A landmark investigation has redefined our understanding of sleep's impact on long-term health . A major UK Biobank study, conducted by researchers from Peking University and Army Medical University, found that irregular sleep patterns , rather than simply sleep duration , are associated with a significantly higher risk of developing up to 172 different diseases . This groundbreaking study, recognized as one of the most comprehensive investigations into the relationship between sleep and health, analyzed objective sleep data from over 88,000 adults  over an average of 6.8 years. The researchers examined six specific sleep characteristics, including nocturnal sleep duration, sleep onset timing, rhythm (such as circadian rhythm strength and stability), and sleep fragmentation. The findings strongly suggest that inconsistent sleep behaviors are causally linked to numerous health complications. A key discovery is that for 92 distinct diseases, over 20% of the associated risk  can be attributed to irregular sleep patterns . Examples of significant risks include: Individuals consistently going to bed after 12:30 a.m.  faced a 2.57 times greater risk of developing liver cirrhosis . Low levels of stability in sleep patterns were found to increase the likelihood of gangrene by 2.61 times . A 37% higher risk of Parkinson’s disease , 36% higher risk of Type 2 diabetes , and 22% higher risk of acute kidney failure  were also observed. Additionally, 83 conditions not previously linked to sleep were identified. Interestingly, this study challenges the idea that "too much" sleep  (particularly more than nine hours) is inherently harmful, a notion that previous subjective research had suggested. The new objective data only confirmed this association for one disease. A potential source of confusion is attributed to misclassification , as a staggering 21.67% of individuals categorized as “long sleepers” were actually getting less than six hours of sleep, suggesting that time spent in bed is often mistaken for actual sleep. Professor Shengfeng Wang, the senior author of the study, emphasized: “Our findings underscore the overlooked importance of sleep regularity. It’s time we broaden our definition of good sleep beyond just duration" . Researchers also identified inflammatory pathways  as a possible biological link, observing higher levels of white blood cells and C-reactive protein in people with irregular sleep. The implications of this study extend to public health  policies: health practitioners may need to consider advising patients not only on their sleep duration but also on the importance of establishing a regular sleep schedule . By emphasizing sleep consistency , these findings could pave the way for more comprehensive strategies to combat the rise of sleep-related health issues and promote greater overall wellness. 🔖 Sources Landmark sleep study links objective sleep patterns with 172 diseases—regularity matters more than duration Irregular sleep patterns may trigger over 170 diseases—including diabetes, kidney failure, and Parkinson’s: Study Irregular sleep patterns linked to risk of 172 diseases, study finds Your sleep schedule could be making you sick, says massive new study

A recent study, published in the journal PLOS One , has issued a serious warning about the amount of microplastics that humans are inhaling daily, especially inside their homes and cars . New measurements suggest that we are breathing in significantly greater quantities of these particles than previously thought . Microplastics are tiny plastic fragments, often completely invisible to the naked eye . They are ubiquitous and have been detected in a wide variety of environments, from the outdoors to our most personal spaces. Previous research had primarily focused on larger particles, ranging from 20 to 200 micrometers, which are less likely to penetrate deeply into the lungs. However, the team of Nadiia Yakovenko and Jeroen Sonke from the Université de Toulouse, France, has focused its attention on fragments of 10 micrometers or less, which are small enough to be inhaled deep into the lungs . After collecting air samples in apartments and vehicles under realistic driving conditions, the researchers estimate that adults inhale approximately 68,000 microplastic particles from 1 to 10 micrometers per day . This figure is one hundred times higher than previous estimates  for small-diameter exposures. The findings also reveal that car air has a higher median concentration (2,238 particles per cubic meter) compared to apartments (528 particles per cubic meter), marking the first time microplastics have been measured in vehicle cabins, highlighting it as a major and underestimated exposure route and a clear case of massive microplastic inhalation . The primary concern lies in the potential health effects . These inhaled particles can penetrate the lungs and could pose risks of oxidative stress, immune system effects, and organ damage . Once in the lungs, microplastics have the capacity to release toxic additives that reach our blood and cause multiple diseases . While microplastics have been detected accumulating in human organs, including the brain, heart, and placenta, experts note that the evidence is still insufficient to determine direct risks to human health  and more research is needed to establish whether they cause harm. Nevertheless, many experts cite the precautionary principle , emphasizing that policy decisions to limit exposure cannot wait for complete data given the omnipresence of this threat. This study underscores the urgency for more research to confirm and expand upon these results  and, ultimately, to guide future public health recommendations and indoor air quality standards. 🔖 Sources Measurements suggest we inhale 68,000 lung-penetrating microplastics daily in our homes and cars Microplastics exist in cars and homes, new study finds Humans may be inhaling 100 times more microplastics than previously assumed, scientists warn What are all these microplastics doing to our brains?

In an unprecedented medical breakthrough, eight healthy babies have been born in the United Kingdom using an innovative IVF (In Vitro Fertilization) technique that incorporates DNA from three people, designed to minimize the risk of inheriting devastating genetic diseases. The results of this global trial , published in the New England Journal of Medicine , offer new hope to women with mutations in their mitochondrial DNA. Mitochondrial diseases , affecting approximately one in 5,000 births, are incurable and can cause severe symptoms such as poor vision, diabetes, muscle weakness, organ failure, and even death in infancy. The technique, approved by the UK in 2015 as the first country to do so, involves using a small amount of healthy mitochondrial DNA from a donor, along with the mother's egg and the father's sperm. Although they have been called "three-parent babies," researchers emphasize that only about 0.1% of the newborn's DNA comes from the donor , an insignificant amount that does not affect the child's main traits. The trial, conducted at the Newcastle Fertility Centre, resulted in the birth of four boys and four girls, whose ages range from under six months to over two years. The research demonstrated that the amount of mutated mitochondrial DNA was reduced by 95% to 100% in six babies and by 77% to 88% in the other two, levels considered below the threshold that causes the disease. All children are currently healthy and meeting their developmental milestones. While a "reversal" phenomenon was observed in three children, where the proportion of abnormal mitochondria increased post-birth, it remains at safe levels and requires further study. Despite being hailed as a "major breakthrough," the procedure remains controversial. Countries like the United States and France have not approved it, and ethical concerns persist regarding the destruction of human embryos and the fear of opening the door to genetically modified "designer babies." However, British experts emphasize that the technique is strictly regulated and limited to cases of "very high risk" of mitochondrial disease transmission, with its benefit being "obvious" in this context. The health of the babies will continue to be monitored in the coming years to ensure their long-term well-being. 🔖 Sources How a third parent's DNA can prevent an inherited disease 8 babies born with experimental 3-parent IVF technique Eight healthy babies born after IVF using DNA from three people Babies made using three people's DNA are born free of hereditary disease 8 babies born with DNA from 3 people in world-first IVF trial aimed at minimizing risk of inherited disease

An exciting breakthrough led by researchers from the Hebrew University of Jerusalem  and international partners could redefine cancer immunotherapy . Published in Nature Communications , the study reveals an innovative strategy to enhance the immune system’s ability to fight tumors. The key lies in reprogramming how T cells —the immune system’s "frontline soldiers"—produce energy. The team, co-led by Prof. Michael Berger and PhD student Omri Yosef, discovered that by disabling a protein known as Ant2  in these cells, their effectiveness is dramatically enhanced against tumors. This disabling action triggers a complete shift in how T cells  produce and use energy, "rewiring" their internal power supply at the level of the mitochondria , the energy-producing structures in cells. This transforms T cells  into stronger, faster, and more resilient cancer  fighters, exhibiting greater stamina, more rapid multiplication, and improved precision in homing in on and destroying cancer cells, boosting the immune system's ability to fight tumors . Perhaps most exciting is the possibility of inducing this change pharmacologically, meaning with drugs , not just genetically. This opens the door to much more accessible clinical applications. This strategy aligns with a growing trend in immunotherapy  that focuses not just on guiding immune responses, but on upgrading the cells themselves—enhancing their efficiency from within . The practical applications are potentially far-reaching. It could improve existing CAR-T therapies, making them more durable and effective in hostile tumor environments where cell exhaustion or limited persistence are common issues. Furthermore, by fine-tuning the body’s own immune cells, this approach may avoid some of the severe side effects seen with chemotherapy or full immune activation. Although the study focused on CD8+ T cells  in a model system, the metabolic reprogramming concept could potentially be applied across many types of solid tumors or hematological cancers, including those traditionally resistant to immunotherapy. As Prof. Berger explained, this work highlights how deeply interconnected metabolism  and immunity truly are, promising more natural and effective therapies. "We’re not just helping the immune system aim—we’re giving it better tools to win the fight,"  Berger said. 🔖 Sources Israeli-led breakthrough paves way for next-generation cancer therapies Israeli-led breakthrough discovers way to boost immune system's cancer-fighting ability T cells require mitochondria to proliferate, function and generate memory Powering up T cells: A new path in cancer immunotherapy

Malaria continues to be one of the world's deadliest diseases, with 263 million cases and nearly 600,000 deaths reported in 2023, where 80% of the victims are children. Mosquitoes, the animals that kill more people each year than any other, are the main vectors of this disease. However, science has made significant strides with two promising approaches that could change the course of this fight. Scientists from the University of California San Diego, Johns Hopkins University, and other institutions have developed an innovative method that genetically blocks mosquitoes from transmitting malaria . Published in Nature  in July 2025, this breakthrough uses CRISPR  technology to make a minuscule but dramatic change. The CRISPR-Cas9 gene-editing system replaces a single amino acid (L224 with Q224) in a key protein called FREP1 in the mosquito's genome. This change prevents malaria parasites from reaching the insect's salivary glands, thereby halting transmission. Although genetically modified mosquitoes can still bite infected people and acquire parasites, they can no longer spread the disease to other individuals . The Q224 variant is a naturally occurring allele, and the system is designed to spread this beneficial trait throughout mosquito populations, similar to an "allelic drive". Crucially, this change does not affect the mosquito's normal growth or reproduction. This approach leverages a naturally occurring mosquito gene allele, turning it into a powerful shield that blocks multiple malaria parasite species. In parallel, a large-scale study known as the BOHEMIA trial has shown that the mass administration of ivermectin, an antiparasitic drug, can reduce the incidence of malaria by 26% . This approach is surprising: the pill makes human blood deadly to mosquitoes that bite those who have taken it, killing them after the bite. The study, led by the Barcelona Institute for Global Health (ISGlobal) and published in The New England Journal of Medicine , was conducted in Kenya and Mozambique. Although ivermectin is commonly used to treat diseases like onchocerciasis (river blindness) and lymphatic filariasis (elephantiasis), it has proven to be safe and widely available for this new use. In Kenya's Kwale County, administering a monthly dose for three months to children aged 5 to 15 resulted in a significant reduction in malaria infection rates . The results align with the World Health Organization’s (WHO) criteria for new vector control tools, which require at least a 20% reduction in incidence lasting for at least one month after treatment. Additionally, ivermectin offered collateral benefits , such as the reduction of lice, scabies, and bed bugs in communities. Both strategies are crucial, as traditional mosquito control tools, such as insecticide-treated bed nets, are losing effectiveness due to mosquito resistance to insecticides and changes in their biting behavior. These advances represent a significant step a gainst Malaria , offering complementary and effective tools to protect the most vulnerable populations. While the Mozambique trial faced disruptions from Cyclone Gombe and a cholera outbreak, highlighting the importance of strong community engagement, the overall findings support ivermectin's potential to shape the future of malaria prevention, especially in endemic areas where existing tools are failing. 🔖 Sources A Pill That Makes Your Blood Deadly to Mosquitoes? It’s Real – And It Works New findings support ivermectin for malaria control CRISPR genome editing stops mosquitoes spreading malaria Stealth Genetic Switch in Mosquitoes Halts Malaria Spread

In an astonishing scientific discovery, researchers from the University of California, San Francisco (UCSF) and the Gladstone Institutes have identified a potential new approach to treating Alzheimer's disease using two oncology drugs already approved by the FDA. This research offers new hope for a disease that currently has no cure and affects more than 55 million people worldwide. The drugs in question are Letrozole and Irinotecan. Letrozole is used to treat certain types of breast cancer, while Irinotecan is prescribed for colon and lung cancer. What is most notable is that, while they are already known in the medical field, their potential to address brain damage related to Alzheimer's had not been explored until now. The key to their efficacy lies in their combination, as each drug appears to target different types of brain cells. Letrozole helps neurons, the cells responsible for transmitting information, while Irinotecan acts on glial cells, which support neurons. This dual-target approach is crucial for a disease as complex as Alzheimer's. One of the main markers of Alzheimer's is the accumulation of tau proteins, which form tangles inside the brain and disrupt normal cell function, contributing to cognitive decline. The combination of Letrozole and Irinotecan has been shown to reduce these tau protein tangles in the brains of mouse models. Beyond the elimination of tau tangles, the mice treated with these drugs also showed significant improvements in learning and memory tasks, functions that are often severely affected in patients with Alzheimer's. In fact, mice that had already developed severe symptoms saw their memory restored. This suggests that the drugs not only reduce the physical markers of the disease but could also restore some of the lost cognitive abilities, including short-term and long-term spatial memory, pointing towards a potential reversal of Alzheimer's. Although the results in mice are very promising, the real test is whether these drugs can have the same effect in humans. Since they are already approved by the FDA for other uses, the path to clinical trials for Alzheimer's could be faster than the development of entirely new medications. However, it is essential to evaluate their potential side effects in this new context, as Letrozole can cause hot flashes and Irinotecan can lead to severe diarrhea, nausea, and vomiting. Researchers emphasize the need to balance the potential benefits with these significant adverse effects. This research, published in the journal Cell , marks an exciting step forward in the search for new ways to treat Alzheimer's and highlights the possibility of repurposing existing medications for other complex diseases. In the coming years, more research and clinical trials will be conducted to determine if Letrozole and Irinotecan can fulfill their potential, offering a much-needed therapeutic strategy for millions of people affected by this debilitating condition. 🔖 Sources Alzheimer’s Could Be Treated with These Two FDA-Approved Cancer Drugs, New Research Finds Breakthrough as two FDA-approved drugs are found to reverse Alzheimer’s — including restoring memory Could cancer drugs be the future of Alzheimer's treatment? Dual cancer drugs restore memory and rewire brain cells in Alzheimer’s mouse models

A revolutionary discovery is redefining our understanding of gut-brain communication , uncovering a newly identified system called the " neurobiotic sense ". This innovative finding explains how our brain can respond in real time to signals from the microbes inhabiting our gut. "Neurobiotic Sense" Key to Appetite Regulation. Led by Duke University School of Medicine neurobiologists, including Diego Bohórquez, PhD, and M. Maya Kaelberer, PhD, the research published in the journal Nature  focuses on neuropod cells . These are tiny sensor cells that line the colon's epithelium. Neuropod cells have the ability to detect a common microbial protein and send rapid messages to the brain that can help curb appetite  and guide decision-making about eating. The key player in this process is flagellin , an ancient protein found in bacterial flagella, tail-like structures that bacteria use to move. When we eat, some gut bacteria release flagellin. Neuropod cells detect this flagellin with the help of a specific receptor called TLR5  (Toll-like receptor 5). Once detected, the signal is rapidly transmitted through the vagus nerve, a major communication pathway directly between the gut and the brain. This gut-brain neural circuit forms the aforementioned neurobiotic sense . The researchers demonstrated this mechanism through experiments in mice. By administering a small dose of flagellin directly into the colon of fasted mice, they observed a significant decrease in food intake  within 20 minutes in littermate controls. However, in mice whose TLR5 receptor had been ablated from PYY-labeled cells, flagellin had no effect; these mice ate more (increased meal size in both sexes and longer meal duration in females) and gained more weight than controls. This indicates that the appetite suppression system did not function. This appetite-suppressing effect of flagellin was also observed in germ-free mice, suggesting that flagellin sensing alone is sufficient to suppress food intake, regardless of other microbial signals. The study concluded that PYY-labeled colonic neuropod cells use TLR5  to detect flagellin and rapidly signal to the brain via the vagus nerve, regulating feeding behavior through dedicated NPY2R receptors. In essence, neuropod cells send a "We've had enough" signal to the brain. This "neurobiotic sense" enables the host to adjust behavior by monitoring gut microbial patterns. This discovery is particularly relevant because it suggests that the gut's bacterial system naturally mimics the appetite-suppressing effects of drugs like Ozempic (GLP-1 analogs) , but potentially without the adverse side effects. Scientists believe that manipulating this bacterial system and enhancing natural communication, possibly through specific diets or by ingesting prebiotics and probiotics, could be a strategy for natural weight loss . Looking ahead, this research is crucial for understanding how our behavior is influenced by microbes. A clear next step is to investigate how specific diets alter the microbial landscape in the gut, which could be a key piece of the puzzle in conditions like obesity  or psychiatric disorders . In summary, this new neurobiotic sense  provides us with a capability similar to our other senses (sight, sound, smell, taste, and touch), but operating from an unexpected place: the gut. 🔖 Sources Scientists discover how you can turn on your body's natural Ozempic to lose weight without the nasty side effects Newly Discovered ‘Sixth Sense’ Links Gut Microbes to the Brain in Real Time Gut bacteria send direct signals to the brain to stop you from overeating Real-Time Gut-Brain Communication Mediated by Microbial Protein

Following more than two decades of advancements since the culmination of the Human Genome Project, science has made a monumental leap. An international team of researchers, including scientists from the University of Washington, The Jackson Laboratory, Clemson University, and the European Molecular Biology Laboratory (EMBL), has published the most extensive catalog of human genetic variation ever compiled, promising a new era for precision medicine, thanks to this new human genome map . Published in the journal Nature  this Wednesday, the study delved into the human genome of 1,084 individuals from diverse populations around the world. Using long-read sequencing technologies (PacBio HiFi and Oxford Nanopore Technologies), scientists managed to map the "structural variants" of DNA—large segments of the code that can be deleted, added, flipped, or moved—with unprecedented detail. What makes this work especially revealing is that it has unearthed "hidden" features of the genome that were previously technologically unreachable. This includes vast portions of so-called "junk DNA" or "repetitive DNA," which were believed to be non-functional. Now, we know these sequences are not "junk," and this study sheds light on them. More than half of the newly discovered genomic variation was found in these repetitive regions, including "jumping genes" or transposons, which can destabilize the genome and contribute to diseases like cancer by "hijacking regulatory sequences" to increase their activity. The findings are broad and profound: Structural Variants (SVs):  Up to 26,115 structural variants per individual were identified, with a total of more than 175,000 sequence-resolved events. This is a critical advance, as structural variants are more likely to alter gene expression, and understanding them is fundamental for diseases. Detailed Centromeres:  1,246 centromeres—essential structures for cell division—were completely assembled, revealing up to 30-fold variation in their length. Furthermore, there were indications that approximately 7% of centromeres might have two binding sites for cell division fibers (di-kinetochores), a purely speculative idea that can now be explored. Clinically Relevant Regions:  The study successfully resolved the sequences of crucial genes such as SMN1/SMN2, associated with spinal muscular atrophy, and the Major Histocompatibility Complex (MHC), vital for immune function and susceptibility to autoimmune diseases. The diversity of the samples used—65 individuals from 5 continents and 28 population groups—is crucial. The study revealed that samples of African ancestry showed the greatest structural variance, underscoring the importance of including diverse populations to counteract the historical bias towards European ancestry in reference genomes. This new map of the human genome and its genetic variation not only fills 92% of previously inaccessible genomic data "gaps" but also provides an open and accessible basis for other scientists to delve into the genetic basis of diseases. It is, in the words of Jan Korbel, co-author of the study, as if geneticists have been presented with a "new microscope" to see the true complexity of human genetic variation for the first time. This advancement is a clear sign of where the field of genetics is heading: towards much more personalized genetic diagnoses and treatments, marking a milestone in precision medicine. 🔖 Sources Researchers sequence complex parts of human genome, expanding the future of precision medicine Best-ever map of the human genome sheds light on 'jumping genes,' 'junk DNA' and more Complex genetic variation in nearly complete human genomes Diverse human genomes reveal complex genetic variation

For decades, male contraception options have been limited to condoms and vasectomies, while women have had a wide range of methods at their disposal, including over 20 FDA-approved contraceptive categories. However, a significant shift is on the horizon, promising greater equity in family planning. A Crucial Breakthrough: The Non-Hormonal Male Pill YCT-529 Researchers from the University of Minnesota's College of Pharmacy, in collaboration with Columbia University and YourChoice Therapeutics, have made a monumental stride with the YCT-529 pill, the first oral, non-hormonal male contraceptive of its kind. This innovative pill works by stopping sperm production through blocking a vitamin A metabolite crucial for this process. By being non-hormonal, it's expected to minimize side effects such as changes in sexual function, libido, or mood. Promising Results in Preclinical and Human Trials Initial animal studies yielded very positive results: In male mice, the pill caused infertility and showed 99% effectiveness in preventing pregnancies within four weeks. In non-human primates, a reduction in sperm counts was observed within two weeks. Most importantly, both mice and primates fully recovered their fertility upon discontinuing the medication, within six weeks and 10 to 15 weeks, respectively. No side effects were detected in any of the animal groups. Recently, YCT-529 passed another crucial milestone: it successfully completed its first phase of human clinical trials in 2024, proving to be safe for use. This initial trial, which included 16 men aged 32 to 59 who had already undergone a vasectomy (as a precautionary measure), focused on evaluating tolerability and how the drug accumulates in the body, not its contraceptive efficacy. The results showed good and rapid drug bioavailability, suggesting that a single daily dose might be sufficient. It's important to note that, in this small study, no adverse side effects related to the drug were observed. The Future of Male Contraception Currently, YCT-529 is in its second phase of clinical trials, where both its safety and efficacy are being evaluated in larger cohorts of men. This development is fundamental, especially considering that almost 50% of pregnancies in the U.S. and globally are unintentional. Experts and surveys indicate a growing interest among men in new contraceptive options, with studies showing that up to 75% of men are willing to try new methods. Dr. Gunda Georg, lead author of the University of Minnesota study, highlights that a safe and effective male pill will not only offer more options to couples but also allow for a more equitable distribution of responsibility in family planning and provide reproductive autonomy for men. While YCT-529 advances, other options, such as hormonal gels and implantable devices, are also under development, pointing to a future where contraceptive choice is truly shared. 🔖 Sources Male birth control pill passes early safety test, with more trials underway First hormone-free male birth control pill clears another milestone First Hormone-Free Male Birth Control Pill Shown Safe in Early Human Trial

Two significant breakthroughs in understanding diabetes are poised to shake up the healthcare world, urging an urgent review of how this complex disease is diagnosed and treated globally. These discoveries promise to transform care for millions, especially in low- and middle-income countries (LMICs). Official Recognition of Type 5 Diabetes The International Diabetes Federation (IDF) has formally announced the long-awaited official recognition of Type 5 diabetes , a historic milestone. This form of diabetes is primarily linked to chronic malnutrition, particularly during childhood or adolescence, which is believed to affect pancreatic development and reduce insulin production. It's estimated that between 20 and 25 million people worldwide, mainly in Asia and Africa, live with this condition. Even in the United States, children in foster care or food-insecure migrants could be at risk. Unlike Type 2 diabetes (characterized by insulin resistance) or Type 1 diabetes (an autoimmune disease that destroys insulin-producing cells), Type 5 diabetes—also known as Severe Insulin-Deficient Diabetes (SIDD) or malnutrition-related diabetes—is distinguished by its metabolic profile: individuals are insulin-deficient but not insulin-resistant. This is crucial because many can manage their condition with oral medication instead of insulin injections, a more cost-effective and accessible solution in low-resource settings. Dr. Meredith Hawkins, co-chair of the IDF's task force for Type 5 diabetes, led the research that confirmed the distinct profile of this condition, which has been observed but often misclassified for over 70 years. The IDF is working to establish formal diagnostic criteria and therapeutic guidelines, as well as a global research registry and educational modules for healthcare professionals. A New Diabetes Subtype Identified in Africa In parallel, a large-scale study, the Young-Onset Diabetes in Sub-Saharan Africa (YODA) study, has identified a new diabetes subtype in children, adolescents, and young adults in sub-Saharan Africa. Published in The Lancet Diabetes & Endocrinology , the findings reveal that approximately 65% of participants previously diagnosed with Type 1 diabetes lacked the typical autoimmune signs and genetic predisposition of the classic disease. Only 8.5% carried more than one diabetes-related autoantibody, a drastic difference from the 90% observed in Western cohorts. This new subtype is an insulin-deficient condition that fits neither Type 2 diabetes nor malnutrition-related diabetes (Type 5). The findings challenge global assumptions about Type 1 diabetes, as most prior data comes from Western populations. Dr. Jean-Claude Katte from the University of Exeter and Professor Moffat Nyirenda, Director of the MRC/UVRI-LSHTM Research Unit in Uganda, emphasize the urgent need to investigate the biological and environmental factors behind this form of diabetes, such as infections, nutrition, or environmental toxins, and adapt diagnostic and treatment approaches for African settings. These discoveries highlight the importance of equity in science and the need for more inclusive and "context-specific" research to prevent the misdiagnosis and mistreatment of millions worldwide. The impact of an accurate diagnosis can be the difference between appropriate treatment and severe complications, or even death, especially for those in limited-resource environments. 🔖 Sources Scientists identify a new subtype of diabetes that will change how the disease is treated IDF launches new type 5 diabetes working group New subtype of diabetes identified in Africa in first largescale study What Is Type 5 Diabetes? A New Form of Diabetes Linked to Childhood Malnutrition