Climate Change Is Ruining Cheese, Scientists and Farmers Warn
Climate change is making everything worse — including apparently threatening the dairy that makes our precious cheese.
In interviews with Science News, veterinary researchers and dairy farmers alike warned that changes to the climate that affect cows are impacting not only affects the nutritional value of the cheeses produced from their milk, but also the color, texture, and even taste.
Researchers from the Université Clermont Auvergne, which is located in the mountainous Central France region that produces a delicious firm cheese known as Cantal, explained in a new paper for the Journal of Dairy Science that grass shortages caused by climate change can greatly affect how cows' milk, and the subsequent cheese created from it, tastes.
At regular intervals throughout a five-month testing period in 2021, the scientists sampled milk from two groups of cows, each containing 20 cows from two different breeds that were either allowed to graze on grass like normal or only graze part-time while being fed a supplemental diet that featured corn and other concentrated foods.
As the researchers found, the corn-fed cohort consistently produced the same amount of milk and less methane than their grass-fed counterparts — but the taste of the resulting milk products was less savory and rich than the grass-fed bovines.
Moreover, the milk from the grass-fed cows contained more omega-3 fatty acids, which are good for the heart, and lactic acids, which act as probiotics.
"Farmers are looking for feed with better yields than grass or that are more resilient to droughts," explained Matthieu Bouchon, the fittingly-named lead author of the study.
Still, those same farmers want to know how supplementing their cows' feed will change the nutritional value and taste, Bouchon said — and one farmer who spoke to Science News affirmed anecdotally, this effect is bearing out in other parts of the world, too.
"We were having lots of problems with milk protein and fat content due to the heat," Gustavo Abijaodi, a dairy farmer in Brazil, told the website. "If we can stabilize heat effects, the cattle will respond with better and more nutritious milk."
The heat also seems to be getting to the way cows eat and behave as well.
"Cows produce heat to digest food — so if they are already feeling hot, they'll eat less to lower their temperature," noted Marina Danes, a dairy scientist at Brazil's Federal University of Lavras. "This process spirals into immunosuppression, leaving the animal vulnerable to disease."
Whether it's the food quality or the heat affecting the cows, the effects are palpable — or, in this case, edible.
"If climate change progresses the way it's going, we'll feel it in our cheese," remarked Bouchon, the French researcher.
More on cattle science: Brazilian "Supercows" Reportedly Close to Achieving World Domination
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3 hours ago
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Dupixent® (dupilumab) Demonstrated Superiority Over Xolair® (Omalizumab) in Chronic Rhinosinusitis with Nasal Polyps (CRSwNP) in Patients with Coexisting Asthma in First-ever Presented Phase 4 Head-to-Head Respiratory Trial
New late-breaking data at EAACI showed Dupixent outperformed Xolair across all primary and secondary efficacy endpoints of CRSwNP and in all asthma-related endpoints Dupixent also outperformed Xolair in improving such key signs and symptoms as nasal polyp size and sense of smell in CRSwNP, and lung function and disease control in asthma, with rapid improvements seen as early as 4 weeks Results reinforce the efficacy of Dupixent in treating both upper and lower respiratory diseases by targeting IL-4 and IL-13, two key drivers of type 2 inflammation TARRYTOWN, N.Y. and PARIS, June 15, 2025 (GLOBE NEWSWIRE) -- Regeneron Pharmaceuticals, Inc. (NASDAQ: REGN) and Sanofi today presented positive results from the EVEREST Phase 4 trial in adults with severe chronic rhinosinusitis with nasal polyps (CRSwNP) and coexisting asthma. In the trial, Dupixent® (dupilumab) outperformed Xolair® (omalizumab) on all primary and secondary efficacy endpoints of CRSwNP, and in all asthma-related endpoints. The data are from the first-ever presented head-to-head respiratory trial with biologic medicines and were shared in a late-breaking oral presentation at the 2025 European Academy of Allergy and Clinical Immunology (EAACI) Annual Congress. 'Patients suffering from chronic rhinosinusitis with nasal polyps often live with the constant obstruction of their nasal passages that can lead to burdensome nasal congestion and loss of smell. What's more, a majority of these individuals also have asthma that can substantially impact their quality of life,' said Eugenio De Corso, M.D., Ph.D., ENT Specialist, Otolaryngology, Head and Neck Surgery, Rhinology, A. Gemelli University Hospital Foundation, IRCSS, Rome, Italy, and lead investigator of the study. 'EVEREST is the first-ever trial to demonstrate the superiority of Dupixent over Xolair on CRSwNP endpoints in patients with coexisting asthma, along with generally similar safety profiles. Together, these Dupixent outcomes provide important insights that will help guide patients and physicians through the treatment decision-making process.' In the EVEREST trial, 360 adults with severe, uncontrolled CRSwNP and coexisting asthma were randomized to receive Dupixent 300 mg (n=181) every two weeks or a weight- and immunoglobulin E (IgE) level-based dosing regimen of Xolair (n=179) every two or four weeks. Both Dupixent and Xolair were added to background mometasone furoate nasal spray (MFNS). Primary and secondary endpoint results in CRSwNP for patients treated with Dupixent compared to Xolair at 24 weeks were as follows, with differences seen as early as 4 weeks: 1.60-point superior reduction in nasal polyp size, a primary endpoint (p<0.0001a) 8.0-point superior improvement in ability to identify different smells, a primary endpoint (p<0.0001a). More patients on Dupixent improved above the anosmia threshold compared to Xolair. 0.58-point superior reduction in nasal congestion/obstruction, a key secondary endpoint (p<0.0001a) 0.81-point superior improvement in loss of smell, a key secondary endpoint (p<0.0001a) 1.74-point superior reduction in symptom severity (p<0.0001a) 12.7-point difference in health-related quality of life (p<0.0001b) 31.27-point difference in peak nasal inspiratory flow (p<0.0001b) 1.87-point difference in overall severity of rhinosinusitis (p<0.0001b) Asthma endpoint results for patients treated with Dupixent compared to Xolair at 24 weeks were as follows, with differences seen as early as 4 weeks: 150 mL difference in lung function (pre-bronchodilator FEV1; p=0.003b) 0.48-point difference in asthma control (p<0.0001b) aStatistically significantbNominally significant as the endpoint was not included in the multiplicity adjustment hierarchy The safety results in the EVEREST trial were generally consistent with the known safety profile of Dupixent in its approved respiratory indications, with similar overall rates of adverse events (AEs) observed between Dupixent (64%) and Xolair (67%). Serious AEs were reported in 2% and 4% of patients treated with Dupixent and Xolair, respectively. Additionally, AEs leading to trial discontinuation were reported in 3% of Dupixent patients and 1% of Xolair patients. About the Dupixent Phase 4 TrialEVEREST is a randomized, double-blind Phase 4 trial comparing the efficacy and safety of Dupixent to Xolair in adults with severe, uncontrolled CRSwNP and coexisting mild, moderate or severe asthma. During the 24-week trial, patients received Dupixent 300 mg every two weeks or Xolair 75 to 600 mg every two or four weeks, which was added to background MFNS. Xolair dosing was determined based on body weight and serum total IgE levels as per the approved label. All endpoints were assessed at 24 weeks. The primary endpoints assessed change from baseline in nasal polyp score (NPS; scale: 0-8) and the University of Pennsylvania Smell Identification Test (UPSIT; scale: 0-40). Secondary endpoints included change from baseline in nasal congestion (NC; scale: 0-3), loss of smell (LoS; scale: 0-3), total symptom score (TSS; scale: 0-9), Sino-Nasal Outcome Test-22 (SNOT-22; scale: 0-110), peak nasal inspiratory flow, and rhinosinusitis disease severity (visual analogue scale: 0-10 cm). Other endpoints assessed pre-bronchodilator forced expiratory volume over one second (pre-BD FEV1) and the 7-item Asthma Control Questionnaire (ACQ-7; scale: 0-6). About DupixentDupixent, which was invented using Regeneron's proprietary VelocImmune® technology, is a fully human monoclonal antibody that inhibits the signaling of the interleukin-4 (IL-4) and interleukin-13 (IL-13) pathways and is not an immunosuppressant. The Dupixent development program has shown significant clinical benefit and a decrease in type 2 inflammation in Phase 3 trials, establishing that IL-4 and IL-13 are two of the key and central drivers of the type 2 inflammation that plays a major role in multiple related and often co-morbid diseases. Dupixent has received regulatory approvals in more than 60 countries in one or more indications including certain patients with atopic dermatitis, asthma, CRSwNP, eosinophilic esophagitis (EoE), prurigo nodularis, chronic spontaneous urticaria (CSU) and chronic obstructive pulmonary disease (COPD) in different age populations. More than 1,000,000 patients are being treated with Dupixent globally.1 About Regeneron's Technology Regeneron's VelocImmune technology utilizes a proprietary genetically engineered mouse platform endowed with a genetically humanized immune system to produce optimized fully human antibodies. When Regeneron's co-Founder, President and Chief Scientific Officer George D. Yancopoulos was a graduate student with his mentor Frederick W. Alt in 1985, they were the first to envision making such a genetically humanized mouse, and Regeneron has spent decades inventing and developing VelocImmune and related VelociSuite® technologies. Dr. Yancopoulos and his team have used VelocImmune technology to create a substantial proportion of all original, FDA-approved fully human monoclonal antibodies. This includes Dupixent® (dupilumab), Libtayo® (cemiplimab-rwlc), Praluent® (alirocumab), Kevzara® (sarilumab), Evkeeza® (evinacumab-dgnb), Inmazeb® (atoltivimab, maftivimab and odesivimab-ebgn) and Veopoz® (pozelimab-bbfg). In addition, REGEN-COV® (casirivimab and imdevimab) had been authorized by the FDA during the COVID-19 pandemic until 2024. Dupilumab Development Program Dupilumab is being jointly developed by Regeneron and Sanofi under a global collaboration agreement. To date, dupilumab has been studied across more than 60 clinical trials involving more than 10,000 patients with various chronic diseases driven in part by type 2 inflammation. In addition to the currently approved indications, Regeneron and Sanofi are studying dupilumab in a broad range of diseases driven by type 2 inflammation or other allergic processes in Phase 3 trials, including chronic pruritus of unknown origin, bullous pemphigoid and lichen simplex chronicus. These potential uses of dupilumab are currently under clinical investigation, and the safety and efficacy in these conditions have not been fully evaluated by any regulatory authority. U.S. INDICATIONS DUPIXENT is a prescription medicine used: to treat adults and children 6 months of age and older with moderate-to-severe eczema (atopic dermatitis or AD) that is not well controlled with prescription therapies used on the skin (topical), or who cannot use topical therapies. 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It is not known if DUPIXENT is safe and effective in children with chronic rhinosinusitis with nasal polyps under 12 years of age. to treat adults and children 1 year of age and older with eosinophilic esophagitis (EoE), who weigh at least 33 pounds (15 kg). It is not known if DUPIXENT is safe and effective in children with eosinophilic esophagitis under 1 year of age, or who weigh less than 33 pounds (15 kg). to treat adults with prurigo nodularis (PN). It is not known if DUPIXENT is safe and effective in children with prurigo nodularis under 18 years of age. with other medicines for the maintenance treatment of adults with inadequately controlled chronic obstructive pulmonary disease (COPD) and a high number of blood eosinophils (a type of white blood cell that may contribute to your COPD). DUPIXENT is used to reduce the number of flare-ups (the worsening of your COPD symptoms for several days) and can improve your breathing. It is not known if DUPIXENT is safe and effective in children with chronic obstructive pulmonary disease under 18 years of age. to treat adults and children 12 years of age and older with chronic spontaneous urticaria (CSU) who continue to have hives that are not controlled with H1 antihistamine treatment. It is not known if DUPIXENT is safe and effective in children with chronic spontaneous urticaria under 12 years of age, or who weigh less than 66 pounds (30 kg). DUPIXENT is not used to relieve sudden breathing problems and will not replace an inhaled rescue medicine. DUPIXENT is not used to treat any other forms of hives (urticaria). IMPORTANT SAFETY INFORMATION Do not use if you are allergic to dupilumab or to any of the ingredients in DUPIXENT®. Before using DUPIXENT, tell your healthcare provider about all your medical conditions, including if you: have eye problems. have a parasitic (helminth) infection. are scheduled to receive any vaccinations. You should not receive a 'live vaccine' right before and during treatment with DUPIXENT. are pregnant or plan to become pregnant. It is not known whether DUPIXENT will harm your unborn baby. A pregnancy registry for women who take DUPIXENT during pregnancy collects information about the health of you and your baby. To enroll or get more information call 1-877-311-8972 or go to . are breastfeeding or plan to breastfeed. It is not known whether DUPIXENT passes into your breast milk. Tell your healthcare provider about all the medicines you take, including prescription and over-the-counter medicines, vitamins, and herbal supplements. Especially tell your healthcare provider if you are taking oral, topical, or inhaled corticosteroid medicines; have asthma and use an asthma medicine; or have atopic dermatitis, chronic rhinosinusitis with nasal polyps, eosinophilic esophagitis, prurigo nodularis, chronic obstructive pulmonary disease, or chronic spontaneous urticaria, and also have asthma. Do not change or stop your other medicines, including corticosteroid medicine or other asthma medicine, without talking to your healthcare provider. This may cause other symptoms that were controlled by those medicines to come back. DUPIXENT can cause serious side effects, including: Allergic reactions. DUPIXENT can cause allergic reactions that can sometimes be severe. Stop using DUPIXENT and tell your healthcare provider or get emergency help right away if you get any of the following signs or symptoms: breathing problems or wheezing, swelling of the face, lips, mouth, tongue or throat, fainting, dizziness, feeling lightheaded, fast pulse, fever, hives, joint pain, general ill feeling, itching, skin rash, swollen lymph nodes, nausea or vomiting, or cramps in your stomach-area. Eye problems. Tell your healthcare provider if you have any new or worsening eye problems, including eye pain or changes in vision, such as blurred vision. Your healthcare provider may send you to an ophthalmologist for an exam if needed Inflammation of your blood vessels. Rarely, this can happen in people with asthma who receive DUPIXENT. This may happen in people who also take a steroid medicine by mouth that is being stopped or the dose is being lowered. Tell your healthcare provider right away if you have: rash, chest pain, worsening shortness of breath, brown or dark colored urine, persistent fever, or a feeling of pins and needles or numbness of your arms or legs. Psoriasis. This can happen in people with atopic dermatitis and asthma who receive DUPIXENT. Tell your healthcare provider about any new skin symptoms. Your healthcare provider may send you to a dermatologist for an examination if needed. Joint aches and pain. Some people who use DUPIXENT have had trouble walking or moving due to their joint symptoms, and in some cases needed to be hospitalized. Tell your healthcare provider about any new or worsening joint symptoms. 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Prurigo Nodularis: eye and eyelid inflammation, including redness, swelling, and itching, sometimes with blurred vision, herpes virus infections, common cold symptoms (nasopharyngitis), dizziness, muscle pain, and diarrhea. Chronic Obstructive Pulmonary Disease: injection site reactions, common cold symptoms (nasopharyngitis), high count of a certain white blood cell (eosinophilia), viral infection, back pain, inflammation inside the nose (rhinitis), diarrhea, gastritis, joint pain (arthralgia), toothache, headache, and urinary tract infection. Chronic Spontaneous Urticaria: injection site reactions. Tell your healthcare provider if you have any side effect that bothers you or that does not go away. These are not all the possible side effects of DUPIXENT. Call your doctor for medical advice about side effects. You are encouraged to report negative side effects of prescription drugs to the FDA. Visit or call 1-800-FDA-1088. Use DUPIXENT exactly as prescribed by your healthcare provider. It's an injection given under the skin (subcutaneous injection). Your healthcare provider will decide if you or your caregiver can inject DUPIXENT. Do not try to prepare and inject DUPIXENT until you or your caregiver have been trained by your healthcare provider. In children 12 years of age and older, it's recommended DUPIXENT be administered by or under supervision of an adult. In children 6 months to less than 12 years of age, DUPIXENT should be given by a caregiver. Please see accompanying full Prescribing Information including Patient Information. About RegeneronRegeneron (NASDAQ: REGN) is a leading biotechnology company that invents, develops and commercializes life-transforming medicines for people with serious diseases. Founded and led by physician-scientists, our unique ability to repeatedly and consistently translate science into medicine has led to numerous approved treatments and product candidates in development, most of which were homegrown in our laboratories. Our medicines and pipeline are designed to help patients with eye diseases, allergic and inflammatory diseases, cancer, cardiovascular and metabolic diseases, neurological diseases, hematologic conditions, infectious diseases, and rare diseases. Regeneron pushes the boundaries of scientific discovery and accelerates drug development using our proprietary technologies, such as VelociSuite, which produces optimized fully human antibodies and new classes of bispecific antibodies. We are shaping the next frontier of medicine with data-powered insights from the Regeneron Genetics Center® and pioneering genetic medicine platforms, enabling us to identify innovative targets and complementary approaches to potentially treat or cure diseases. For more information, please visit or follow Regeneron on LinkedIn, Instagram, Facebook or X. About Sanofi Sanofi is an R&D driven, AI-powered biopharma company committed to improving people's lives and delivering compelling growth. We apply our deep understanding of the immune system to invent medicines and vaccines that treat and protect millions of people around the world, with an innovative pipeline that could benefit millions more. Our team is guided by one purpose: we chase the miracles of science to improve people's lives; this inspires us to drive progress and deliver positive impact for our people and the communities we serve, by addressing the most urgent healthcare, environmental, and societal challenges of our time. Sanofi is listed on EURONEXT: SAN and NASDAQ: SNY. Regeneron Forward-Looking Statements and Use of Digital Media This press release includes forward-looking statements that involve risks and uncertainties relating to future events and the future performance of Regeneron Pharmaceuticals, Inc. ('Regeneron' or the 'Company'), and actual events or results may differ materially from these forward-looking statements. Words such as 'anticipate,' 'expect,' 'intend,' 'plan,' 'believe,' 'seek,' 'estimate,' variations of such words, and similar expressions are intended to identify such forward-looking statements, although not all forward-looking statements contain these identifying words. 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Yahoo
5 hours ago
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Who's the real invasive species: us or them? Ecologists are rethinking urban biodiversity
Climate change is already having a profound impact on cities, as global urbanization pushes more and more people to live in them. The animals who cohabitate with human, whether we appreciate their presence or not, are changing too. Specifically, there's been an increase in invasive species — a term used to describe introduced organisms that bring dramatic and often destructive changes, and sometimes can drive other species to extinction. But here's the thing: Invasive species don't stop evolving themselves. Consider the infamous brown rats of New York City, which have evolved longer noses and shorter upper molar tooth rows, the better to enjoy the Big Apple's colder weather and higher-quality food. Other invasive species are adapting behaviorally, physically and genetically to life in cities as well. While invasive species pose major public health implications and can certainly affect humans' quality of life, their adaptive abilities can rival those of human migrants and pose a puzzling question: Who's the real invader here? Brian Verrelli, a professor in the Center of Biological Data Science at Virginia Commonwealth University, sees many of these questions as philosophical. "What does it mean to invade something, right?" he asked in a video interview. "What does it mean for humans to invade one area or another? Are there areas that we invade, or are humans welcome freely to move around the planet? We know that's the case in some places, and certainly not the case in others. "It's a bit of an interesting, hypocritical conversation," Verrelli added, given that "we are facilitating the movement of these organisms around the planet." Rats have invaded new continents because ships carrying them in the hold. Spiders move across continents inside our cars. And we have all literally "translocated" organisms from one place to another, Verrelli said, because we wanted to — flowers and household pets, for example. "Traveling globally, one can notice the same suite of species in many cities around the world — biological invasions creating a kind of global Cuisinart where the urban biota becomes homogeneous," Laura Meyerson, a professor at the University of Rhode Island who studies invasive species and ecological restoration, told Salon. " She cited the nearly ubiquitous tree of heaven (Ailanthus altissima), which is found in cities around the world. "This introduced tree is threatening important ancient ruins such as the Roman Colosseum. Interestingly, it is the host plant in its native range for the spotted lanternfly," an invasive pest that has recently gotten a lot of attention in North America. "Other common species in urban areas globally are Norway rats and English pigeons, both of which can spread disease," Meyerson said, along with "European starlings and the common reed (Phragmites australis), both of those being aggressive introduced species that displace native species." But Verrelli believes that if we can't exactly determine who counts as an invader, we also can't really say what's being invaded. That might sound like an abstruse philosophical argument, but he says it's a hot debate within the scientific community. "We have what are called 'stud books' for our primates at zoos all over the world," Verrelli said. "We don't count that as invasion, but we are directly facilitating that. I'm hitting this note because it very much underlies our idea of invasion and gene flow, how genetics moves around and what it means to point to an organism and say it belongs to a certain species." Verrelli has studied the spread of black widow spiders, an increasing medical health concern in cities along the West Coast. People now encounter these potentially deadly spiders, which used to be found in isolated desert areas, in urban or suburban garages and yards. "As we're altering the landscape within cities, these areas are becoming attractive to black widows," Verrelli said. "They're all around us now, so we need to be able to understand what's happening as they're moving into cities." There are important health and environmental questions about whether black widows are becoming more deadly or displacing other arachnid species, but Verrelli raises a different question: "They were here first. Are they really invading the urban area? Yes, because we plopped the urban area down in the middle of the desert." Verrelli spent nine years in Arizona, an arid environment where many organisms struggle to survive, but that has now been altered and made more hospitable by human habitation. Indeed, the American Southwest is particularly vulnerable to invasive species, including highly adaptive species that can affect human health, largely thanks to the rapid spread of urbanism — which can bring water to desert environments while also creating artificial heat islands in colder climates, and allowing tropical species to expand their ranges. Meyerson defines invasive species as "non-native species introduced either intentionally or accidentally by humans outside of their native range," while noting a crucial distinction between non-native but non-invasive species — tulips were imported to North America from Europe, for example, but do no ecological harm — and invasive ones. Most invasion scientists aim "to prevent introductions of harmful invasive species in the first place through public education, better screening tools and risk assessments," she said. But once such species are introduced, detecting and eradicating them quickly becomes the goal. If that doesn't work, the next goal is about managing and containing them, preventing further spread, and supporting native species by managing green spaces and natural habitats within the urban environment. "Urban areas can also be important stopover sites for migrating species," she added. "We need to manage these areas to help support these seasonal migrations." It's no longer reasonable, Verrelli believes, to draw a neat line between urban and wild spaces. "For a very long time, even most scientists studying urban areas as ecologists didn't really treat urban areas as 'natural' environments, because humans lived in them," he said. "That's something that I smile at, because if we don't believe humans are part of the natural world, we're in trouble. Most of our natural world is going to be consumed by humans, in which case we're ignoring a major influence on how organismal biodiversity is successful." Patterns of evolution play out in urban environments. A classic example often taught in high school biology classes is that of industrial melanism in the peppered moth, a British species tha looks, well, "peppered," with black dots on a mostly white background. There had always been occasional all-black moths, but from the mid-19th century, observers began to see more and more black moths in the industrial cities of England and Scotland. The mostly white moths stood out in the sooty environment and became easy prey for predators. Ultimately, the ones able to blend in were more likely to survive and reproduce. This is an adaptation — in evolutionary biology, a trait that arose due to natural selection. But when we casually talk about species adapting to life in the big city, that's not always what we're describing. A bear that overturns your trash can and figures out how to get your leftovers isn't "adapting"; it's just repurposing a behavior that evolved in its natural or ancestral environment. This kind of transfer of an evolutionary adaptation to a new context is called "exaptation." "It's really important that we know the difference between these two," Verrelli said. "We're not just trying to classify for the purpose of classification. If we can tell the exaptations versus the adaptations, then we are going to really understand the selective agents." Verrelli cites the work of Kristen Winchell at NYU, who has studied anoles lizards moving from forests into urban areas in Puerto Rico. In cities, she found, these lizards evolved longer legs relative to their body size, allowing them to crawl up metal pipes. That's not an exaptation, where the same structures that let them climb trees are applied to the new setting, but actual evolutionary adaptations. In Verrelli's view, understanding this difference isn't about discouraging these animals' presence, but making it easier for us and them to live in harmony and reasonable comfort. If an urban lizard can't climb up a pipe, an urban cat may select it right out of existence. "How do we design the urban environment to make them more readily livable to these organisms?" Verrelli asks. "What kind of surfaces should we be developing? What kind of areas? Where do we put light, where do we not put light?" Such questions will be "very important to understanding how organisms can move through urban environments." Sometimes our attempts to address invasive species can be counterproductive: Meyerson cites the example of the American elm, a formerly popular street tree appreciated not only for their beauty but also their hardiness under harsh urban conditions. But Dutch elm disease, an invasive fungus spread by bark beetles to which the native trees had no defense, has decimated the elm by tens of millions across the continent. "Ironically, many of these street trees were replaced by other introduced invasive species such as Norway maple or callery pear," she said, "which in turn have their own impacts." Introduced species are wreaking havoc due to similar lack of evolved defenses in the American beech, many amphibian species and North American bats of different kinds. Generalist creatures, those that can thrive in a variety of environments, will most easily adapt to city life and may go on to decimate native species. There is general agreement that we are no longer dealing with either a purely urban, human environment or a purely wild and untouched one. But while Verrelli belongs to one side in the ongoing debate among conservation biologists, the other includes those who believe cities are an incurable blight and that their spread must be reduced or reversed. His side, roughly speaking, sees urbanization as a permanent reality and harmonious biodiversity — sharing these spaces with our plant and animal relatives — as the most important goal. They see the distinction between wild spaces and urban spaces collapsing, which is happening anyway, not always harmoniously. "In understanding invasion, we need to learn more about cities," Verrelli said. "We need to learn more about invaders. We need to learn more about how they're doing, what they're doing. That's why we study things like bedbugs and black widows, because these are good models to learn about how this is happening, and because it's going to keep happening. "Instead of the idea of, let's go study things outside of cities, because this are the important areas we need to conserve, I'm on the other side. We need to study invasions in cities, because this is largely the future, whether we like it or not. As we move into the future, we're preparing a new landscape that's evolving all the time. Let's prepare biodiversity for it as well."


Gizmodo
8 hours ago
- Gizmodo
Climate Disasters Hit the Brain Before Babies Are Even Born, Study Suggests
When Superstorm Sandy made a beeline for New York City in October 2012, it flooded huge swaths of downtown Manhattan, leaving 2 million people without electricity and heat and damaging tens of thousands of homes. The storm followed a sweltering summer in New York City, with a procession of heat waves nearing 100 degrees. For those who were pregnant at the time, enduring these extreme conditions wasn't just uncomfortable—it may have left a lasting imprint on their children's brains. That's according to a new study published on Wednesday in the peer-reviewed journal PLOS One. Using MRI scans, researchers at Queens College, City University of New York, found that children whose mothers lived through Superstorm Sandy had distinct brain differences that could hinder their emotional development. The effects were even more dramatic when people were exposed to extreme heat during their pregnancy, in addition to the tropical storm, the researchers found. 'It's not just one climate stressor or one isolated event, but rather a combination of everything,' said Donato DeIngeniis, the lead author of the study and a doctoral student in neuropsychology at the CUNY Graduate Center. DeIngeniis' study is the first of its kind to examine the joint effects of natural disasters and extreme heat—events that often coincide. A few years ago, scientists dubbed summer 'danger season' since it's a time of colliding risks, including heat, hurricanes, wildfires, and toxic smoke. And summertime temperatures keep climbing to new heights. The study analyzed brain imaging data from a group of 34 children, approximately 8 years old, whose mothers were pregnant during Superstorm Sandy—some of whom were pregnant at the time that Sandy made landfall, and some of whom were exposed to heat 95 degrees F or higher during their pregnancy. While the researchers didn't find that heat alone had much of an impact, living through Superstorm Sandy led to an increase in the basal ganglia's volume, a part of the brain that deals with regulating emotions. While that larger size could be a compensation in response to stress, changes in the basal ganglia have been linked to behavioral challenges for children, such as depression and autism, DeIngeniis said. 'What we are seeing is compelling evidence that the climate crisis is not just an environmental emergency, it is potentially a neurological one with consequence for future generations who will inherit our planet,' said Duke Shereen, a co-author of the study and the director of the MRI facility at CUNY Graduate Center, in a press release. Global warming made Superstorm Sandy more damaging as a result of rising sea levels and higher ocean temperatures that might have amped up its rainfall. Yoko Nomura, a co-author of the study and a psychology professor at the Queens College, CUNY, said that the time before birth is 'very, very sensitive' for development because the fetus' body is changing so drastically. The human brain grows the most rapidly in the womb, reaching more than a third of its full adult volume before birth, according to the study. Any added stress at that time, even if small, 'can have a much bigger impact,' Nomura said. But that extra-sensitive period also presents a window of opportunity. 'Developmental science, including the science in this paper, is exciting because it not only tells us what we can do to protect children from the effects of climate change, but it also tells us when we can step in to protect children to make the greatest difference,' Lindsey Burghardt, chief science officer at the Center on the Developing Child at Harvard University, said in an email. Although there's a lot of evidence that prenatal stress generally can affect child brain development, according to DeIngeniis, research on climate-related stress specifically is lacking. 'It is still a field that has potential for explosive growth,' said Jennifer Barkin, a professor at Mercer University School of Medicine in Macon, Georgia, who is studying the effects of last year's Hurricane Helene on maternal health. DeIngeniis' study offers concrete evidence of how climate-charged events can affect the brain, Barkin said. 'People have a hard time sometimes with mental health, because it's not like you can take an X-ray and see a broken bone.' But it's easier to understand imaging showing a difference in brain volume based on exposure to environmental stress, she said. Barkin, who developed an index for measuring maternal health after childbirth, says that people are beginning to pay more attention to mothers and their mental health—not just in terms of delivering a healthy baby, but over the long term. 'We tend to focus things on the child's outcome, which is important, but to keep the child healthy, the mother has to be healthy, too,' she said. 'Because when Mom's struggling, the family's going to struggle.' This article originally appeared in Grist at Grist is a nonprofit, independent media organization dedicated to telling stories of climate solutions and a just future. Learn more at