100 years ago, scientists predicted we'd live to 1,000 years old
The foundations for this optimism had been building for decades. Germs were first discovered in the 1880s, ushering in the golden age of bacteriology and numerous life-saving vaccines. Vitamins got their name in the early 1900s when London-based Polish biochemist Casimir Funk—one of many scientists seeking cures for common diseases by linking them to vital nutrient deficiencies—combined 'vital' and 'amines.' Rickets led to the discovery of vitamin D, scurvy to vitamin C, and vitamin B was tied to beriberi, a disease that causes weakness, weight loss, confusion, and, in extreme cases, death. Meanwhile, anesthesia transformed surgery from a grisly performing art with low survival rates to more precise procedures conducted in germ-free operating rooms. Bit by bit, medicine appeared to be conquering many of humanity's most pernicious plagues and thereby extending our average lifespan.
By July 1925, Popular Science writer John E. Lodge even suggested that humans might soon be able to extend their life expectancy to 1,000 years. 'Thanks to the efforts of science in combatting the ravages of disease, the average span of life is increasing every year,' Lodge wrote. 'Are we to expect, then, that in time science will succeed in prolonging the average life until, like Methuselah, we measure our lives by centuries instead of by years.' Lodge envisioned a world where aging could be halted by replacing worn-out enzymes, transplanting organs, or manipulating an elusive 'vital spark.' Scientists, he claimed, might be on the verge of conquering death itself.
A hundred years later, we're still not there, but we continue to chase immortality with the same zest. Just as a century ago, today that quest is fueled not by glamorous breakthroughs—even if history makes it seem so—but by painstaking, collaborative scientific research, yielding fresh medical insights. In place of insulin, vaccines, and vitamins, today we're captivated by gene-editing, cellular reprogramming, and immunotherapy. From biohackers injecting stem cells in search of cellular youth to billionaires like Bryan Johnson leaning on wearable tech for preventative health, blood plasma exchanges, and caloric restriction, the goal of outsmarting death hasn't diminished—the elixirs are just more sophisticated.
And yet, we've come a long way in a century. In 1925, the average American lifespan was 58 years; today, it's 78.4 years, according to the US Centers for Disease Control. Such progress might seem meager compared to our grandiose early 20th century expectations, but the trend suggests that by the next century the average American would live to be a centenarian. There's even reason to believe—as there was in 1925—that current promising research might yield treatments as soon as the next few decades that significantly extend our lifespans while improving disease resistance.
Consider how researchers in Singapore have extended the lives of mice 25 percent by blocking the protein interleukin-11. Scientists at the University of Rochester have successfully transferred a longevity gene to mice from naked mole rats, which live ten times longer than similar rodents. The gene, known for producing high molecular weight hyaluronic acid, or HMW-HA, extended mouse lives by 4.4% and improved their overall health. The researchers now aim to transfer these benefits to humans.
In an ironic twist, a century after Banting's insulin discovery displaced goat's rue, a derivative of the pink-and-white flowering plant is back in favor. Metformin, a biguanide medication, has become one of the leading drugs for managing type 2 diabetes. Like its medieval predecessor, which was used for everything from increasing milk flow in livestock to alleviating plague symptoms, metformin has been similarly used or tested in myriad applications: as an antimalarial drug, influenza treatment, lactation enhancer, arthritis remedy, and cardiovascular medicine. Now, scientists have begun to piece together the mystery of metformin's versatility by mapping how it works at a cellular level. Recent research has shown that it may slow or inhibit cellular changes leading to inflammation and age-related diseases, extending lifespan.
The cellular aging story stretches back to the late 19th century. As scientists were discovering germs, developing vaccines, uncovering the link between vital nutrients and common diseases, and improving surgery, evolutionary biologist August Weismann theorized that human cells had replication limits, which explained why the ability to heal diminished with age. By the 1960s, scientists had proven Weismann correct. Today, researchers are learning to halt and reverse cellular aging through reprogramming, an idea first attempted in the 1980s and advanced by Nobel Prize recipient Shinya Yamanaka, who discovered how to revert mature, specialized cells back to their embryonic, or pluripotent state, enabling them to regenerate into new tissue like liver cells or teeth.
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But none of this means we're approaching thousand-year lifespans. Most longevity interventions work only in tightly controlled laboratory settings or short-lived animals. Translating them into humans presents entirely different—and enormously complex—challenges. Even if we managed to double or triple the human lifespan, equally complex social challenges would follow: Who would get access to life-extending therapies? How do we support a society where most people live into their third or fourth century? What psychological toll does such extreme longevity take?
The optimism of 1925 wasn't misplaced; it was simply premature. It still might be, but today's longevity researchers are armed with more sophisticated tools and a deeper understanding of biological processes. Whether today's tools and knowledge will finally enable us to defy death remains to be seen. If there's a lesson to draw from the past hundred years, however, it's that life extension is incremental, fragile, and often humbling. We've added decades to average life expectancy, transformed once-fatal diseases into manageable conditions, and dramatically improved the quality of life in later years. That's no small feat—but it's not immortality.
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25 minutes ago
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Astronaut captures amazing red sprite phenomenon from space
Speeding around the Earth at 28,000 km/h, NASA astronaut Nichole Ayers captured an incredible view of a phenomenon known as a red sprite. Here's the science behind this 'transient luminous event'. Lightning flashes through the air several million times every day, all around the world. The vast majority of those bolts occur inside clouds, between different clouds, or between the clouds and the ground. They happen as a result of large build-ups of negative or positive charge within clouds and along the ground, and act to balance out those charges. A small fraction of these discharges — about one in every 1,600 on average — actually occur above the clouds. These 'transient luminous events' or TLEs happen when the charge build-up within a thunderstorm balances out between the cloud and the upper atmosphere, near the edge of space. The different forms of transient luminous events. (NOAA) On July 3, 2025, from her vantage point in the cupola of the International Space Station, astronaut Nichole Ayers was snapping pictures of thunderstorms as the station passed over Mexico and the United States. In a spectacular feat of timing, one of her photographs managed to catch one of these TLEs, known as a red sprite, right in the middle of discharging! This cropped view of the image snapped by astronaut Nichole Ayers zooms in on the red sprite she captured on July 3, 2025. (astro_ayers/X/NASA) READ MORE: Sprites are rapid flashes of red light that occur high up in the atmosphere, over 50 kilometres above the ground. While they are referred to as upper atmospheric lightning, the only thing red sprites have in common with the typical form of lightning we see is the movement of electric charge from one part of the atmosphere to another. Other than that, they are very different phenomena. Another sprite seen from the ISS on August 10, 2015, over Central America. (NASA) Lightning only occurs in the lowest part of the atmosphere — the troposphere — and as it flashes through the air, it heats that air to temperatures hotter than the surface of the Sun. Sprites, on the other hand, only happen in the thin upper atmosphere — the mesosphere and ionosphere — and they are a cold plasma phenomenon. Their glow probably has more in common with that of a fluorescent light bulb, or the Aurora Borealis. The colour of a sprite comes from the fact that our atmosphere is mostly nitrogen. When an air molecule becomes energized, one of the electrons orbiting around it will jump up to a higher level. To return to its 'ground state', where the electron drops back down into its normal orbit, it emits a flash of light to dump its excess energy. In the case of nitrogen, the light emitted has a very strong red component, along with a bit of blue and purple. This immense 'jellyfish sprite' was captured over a storm in West Texas on July 2, 2020. (Stephen Hummel) It seems that we've known about sprites, or at least transient luminous events in general, for around 300 years. According to NASA, pilots apparently were reporting sightings of them since the first military and commercial flights in the early part of the 20th century. It wasn't until 1989, though, that they were finally caught on camera. While we know what sprites are, explaining how they form is a bit more challenging. However, here's what we know, as well as what researchers speculate, about the process. The formation of a sprite starts inside a thunderstorm. There, the exchange of electrons between colliding ice crystals and snow pellets produces distinct regions of electric charge within the cloud. Weak positive charge collects at the base, strong negative charge accumulates in the middle, and strong positive charge builds at the top. Most often, lightning will balance the negative charge at the core of the cloud by linking it with a region of positive charge on the ground, inside another nearby cloud, or even within the same cloud. This is the common negative lightning that occurs millions of times per day. The likely distribution of electric charge of a cumulonimbus cloud has been drawn onto this User-generated Content image of a storm taken on Aug 27, 2022, from Carrot River, SK, and uploaded to the Weather Network's UGC gallery. (Fran Bryson/UGC) Occasionally, though, the strong positive charge accumulated at the top of the thunderstorm cloud has a chance to discharge, by linking with a region of negative charge along the ground. When this happens, we see a powerful stroke of positive lightning. This appears to be the point where a sprite has a chance to form. Normally, as a thunderstorm cloud is rolling along through the troposphere, at the same time, the air much higher up has a strong positive charge due to interactions with particles streaming into the atmosphere from space. Usually, this upper atmospheric positive charge doesn't have anywhere to go. It needs a region of negative charge to balance out. The negatively charged core of the thunderstorm could do this. However, the positive charge accumulated at the top of the cloud stands in the way. When a positive lightning strike lances out between the top of the cloud and the ground, though, much of that excess positive charge is stripped away. At that moment, the negative charge in the middle of the cloud becomes directly exposed to the positively charged mesosphere, allowing a connection to form. Based on observations, sprites are almost always preceded by a positive lightning strike. Thus, they are a potential trigger for the phenomenon. Even so, a positive lightning strike doesn't always guarantee that a sprite will appear. Thus, it's likely that some other component needs to be present for the sprite to form. That other component could be gravity waves. The video above was recorded from atop Mount Locke in West Texas, in May 2020, by Stephen Hummel, the dark sky specialist at the McDonald Observatory. In the video, gravity waves can clearly be seen, illuminated by a phenomenon called airglow, radiating away from a storm along the horizon to the lower right. Amid the gravity waves streaming through the field of view, several sprites are also captured (watch closely at 1s, 3s, 7s and 12s into the video). Gravity waves behave like ripples on the surface of a pond, with air rising and falling as it tries to balance out the forces of gravity and buoyancy. When a powerful thunderstorm's strong updraft winds reach the top of the troposphere, they are deflected by the stable air of the lower stratosphere, and are forced to spread outward instead. Research has already shown that the action of gravity waves can have an impact on the upper atmosphere. This could be another way they influence what happens, far above the surface. Now, exactly how gravity waves might play a role in sprite formation isn't yet known. Some researchers have noted that sprites appear to form at what they call "plasma irregularities" in the ionosphere. However, these irregularities are themselves, also a mystery. It could be that gravity waves play a role in forming these irregularities. For now, though, no one knows. To understand this phenomenon better, more sightings, more captures, and more research are required. Click here to view the video
Yahoo
35 minutes ago
- Yahoo
Celltrion USA announces U.S. launch of denosumab biosimilars, STOBOCLO® and OSENVELT® (denosumab-bmwo)
STOBOCLO® (denosumab-bmwo) and OSENVELT® (denosumab-bmwo) are approved by FDA for all indications of PROLIA® (denosumab) and XGEVA® (denosumab) respectively[1],[2] STOBOCLO and OSENVELT, among the first wave of biosimilars referencing PROLIA and XGEVA respectively, are commercially available in the U.S. Celltrion further expands its portfolio, delivering cost-effective and high-quality biologic medicines to wider range of patients in the U.S. JERSEY CITY, N.J., July 7, 2025 /PRNewswire/ -- Celltrion USA today announced that STOBOCLO® (denosumab-bmwo) and OSENVELT® (denosumab-bmwo), biosimilars referencing PROLIA® (denosumab) and XGEVA® (denosumab) respectively, are commercially available in the United States. STOBOCLO is available in 60 mg/mL injection and is approved to treat postmenopausal women with osteoporosis at high risk for fracture, to increase bone mass in men with osteoporosis at high risk for fracture, to treat glucocorticoid-induced osteoporosis in men and women at high risk for fracture, to increase bone mass in men at high risk for fracture receiving androgen deprivation therapy for nonmetastatic prostate cancer, and to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer.[1] OSENVELT is available in 120 mg/1.7 mL (70 mg/mL) injection and is indicated to prevent skeletal-related events in patients with multiple myeloma and in patients with bone metastases from solid tumors, to treat adults and skeletally mature adolescents with giant cell tumor of bone that is unresectable or where surgical resection is likely to result in severe morbidity, and to treat hypercalcemia of malignancy refractory to bisphosphonate therapy.[2] "We are pleased to have achieved a global settlement with Amgen regarding our denosumab biosimilars," said Thomas Nusbickel, Chief Commercial Officer at Celltrion USA. "We are proud to introduce our denosumab biosimilars to the U.S. market, offering patients and healthcare professionals a valuable alternative treatment option. Building on our strong heritage in biosimilars, Celltrion remains committed to being a trusted partner for both patients and physicians, while contributing to the overall sustainability of healthcare systems." STOBOCLO and OSENVELT are supported by Celltrion's comprehensive patient support programs designed to help empower patients to navigate their treatment journeys. Celltrion offers a suite of resources, including the Celltrion CONNECT® Patient Support Program and the Celltrion CARES™ Co-pay Assistance Program. Patients who are uninsured may be able to receive STOBOCLO and OSENVELT at no cost. Visit and to learn more. Celltrion's biosimilars portfolio covers the areas of immunology, oncology, gastroenterology, allergy, and endocrinology. About STOBOCLO® (denosumab-bmwo) STOBOCLO® (denosumab-bmwo) is a receptor activator of NF-κb ligand (RANKL) inhibitor referencing PROLIA® (denosumab). STOBOCLO 60 mg/mL injection is approved by the FDA based on comprehensive data and clinical evidence confirming the therapeutic equivalence to PROLIA. In the U.S., STOBOCLO is approved to treat postmenopausal women with osteoporosis at high risk for fracture, to increase bone mass in men with osteoporosis at high risk for fracture, to treat glucocorticoid-induced osteoporosis in men and women at high risk for fracture, to increase bone mass in men at high risk for fracture receiving androgen deprivation therapy for nonmetastatic prostate cancer, and to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. INDICATIONS STOBOCLO® (denosumab-bmwo) is a RANK ligand (RANKL) inhibitor indicated for treatment: of postmenopausal women with osteoporosis at high risk for fracture to increase bone mass in men with osteoporosis at high risk for fracture or in men at high risk for fracture receiving androgen deprivation therapy for nonmetastatic prostate cancer of glucocorticoid-induced osteoporosis in men and women at high risk for fracture to increase bone mass in women at high risk for fracture receiving an adjuvant aromatase inhibitor therapy for breast cancer IMPORTANT SAFETY INFORMATION WARNING: SEVERE HYPOCALCEMIA IN PATIENTS WITH ADVANCED KIDNEY DISEASE Patients with advanced chronic kidney disease, including those on dialysis, face a higher risk of severe hypocalcemia after denosumab administration, with reported cases leading to hospitalization, life-threatening events, and fatalities. The presence of chronic kidney disease-mineral bone disorder (CKD-MBD) markedly increases the risk of hypocalcemia in these patients Before starting STOBOCLO® (denosumab-bmwo) in advanced chronic kidney disease patients, assess for CKD-MBD. Treatment should be supervised by a healthcare provider experienced in diagnosing and managing CKD-MBD. STOBOCLO is contraindicated in hypocalcemia, pregnant women, and in patients with known hypersensitivity to denosumab. Severe Hypocalcemia: Ensure adequate calcium and vitamin D; monitor for severe hypocalcemia. Drug Products with Same Active Ingredient: Do not use with other denosumab products. Hypersensitivity: If an anaphylactic or other clinically significant allergic reaction occurs, initiate appropriate therapy and discontinue further use of STOBOCLO. Osteonecrosis of the Jaw (ONJ): ONJ can occur in patients on STOBOCLO. Conduct oral exams before treatment; maintain oral hygiene; consider discontinuation of STOBOCLO if ONJ develops. Atypical Subtrochanteric and Diaphyseal Femoral Fractures: Monitor for thigh, hip, or groin pain; evaluate for fractures. Interruption of STOBOCLO therapy should be considered, pending a benefit-risk assessment, on an individual basis. Multiple Vertebral Fractures (MVF) Following Discontinuation of Treatment: Increased risk post-discontinuation of denosumab; transition to alternative therapy if discontinuing STOBOCLO. Serious Infections: Higher risk in denosumab users; assess benefit-risk profile, especially in immunocompromised patients. Assess the benefit-risk profile before starting STOBOCLO and reconsider its use if serious infections develop. Dermatologic Adverse Reactions: Consider discontinuing STOBOCLO if severe dermatitis, eczema, or rashes occur. Musculoskeletal Pain: Consider discontinuation of STOBOCLO if severe pain develops. Bone Turnover Suppression: In clinical trials in women with postmenopausal osteoporosis, denosumab significantly suppressed bone remodelling; patients should be monitored for these outcomes. Hypercalcemia in Pediatrics Patients with Osteogenesis Imperfecta: Not for pediatric use; hypercalcemia reported in patients osteogenesis imperfecta treated with denosumab products. Most common Adverse Reactions: In (>5%) of patients with: Postmenopausal osteoporosis were back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. Male osteoporosis were back pain, arthralgia, and nasopharyngitis. Glucocorticoid-induced osteoporosis (> 3%) were back pain, hypertension, bronchitis, and headache. Bone loss due to hormone ablation for cancer (≥ 10%) were arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials. For more information, see Full Prescribing Information. About OSENVELT® (denosumab-bmwo) OSENVELT® (denosumab-bmwo) is a receptor activator of NF-κb ligand (RANKL) inhibitor referencing XGEVA® (denosumab). OSENVELT 120 mg/1.7 mL (70 mg/mL) injection is approved by the FDA based on a robust clinical trial and comprehensive data confirming the therapeutic equivalence to XGEVA. In the U.S., OSENVELT is indicated to prevent skeletal-related events in patients with multiple myeloma and in patients with bone metastases from solid tumors, to treat adults and skeletally mature adolescents with giant cell tumor of bone that is unresectable or where surgical resection is likely to result in severe morbidity, and to treat hypercalcemia of malignancy refractory to bisphosphonate therapy. INDICATION OSENVELT® (denosumab-bmwo) is indicated for: Prevention of skeletal-related events in patients with multiple myeloma and in patients with bone metastases from solid tumors. Treatment of adults and skeletally mature adolescents with giant cell tumor of bone that is unresectable or where surgical resection is likely to result in severe morbidity. Treatment of hypercalcemia of malignancy refractory to bisphosphonate therapy. IMPORTANT SAFETY INFORMATION Contraindications: Patients with hypocalcemia or with known clinically significant hypersensitivity to denosumab products. Drug Products with Same Active Ingredient. Patients receiving OSENVELT should not receive other denosumab products concomitantly. Hypersensitivity. If an anaphylactic or other clinically significant allergic reaction occurs, initiate appropriate therapy and discontinue further use of OSENVELT. Hypocalcemia. Severe hypocalcemia can occur, and fatal cases have been reported. Monitor calcium levels and calcium and vitamin D intake. Osteonecrosis of the Jaw (ONJ): ONJ can occur in patients on OSENVELT. Conduct oral exams and appropriate preventive dentistry before and during treatment; maintain oral hygiene and avoid invasive dental procedures; consider discontinuation of OSENVELT if ONJ develops. Atypical Subtrochanteric and Diaphyseal Femoral Fractures: Monitor for thigh, hip, or groin pain; evaluate for fractures. Interruption of OSENVELT therapy should be considered, pending a benefit-risk assessment, on an individual basis. Hypercalcemia Following Treatment Discontinuation in Patients with Giant Cell Tumor of Bone and in Patients with Growing Skeletons. Clinically significant hypercalcemia, potentially requiring hospitalization, can occur within a year after stopping denosumab in patients with giant cell tumor of bone or growing skeletons; monitor serum calcium and manage calcium and vitamin D needs post-discontinuation. Multiple Vertebral Fractures (MVF) Following Treatment Discontinuation. Increased risk post-discontinuation of denosumab; evaluate for risk for vertebral fractures after discontinuing OSENVELT. Embryo-Fetal Toxicity. Denosumab may cause fetal harm; verify pregnancy status before starting OSENVELT and advise effective contraception during treatment and for 5 months after the last dose. Most common Adverse Reactions: Bone Metastasis from Solid Tumors (≥ 25%) were fatigue/asthenia, hypophosphatemia, and nausea. In patients (≥ 10%) with: Multiple Myeloma were diarrhea, nausea, anemia, back pain, thrombocytopenia, peripheral edema, hypocalcemia, upper respiratory tract infection, rash, and headache; Giant Cell Tumor of Bone were arthralgia, headache, nausea, back pain, fatigue, and pain in extremity. Hypercalcemia of Malignancy (> 20%) were nausea, dyspnea, decreased appetite, headache, peripheral edema, vomiting, anemia, constipation, and diarrhea. For more information, see Full Prescribing Information. About Celltrion, Inc. Celltrion is a leading biopharmaceutical company that specializes in researching, developing, manufacturing, marketing and sales of innovative therapeutics that improve people's lives worldwide. Celltrion is a pioneer in the biosimilar space, having launched the world's first monoclonal antibody biosimilar. Our global pharmaceutical portfolio addresses a range of therapeutic areas including immunology, oncology, hematology, ophthalmology and endocrinology. Beyond biosimilar products, we are committed to advancing our pipeline with novel drugs to push the boundaries of scientific innovation and deliver quality medicines. For more information, please visit our website and stay updated with our latest news and events on our social media - LinkedIn, Instagram, X, and Facebook. About Celltrion USA Celltrion USA is Celltrion's U.S. subsidiary established in 2018. Headquartered in New Jersey, Celltrion USA is committed to expanding access to innovative biologics to improve care for U.S. patients. Celltrion's FDA-approved biosimilar products in immunology, oncology, hematology, and endocrinology include: INFLECTRA® (infliximab-dyyb), TRUXIMA® (rituximab-abbs), HERZUMA® (trastuzumab-pkrb), VEGZELMA® (bevacizumab-adcd), YUFLYMA®(adalimumab-aaty), AVTOZMA® (tocilizumab-anho), STEQEYMA® (Ustekinumab-stba) STOBOCLO® (denosumab-bmwo), OSENVELT® (denosumab-bmwo), and OMLYCLO® (omalizumab-igec), as well as the novel biologic ZYMFENTRA® (infliximab-dyyb). Celltrion USA will continue to leverage Celltrion's unique heritage in biotechnology, supply chain excellence and best-in-class sales capabilities to improve access to high-quality biopharmaceuticals for U.S. patients. For more information, please visit and stay updated with our latest news and events on our social media - LinkedIn. FORWARD-LOOKING STATEMENT Certain information set forth in this press release contains statements related to our future business and financial performance and future events or developments involving Celltrion, Inc. and its subsidiaries that may constitute forward-looking statements, under pertinent securities laws. These statements may be also identified by words such as "prepares", "hopes to", "upcoming", "plans to", "aims to", "to be launched", "is preparing", "once gained", "could", "with the aim of", "may", "once identified", "will", "working towards", "is due", "become available", "has potential to", the negative of these words or such other variations thereon or comparable terminology. In addition, our representatives may make oral forward-looking statements. Such statements are based on the current expectations and certain assumptions of Celltrion, Inc. and its subsidiaries' management, of which many are beyond its control. Forward-looking statements are provided to allow potential investors the opportunity to understand management's beliefs and opinions in respect to the future so that they may use such beliefs and opinions as one factor in evaluating an investment. These statements are not guarantees of future performance and undue reliance should not be placed on them. Such forward-looking statements necessarily involve known and unknown risks and uncertainties associated with the company's business, including the risk factors disclosed in its Annual Report and/or Quarterly Reports, which may cause actual performance and financial results in future periods to differ materially from any projections of future performance or results expressed or implied by such statements. Celltrion, Inc. and its subsidiaries undertake no obligation to update forward-looking statements if circumstances or management's estimates or opinions should change except as required by applicable securities laws. Trademarks STOBOCLO® and OSENVELT® are registered trademarks of Celltrion, and XGEVA® are registered trademarks of Amgen Inc. References [1] STOBOCLO U.S. prescribing information (2025) [2] OSENVELT U.S. prescribing information (2025) US-CT-P41-25-00006 For further information please contact:Andria Arenaaarena@ 516-578-0057 View original content to download multimedia: SOURCE Celltrion Error in retrieving data Sign in to access your portfolio Error in retrieving data Error in retrieving data Error in retrieving data Error in retrieving data
Yahoo
an hour ago
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Children in the U.S. Are Dying at a Higher Rate than Kids in Similar Countries, Study Says
A new study published by the Journal of the American Medical Association suggested that American children are in worse health than their counterparts in other countries Babies are 1.78 times more likely to perish, and children aged 1 to 19 are 1.8 times more likely to die than those in comparable countries Author Dr. Chris Forrest pointed out that the worrying trends are like a "proverbial canary in the coal mine," pointing to a larger problem within AmericaA new study shed light on a worrying trend in the health of American children. In a Monday, July 7 study published by the Journal of the American Medical Association (JAMA), research suggested that American children are in worse health than those growing up in other developed countries. Additionally, they are progressively less healthy than they were in previous years. The study examined trends in the health of children between 2007 and 2023. It found that in the U.S., "children's health has deteriorated across a broad spectrum of indicators." Data and trends between 2007 and 2022 suggest that infants are 1.78 times more likely to die in the U.S. than in other countries of a similar standing. Children between the ages of 1 and 19 were also 1.8 times more likely to die than their counterparts in other countries. In the latter group, there was a marked difference in the likelihood of dying from "firearm-related incidents" and "motor vehicle crashes," with American children dramatically more likely to perish as a result of these avoidable tragedies. In perspective, this amounts to approximately 54 more children dying per day in America, per the study. The findings come after deaths in the U.S. were in line with other countries in the 1960s. The study also suggested that American children were 14% more likely to suffer a chronic condition than their counterparts. The likelihood of being diagnosed with a chronic condition also increased from 39.9% to 45.7% in America between 2011 and 2023. Examples of chronic issues that children are now battling include the likes of "depression, anxiety and loneliness increased, as did rates of autism, behavioral conduct problems, developmental delays, speech language disorders and attention-deficit hyperactivity disorders." 'I think we all should be disturbed by this,' Dr. Chris Forrest, a professor of pediatrics at Children's Hospital of Philadelphia and director of the Applied Clinical Research Center, told CNN. 'Kids in this country are really suffering.' Never miss a story — sign up for to stay up-to-date on the best of what PEOPLE has to offer, from celebrity news to compelling human interest stories. Speaking to the outlet, Forrest noted that he has seen a change in his patients since he started practicing medicine in the '90s. He attributed that to a variety of elements, saying that it comes together to create "a very toxic environment." While the Make America Healthy Again Commission, fronted by U.S. Secretary of Health and Human Services Robert F. Kennedy has targeted chemicals in food and elsewhere as a cause for America's worsening health, Forrest said that the problem runs much deeper. "It's not just the chemicals. It's not just the food and the iPhones. It's a much broader. It's much deeper. It's what we call the developmental ecosystem, and it makes it very challenging to change it,' Forrest told CNN. 'That's a hard answer for people who want a pithy message that tells them how to fix the issues. It's about where they're growing up, where they're going to school, they're playing, where their families live, their neighborhoods, and it's not just one population. It's the whole nation that needs help.' Another element that he highlighted was that "women are also suffering in this country," suggesting that children are being born into already sickening households. Citing the research, he said, 'This means the same kid born in this country is much more likely to die than if they were born in Germany or Denmark. Why are we allowing this to happen?' For Forrest, the research is comparable to "the proverbial canary in the coal mine." "When [children's] health is deteriorating, that means the foundation of our nation is also deteriorating," he concluded. Read the original article on People