had flu before—that's most people over the age of 5—might have enough immunity to stifle the worst consequences of H5N1 flu. In her experiments, ferrets earlier exposed to the 2009 H1N1 swine flu were protected from the worst symptoms and death when later exposed to H5N1 from Texas cattle. Ferrets that were just given H5N1 flu got sick and died. "I can't tell you exactly how long this protection lasts, but it is nice to see," says Le Sage. Also good news is the observation that the virus isn't hitting anywhere near the reported 50 percent mortality rate in recent U.S. infections. Such rates are imperfect calculations, Friedrich notes, as they are based on people who were sick enough to get tested for H5N1; people who didn't get very ill would not be tallied as survivors. That would artificially inflate the death rate, though it's unclear how much this has affected calculations. Asymptomatic infections may not be uncommon, at least in current U.S. cases: A recent CDC study found that three dairy veterinarians had antibodies to H5N1, indicating they'd been infected, but had never noticed symptoms. The other gene variants that H5N1 has acquired also seem to be a factor, and here the news may be less good. The earlier B3.13 virus seemed to cause mild infections, says David Hamer, a public health epidemiologist at the Boston University Center on Emerging Infectious Diseases. From 2024 through spring 2025, the CDC had tracked 70 H5N1 cases, of any type, in the U.S., and most have been mild. The one person who died was over 65 and had underlying health conditions—but he also had the newer D1.1 strain, as did a teen in Canada who became severely ill. Although it's not fully clear what D1.1 means for people, it could be bad news, speculates Friedrich. "I have this gut feeling, and colleagues of mine do too, that something about the D1.1 genotype may be more permissive for mutations that adapt the virus to humans," he says. For the general public, the main advice experts offer is to not consume raw milk or undercooked poultry products. Though no human infections from raw milk or undercooked food have been reported to the CDC as of spring 2025, the virus may have been transmitted via raw poultry products in a small number of cases in Southeast Asia, and it has infected cats that drank unpasteurized milk. Pasteurization kills the virus; so does cooking of eggs, chicken and beef. The U.S. does have some protections ready, including a stockpile of personal protective equipment, antiviral medication—Tamiflu reportedly works on this virus—and the ingredients for making human vaccines. Those ingredients include virus bits, as well as chemicals that help stimulate the immune system. These are stored in bulk, and could be assembled into ready-to-use vaccine doses within weeks to months. Although those vaccine materials were designed using versions of H5N1 flu from the early 2000s, a recent study suggests that they create an antibody response to the newer 2.3.4.4b versions that have spread globally since 2020, and include both B3.13 and the newly circulating D1.1. Scientists are also working on updated vaccines that would more closely match the virus circulating now. Social factors could also influence the detection of, and response to, a potential pandemic. Many farm workers are undocumented immigrants, making many reluctant to be screened or seek medical attention. "The population we should be surveilling the most is the population we're probably not surveilling at a robust enough level," says Pitesky. And Friedrich notes the great paradox of the Covid-19 pandemic: It spawned a society that's less prepared to manage the next outbreak. "The pandemic eroded public trust in science," he says. "There has been a backlash against the power of public health agencies to do what they need to do to control an outbreak." In early 2025, publication of a CDC report on H5N1 flu spreading from cattle to people was delayed. USDA personnel working on bird flu response were laid off; the department later struggled to reinstate them. And $590 million in funding for an RNA-based vaccine (of the kind that proved successful during the Covid pandemic) was put under review. The changes continue, with the resignation of a top vaccine official within the US Food and Drug Administration in March and movements starting in April to lay off thousands of federal health workers. Regardless of whether H5N1 jumps from person to person sooner, later or never, it's raging in wild animals. In the U.S., thousands of birds of more than 160 native species, including mallards, sparrows, pigeons and bald eagles, have been infected. So have hundreds of mammals of more than two dozen native species, including raccoons, bears and opossums. Some of these get sick, and some die. Many of these infections are "dead ends," Richards notes: They don't pass the virus on. It's mainly far-flying ducks that have done that. By late 2022, H5N1 had entered South America and was thundering down the continent's Pacific coast. "It then traveled the 6,000-kilometer spine of South America in six months, so that's very fast for a virus that's not assisted by planes," says Wille. It hit the tip of South America and jumped to Antarctica. En route, it killed 40 percent of Peruvian pelicans, at least 24,000 South American sea lions and more than 17,000 southern elephant seal pups. Wild birds have been affected around the world, and even waterbirds, which normally harbor influenza A without symptoms, have suffered. Though a full census is lacking, individual examples are sobering. The population of great skuas, found primarily in Scotland, is down by a reported 75 percent. An outbreak in California condors in 2023 killed 21 animals, in a species with fewer than 1,000 in existence. "An event like that could change the course of a species," says Wille. "Are they going to come back or not?" H5N1 hasn't reached Australia or New Zealand, but Wille thinks it's just a matter of time. For the world, the future of this virus, with its propensity to defy expectations, is up in the air. "I think we're on the precipice of something," says Wille. "What that something is, I'm not sure." This story was produced by Knowable Magazine and reviewed and distributed by Stacker.
