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Long-term exposure to fine particulate air pollution may contribute to subtle heart tissue changes associated with the early signs of heart damage, according to research published in Radiology.
The study, which used cardiac MRI, found a connection between higher exposure to particulate matter and diffuse myocardial fibrosis – microscopic scarring in the heart muscle.
Although the relationship between air pollution and cardiovascular disease is well established, the specific tissue-level changes driving this risk remain unclear. This investigation aimed to clarify that link using imaging-based assessments of myocardial health.
The study examined 694 individuals in total, including 201 healthy participants and 493 people with dilated cardiomyopathy. Researchers measured each participant’s myocardial extracellular volume, a marker of fibrosis, using cardiac MRI. These values were then compared with estimates of long-term exposure to fine particulate matter, also known as PM2.5.
PM2.5 refers to airborne particles with a diameter of 2.5 micrometers or smaller. These particles are small enough to be inhaled deeply into the lungs and pass into the bloodstream. Common sources include traffic emissions, industrial activity and wildfires.
“We know that if you’re exposed to air pollution, you’re at higher risk of cardiac disease, including higher risk of having a heart attack,” said the study’s senior author Kate Hanneman, MD, MPH, from the Department of Medical Imaging at the Temerty Faculty of Medicine, University of Toronto and University Health Network in Toronto. “We wanted to understand what drives this increased risk at the tissue level.”
Participants with higher long-term exposure to PM2.5 exhibited greater levels of myocardial fibrosis. This association held true for both healthy individuals and those with existing heart disease. The most pronounced effects were observed in women, people who smoke and individuals with hypertension.
The findings contribute to a growing body of evidence suggesting that air pollution is an independent cardiovascular risk factor. This risk persists even when other major contributors, such as smoking and high blood pressure, are accounted for. The study also showed that health impacts may occur even when pollution levels fall below current global guidelines.
“Even modest increases in air pollution levels appear to have measurable effects on the heart,” Hanneman said. “Our study suggests that air quality may play a significant role in changes to heart structure, potentially setting the stage for future cardiovascular disease.”
“Public health measures are needed to further reduce long-term air pollution exposure,” continued Hanneman. “There have been improvements in air quality over the past decade, both in Canada and the United States, but we still have a long way to go.”
This research may support efforts to improve cardiovascular risk prediction. For example, air pollution exposure history could help clinicians refine risk assessments for patients in high-exposure settings, including outdoor workers or those living in highly polluted regions.
The results also underscore the role of radiologists and medical imaging in environmental health research.
“Medical imaging can be used as a tool to understand environmental effects on a patient’s health,” Hanneman said. “As radiologists, we have a tremendous opportunity to use imaging to identify and quantify some of the health effects of environmental exposures in various organ systems.”
Reference: Du Plessis J, DesRoche C, Delaney S, et al. Association between long-term exposure to ambient air pollution and myocardial fibrosis assessed with cardiac MRI. Radiology. 2025. doi: 10.1148/radiol.250331
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Scientists have found that eating too much dairy could ruin your sleep. Researchers questioned more than 1,000 students about the quality of their sleep, their eating habits, and any perceived link between the two, and found a strong association between nightmares and lactose intolerance — potentially because gas or stomach pain during the night affects people’s dreams.
“Nightmare severity is robustly associated with lactose intolerance and other food allergies,” said Dr Tore Nielsen of Université de Montréal, lead author of the article in Frontiers in Psychology. “These new findings imply that changing eating habits for people with some food sensitivities could alleviate nightmares. They could also explain why people so often blame dairy for bad dreams!”
Sweet dreams?
Although folk beliefs have long held that what you eat affects how you sleep, there’s very little evidence to prove or disprove them. To investigate, researchers surveyed 1,082 students at MacEwan University. They asked about sleep time and quality, dreams and nightmares, and any perceived association between different kinds of dreams and different foods. They also asked about participants’ mental and physical health and their relationship with food.
About a third of respondents reported regular nightmares. Women were more likely to remember their dreams and to report poor sleep and nightmares, and nearly twice as likely as men to report a food intolerance or allergy. About 40% of participants said that they thought eating late at night or specific foods affected their sleep; roughly 25% thought particular foods could make their sleep worse. People who ate less healthily were more likely to have negative dreams and less likely to remember dreams.
“We are routinely asked whether food affects dreaming — especially by journalists on food-centric holidays,” said Nielsen. “Now we have some answers.”
Cheesy culprits
Most participants who blamed their bad sleep on food thought sweets, spicy foods, or dairy were responsible. Only a comparatively small proportion — 5.5% of respondents — felt that what they ate affected the tone of their dreams, but many of these people said they thought sweets or dairy made their dreams more disturbing or bizarre.
When the authors compared reports of food intolerances to reports of bad dreams and poor sleep, they found that lactose intolerance was associated with gastrointestinal symptoms, nightmares, and low sleep quality. It’s possible that eating dairy activates gastrointestinal disturbance, and the resulting discomfort affects people’s dreams and the quality of their rest.
“Nightmares are worse for lactose intolerant people who suffer severe gastrointestinal symptoms and whose sleep is disrupted,” said Nielsen. “This makes sense, because we know that other bodily sensations can affect dreaming. Nightmares can be very disruptive, especially if they occur often, because they tend to awaken people from sleep in a dysphoric state. They might also produce sleep avoidance behaviors. Both symptoms can rob you of restful sleep.”
Eat well to sleep well?
This could also explain why fewer participants reported a link between their food and their dreams than in a previous study by Nielsen and his colleague Dr Russell Powell of MacEwan University, conducted eleven years earlier on a similar population. Improved awareness of food intolerances could mean that the students in the present study ate fewer foods likely to activate their intolerances and affect their sleep. If this is the case, then simple dietary interventions could potentially help people improve their sleep and overall health.
However, besides the robust link between lactose intolerance and nightmares, it’s not clear how the relationship between sleep and diet works. It’s possible that people sleep less well because they eat less well, but it’s also possible that people don’t eat well because they don’t sleep well, or that another factor influences both sleep and diet. Further research will be needed to confirm these links and identify the underlying mechanisms.
“We need to study more people of different ages, from different walks of life, and with different dietary habits to determine if our results are truly generalizable to the larger population,” said Nielsen. “Experimental studies are also needed to determine if people can truly detect the effects of specific foods on dreams. We would like to run a study in which we ask people to ingest cheese products versus some control food before sleep to see if this alters their sleep or dreams.”
Since mid-June, Cambodia’s veterinary authority has confirmed six further highly pathogenic avian influenza (HPAI) outbreaks in poultry flocks.
Based on official notifications to the World Organisation for Animal Health (WOAH), these bring the nation’s total outbreaks over the past 12 months to 16. Directly impacted have been close to 8,000 domestic birds.
In the recent outbreaks, village flocks affected ranged in size from 25 to more than 650 birds. Two were in Pursat — the first infections in this western province. There were also two outbreaks in each of Takeo and Siem Reap, which are located in the far south and northwest of the country, respectively.
Detection of the H5N1 serotype of the HPAI virus at one of the Takeo province outbreaks was confirmed after an infection was suspected in a resident of the village. Sick or dead poultry at the other locations raised suspicions of HPAI in the other village flocks.
Over the past two weeks, HPAI outbreaks linked to the same virus variant have been confirmed in two poultry flocks. The first ended a near two-month hiatus in South Korea.
Testing positive for the virus in mid-June was a flock of around 28,000 birds at a farm in the central province of North Chungcheong, according to the latest WOAH notification.
According to the agriculture ministry, the infection was revealed in ducks as a result of routine pre-shipment testing.
Just last week, a flock of around 1,000 native chickens tested positive for the same virus at a premises in the southeastern province of South Gyeongsang.
The ministry reports that the farm was not authorized to keep livestock, and numerous biosecurity-related deficiencies emerged during the follow-up inspection there.
Following this latest development, the authorities have increased surveillance of native chicken flocks, as well as dealers and traditional markets that handle these birds. Furthermore, for a period of 14 days, the proportion of birds subject to pre-shipment testing will be raised from 10% to 30%.
The risk of further spread of HPAI in South Korea is not considered by the ministry to be high. This is based on experience from 2024, when just four outbreaks were reported in the country during the months of July and August.
These latest outbreaks bring South Korea’s total since October of 2024 to 49.
Animal health agencies of Australia and Japan have recently declared to WOAH that earlier HPAI outbreak series in their respective countries have been “resolved.”
In Australia, a total of more than 596,000 poultry were directly impacted by the disease at four farms in the state of Victoria earlier this year. All these outbreaks started during the month of February, with birds testing positive for the H7N8 serotype of HPAI.
The H5N1 HPAI virus was detected at a total of 51 poultry farms in Japan between October of 2024 and January of this year. As a result, more than 9.2 million birds died or were culled and destroyed to prevent the further spread of the virus.
Among Japan’s wild birds, however, the HPAI situation is ongoing.
After a hiatus of more than two years, the H5N2 variant of HPAI was detected in a wild bird in April, according to a retrospective report to WOAH.
More than 100 wild birds have also tested positive for the H5N1 virus serotype in Japan over recent months, according to a separate notification.
Furthermore, the same virus variant was detected after three sea otters were found dead around the island of Hokkaido in early May.
Most recent disease update from the Department of Agriculture’s Bureau of Animal Industry (dated June 26) in the Philippines indicates no new HPAI cases in poultry since the end of April.
As of June 16, nine HPAI outbreaks had occurred in Vietnamese poultry so far this year, reported DanViet, citing agriculture ministry data. Across six provinces, more than 21,300 birds had died, and 25,200 had been culled in 2025 up to that point.
Compared with 2024, the number of provinces affected this year is lower, but more than twice as many poultry have been lost to the disease, according to this source.
Cambodia has been experiencing a recent spike in human infections with the avian influenza A(H5N1) virus.
A recent update by Avian Flu Diary puts the country’s total cases so far this year at seven. Of these, four have been confirmed during the month of June. This was the situation on June 24, based on data from the country’s health ministry.
As in previous cases in Cambodia, the latest patient is known to have had contact with sick and dead poultry.
The source notes that several of those people infected there have died. This is linked to the greater virulence of the virus circulating in the country — recently designated as clade 2.3.2.1e — than the clade 2.3.4.4b variant circulating elsewhere, including in the U.S. and Europe.
In recent weeks, four human infections with flu viruses of avian origin have been confirmed in China. These are covered in recent updates on the situation in the Western Pacific Region from the World Health Organization (WHO).
Three of these involved the H9N2 virus — one in each of the provinces of Henan, Hunan, and Sichuan. All started in mid-May following contact with poultry. Two adult patients required hospital treatment, but they and a six-year-old boy are reported to have recovered.
The fourth Chinese patient was a farmer from Shaanxi province who may have contracted an H10N3 infection while traveling in Inner Mongolia. While still under treatment in hospital, her condition was reported to be improving. This is the sixth confirmed human infection with this virus in the world.
View our continuing coverage of the global avian influenza situation in poultry, and on disease developments in the U.S. dairy sector.
Top 5 women’s health headlines you missed in June 2025 | Image Credit: © sebra – stock.adobe.com.
June 2025 delivered pivotal updates across the field of women’s health, spanning clinical guidance, therapeutic innovation, policy statements, and new research insights.
From ACOG’s condemnation of violence against reproductive health providers to promising trial data on managing vasomotor symptoms and recurrent bacterial vaginosis, this month’s developments reflect both the clinical and societal forces shaping OB/GYN practice today. Additional highlights include updated AAP recommendations on adolescent contraceptive care and new findings linking ADHD to increased risk of premenstrual dysphoric disorder.
In this monthly roundup, Contemporary OB/GYN summarizes the most significant clinical findings, expert commentary, and policy developments from June 2025.
Click on each headline below for full coverage and analysis.
A phase 3 trial published in the New England Journal of Medicine found that elinzanetant significantly reduced moderate-to-severe vasomotor symptoms in women receiving endocrine therapy for hormone receptor–positive breast cancer. Among the 474 participants, those receiving elinzanetant reported up to 3.5 fewer daily hot flash episodes by week 4 compared to placebo. Improvements in sleep and menopausal quality of life were also greater in the elinzanetant group. These findings address a critical need, as vasomotor symptoms often undermine adherence to endocrine therapy, potentially affecting long-term cancer outcomes.
New data presented at the 2025 ACOG Annual Clinical and Scientific Meeting support the long-term use of secnidazole oral granules for recurrent bacterial vaginosis (BV), a condition affecting nearly 1 in 3 reproductive-aged women in the U.S. In a small trial, once-weekly 2 g doses showed comparable or improved efficacy to CDC-recommended suppressive regimens. Lead investigator Chemen M. Neal, MD, emphasized the potential for simplified dosing to improve adherence and reduce recurrence. The findings also underscore the need for accurate diagnosis and sustained management of BV, which carries both physical and psychosocial burdens.
In a joint statement, ACOG president Steven J. Fleischman, MD, and CEO Sandra E. Brooks, MD, condemned recent acts of violence targeting reproductive health care providers, including a bombing at a Minnesota fertility clinic and online harassment of clinicians. The statement, released following the 2025 ACOG Annual Clinical and Scientific Meeting, underscored the escalating risks ob-gyns face for delivering comprehensive reproductive care. Citing long-standing patterns of ideologically motivated violence, ACOG called for strengthened protections under policies like the Freedom of Access to Clinic Entrances Act and urged political leaders to oppose threats against providers.
The American Academy of Pediatrics updated its guidance on adolescent contraceptive care, urging pediatricians to provide developmentally appropriate, confidential counseling and access to the full spectrum of contraceptive methods. Published in the July 2025 issue of Pediatrics, the policy emphasizes equity, autonomy, and shared decision-making. The AAP highlights the need for proactive engagement given persistent gaps in contraceptive use among teens and calls for expanded access through telehealth and school-based care. Pediatricians are also encouraged to integrate contraception discussions with broader sexual health care, including STI screening and HPV vaccination.
Women with ADHD may face a significantly higher risk of premenstrual dysphoric disorder (PMDD), according to new findings published in the British Journal of Psychiatry. Using survey data from U.K. participants, researchers found PMDD symptoms were over three times more likely in women with ADHD, and risk was even higher when anxiety or depression was also present. PMDD was identified in 31.4% of those with ADHD versus 9.8% of those without. The study’s authors called for increased screening and a better understanding of how hormonal changes affect women with ADHD to address diagnostic disparities.
Using an inexpensive electrode coated with DNA, MIT researchers have designed disposable diagnostics that could be adapted to detect a variety of diseases, including cancer or infectious diseases such as influenza and HIV.
These electrochemical sensors make use of a DNA-chopping enzyme found in the CRISPR gene-editing system. When a target such as a cancerous gene is detected by the enzyme, it begins shearing DNA from the electrode nonspecifically, like a lawnmower cutting grass, altering the electrical signal produced.
One of the main limitations of this type of sensing technology is that the DNA that coats the electrode breaks down quickly, so the sensors can’t be stored for very long and their storage conditions must be tightly controlled, limiting where they can be used. In a new study, MIT researchers stabilized the DNA with a polymer coating, allowing the sensors to be stored for up to two months, even at high temperatures. After storage, the sensors were able to detect a prostate cancer gene that is often used to diagnose the disease.
The DNA-based sensors, which cost only about 50 cents to make, could offer a cheaper way to diagnose many diseases in low-resource regions, says Ariel Furst, the Paul M. Cook Career Development Assistant Professor of Chemical Engineering at MIT and the senior author of the study.
“Our focus is on diagnostics that many people have limited access to, and our goal is to create a point-of-use sensor. People wouldn’t even need to be in a clinic to use it. You could do it at home,” Furst says.
MIT graduate student Xingcheng Zhou is the lead author of the paper, published June 30 in the journal ACS Sensors. Other authors of the paper are MIT undergraduate Jessica Slaughter, Smah Riki ’24, and graduate student Chao Chi Kuo.
An inexpensive sensor
Electrochemical sensors work by measuring changes in the flow of an electric current when a target molecule interacts with an enzyme. This is the same technology that glucose meters use to detect concentrations of glucose in a blood sample.
The electrochemical sensors developed in Furst’s lab consist of DNA adhered to an inexpensive gold leaf electrode, which is laminated onto a sheet of plastic. The DNA is attached to the electrode using a sulfur-containing molecule known as a thiol.
In a 2021 study, Furst’s lab showed that they could use these sensors to detect genetic material from HIV and human papillomavirus (HPV). The sensors detect their targets using a guide RNA strand, which can be designed to bind to nearly any DNA or RNA sequence. The guide RNA is linked to an enzyme called Cas12, which cleaves DNA nonspecifically when it is turned on and is in the same family of proteins as the Cas9 enzyme used for CRISPR genome editing.
If the target is present, it binds to the guide RNA and activates Cas12, which then cuts the DNA adhered to the electrode. That alters the current produced by the electrode, which can be measured using a potentiostat (the same technology used in handheld glucose meters).
“If Cas12 is on, it’s like a lawnmower that cuts off all the DNA on your electrode, and that turns off your signal,” Furst says.
In previous versions of the device, the DNA had to be added to the electrode just before it was used, because DNA doesn’t remain stable for very long. In the new study, the researchers found that they could increase the stability of the DNA by coating it with a polymer called polyvinyl alcohol (PVA).
This polymer, which costs less than 1 cent per coating, acts like a tarp that protects the DNA below it. Once deposited onto the electrode, the polymer dries to form a protective thin film.
“Once it’s dried, it seems to make a very strong barrier against the main things that can harm DNA, such as reactive oxygen species that can either damage the DNA itself or break the thiol bond with the gold and strip your DNA off the electrode,” Furst says.
Successful detection
The researchers showed that this coating could protect DNA on the sensors for at least two months, and it could also withstand temperatures up to about 150 degrees Fahrenheit. After two months, they rinsed off the polymer and demonstrated that the sensors could still detect PCA3, a prostate cancer gene that can be found in urine.
This type of test could be used with a variety of samples, including urine, saliva, or nasal swabs. The researchers hope to use this approach to develop cheaper diagnostics for infectious diseases, such as HPV or HIV, that could be used in a doctor’s office or at home. This approach could also be used to develop tests for emerging infectious diseases, the researchers say.
A group of researchers from Furst’s lab was recently accepted into delta v, MIT’s student venture accelerator, where they hope to launch a startup to further develop this technology. Now that the researchers can create tests with a much longer shelf-life, they hope to begin shipping them to locations where they could be tested with patient samples.
“Our goal is to continue to test with patient samples against different diseases in real world environments,” Furst says. “Our limitation before was that we had to make the sensors on site, but now that we can protect them, we can ship them. We don’t have to use refrigeration. That allows us to access a lot more rugged or non-ideal environments for testing.”
The research was funded, in part, by the MIT Research Support Committee and a MathWorks Fellowship.
PROVIDENCE, R.I. [Brown University] — Sunscreen should be simple: Apply it properly, and it will do its job shielding skin from the sun’s damaging rays. Yet despite the fact that sunscreen has enjoyed popularity for decades — and that it’s recommended for universal use by the American Academy of Dermatology — it is often misunderstood and misused.
Dr. Elnaz Firoz, an associate professor of dermatology, clinician educator, at Brown University’s Warren Alpert Medical School, and medical director of dermatology at Miriam Hospital in Providence, said she spots dozens of sunscreen use mistakes every time she goes to the beach.
“I’m always so shocked at the practices that I see,” Firoz said. “It makes me wonder how we can get more information out to people about how to use sunscreen.”
One way to educate people about sun protection is to connect them with dermatologists. Firoz is one of several Brown-affiliated faculty members who participate in free skin cancer screenings, including at the Amal Clinic at Clínica Esperanza, the Rhode Island Free Clinic and a series of skin check events held at Rhode Island beaches in partnership with the Rhode Island Department of Health.
In this Q&A, Firoz shares sun protection advice and addresses myths about the dangers of sunscreen.
It’s very common for people at the beach to use aerosol bottles of “invisible” chemical sunscreen. Most of the product ends up getting sprayed into the air instead of on the skin, thereby providing less coverage than intended. People will also use the spray sunscreen on faces, where it can get in the eyes, nose and mouth, and cause stinging or a terrible aftertaste. I understand that the spray version is convenient, but it can be difficult to use it in a way that provides adequate protection.
I advise my patients to find a broad-spectrum — meaning it protects against both UVA and UVB sun rays — mineral sunscreen with a sun protection factor (SPF) of at least 30. There are two main product formulations: mineral sunscreens, which have ingredients like zinc oxide and titanium dioxide that sit on the top layer of your skin and block and reflect UV rays; and chemical sunscreens, which sink into your skin and act like sponges, absorbing the sun’s UV rays. Chemical sunscreens are somewhat less photostable than mineral sunscreens, which means they degrade over time slightly more quickly as they are exposed to UV radiation.
I’m a big fan of mineral sunscreen lotion, which is not only broad-spectrum but also safe, and lasts longer both in and out of the water. Mineral formulations tend to be thicker and some may leave a whitish cast on the skin, but technology has advanced to the point that there are now tinted and untinted mineral sunscreens that go on quite easily.
The main reason to use sunscreen is to prevent skin cancer. All types of skin cancer, including basal cell carcinoma, squamous cell carcinoma and melanoma, are unfortunately on the rise. Melanoma is especially worrisome because it can metastasize if not caught early and become fatal, which is why we urge people to get skin checks. Squamous cell carcinoma can also be fatal (albeit rarely), particularly in patients who are elderly or immunocompromised.
UV radiation is a carcinogen — we know that to be 100% true. Each person is going to withstand that carcinogen differently based on their genetics and behavioral practices. And there are, of course, subtypes of melanoma that are not related to the sun. But I tell patients that generally speaking, their risk for skin cancer will be lower if they practice sun safe behaviors, which includes wearing sunscreen. Wearing sunscreen also slows the process of sun damage to the skin.
NEW DELHI: Imagine a routine blood donation quietly holding evidence of a future cancer diagnosis. A recent study published in Cancer Discovery suggests that could soon be a reality: scientists have found cancer-linked DNA mutations in blood plasma collected years before patients showed any signs of disease.In a groundbreaking analysis, Dr Yuxuan Wang and her team at Johns Hopkins University examined plasma samples donated as part of an unrelated study decades ago. By analyzing free-floating DNA fragments, the genetic leftovers from dying cells, they were able to spot warning signs of cancer as far back as 3.5 years before diagnosis, the recent study published on May 22 in the journal Cancer Discovery mentioned.
“It’s an important step toward preclinical cancer detection,” said Catherine Alix-Panabières, a cancer researcher not involved in the study. “Earlier detection typically means better outcomes.”The research focused on 52 people: 26 who developed cancer within six months of donating blood, and 26 who remained cancer-free for at least 17 years. In seven of the cancer patients’ samples, researchers detected common cancer mutations, and in two cases, those same mutations were already present years before any tumors were found.The team dove deeper, sequencing DNA from earlier samples and comparing them to the patients’ white blood cells. In three cases, they uncovered dozens of unique genetic mutations, all hinting at cancer in its earliest molecular form.These findings, though early, shine a spotlight on blood plasma as a potential early-warning system, a kind of molecular time machine. The cancers detected ranged from breast and colon to pancreatic and liver, though some types, like brain cancer, remain elusive due to biological barriers like the blood-brain barrier.Still, it’s not all breakthroughs and optimism.“We didn’t find any mutations in 18 out of 26 cancer patients,” Dr Wang admitted, pointing to the need for larger plasma samples and better detection tools. Cost is another barrier; identifying personalized mutations through DNA sequencing can cost hundreds to thousands of dollars per patient.While full-scale clinical use may be 5–10 years away, experts are cautiously hopeful. With larger trials and stricter ethical guidelines, such tests might one day become routine for high-risk groups, giving doctors a head start before cancer gets one.For now, the study offers a glimpse into a future where a simple blood draw could change the story of cancer, long before the first symptom ever appears.
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In a discovery that overturns old suppositions about the origin of leprosy, researchers have recovered two extremely well-preserved genomes of Mycobacterium lepromatosis—a rare and severe form of bacteria that causes Hansen’s disease—from 4,000-year-old Chilean human skeletons. The finding is the first ancient genetic evidence of this form of leprosy in the Americas and suggests that the disease emerged on the continent independently, centuries before the arrival of Europeans.
The skeletons, unearthed at Chile’s Atacama Desert archaeological sites of El Cerrito and La Herradura, belonged to two adult males who lived around 2000 BCE. The skeletons bore signs of leprosy, such as widened nasal cavities and thickening of the hand bones. When scientists studied the skeletons, they were surprised to find highly intact M. lepromatosis genomes, with better DNA preservation than in many modern samples.
While Mycobacterium leprae has long been known to be the dominant cause of Hansen’s disease—and is found in archaeological remains all over Europe and Asia dating back 5,000 years—M. lepromatosis was only identified in 2008 and is still rare today. This form of leprosy is associated with the most severe manifestations of the disease, such as diffuse lepromatous leprosy (DLL) and the potentially fatal Lucio’s phenomenon.
The two recovered genomes indicate that M. lepromatosis split from M. leprae approximately 26,800 years ago, with the American lineages diverging around 12,600 years ago—presumably coinciding with early human migration into South America. Importantly, the ancient Chilean strain has 94 unique mutations not found in modern genomes, suggesting long-standing isolated evolution.
This deep divergence means that Hansen’s disease did not arrive with European colonists to the Americas, as previously believed, but perhaps originated or was independently introduced much earlier. “So far, the evidence points in the direction of an American origin,” said Kirsten Bos, group leader for Molecular Paleopathology at the Max Planck Institute for Evolutionary Anthropology, “but we’ll need more genomes from other time periods and contexts to be sure.”
The study also raises broader questions about disease evolution and the limitations of our historical knowledge.
Today, M. lepromatosis remains rare, largely confined to Mexico and the Caribbean, but it has also been found in red squirrels in Ireland and the UK, highlighting possible zoonotic transmission routes. Although new cases are limited, finding it in ancient Chile provides evidence that the pathogen also circulated more widely and might have played a significant role in pre-Columbian health.
This finding showcases the ability of ancient DNA studies to reveal the lost epidemics of the past—pathogens that shaped civilizations and disappeared without a trace, until now.