Today, in many countries, polio can seem to be a disease to which little attention is paid. This is especially true among younger generations, who might view it as a thing of the past. But if you ask their grandparents, or people aged 70 years or older, they may well have relatives and acquaintances who suffered from polio, or may have contracted the disease themselves. This is because it was very common around the world until the second half of the 20th century. It is thanks to vaccination that polio is only found in endemic form in a handful of countries today. That said, isolated cases have appeared a little more widely in recent years.
In Sweden, no domestic case has been registered since 1977. Europe was declared polio-free in 2002, a status South and North America achieved in 1994. However, since September 2024, authorities in five European countries have detected poliovirus in wastewater. As a consequence, the European Centre for Disease Prevention and Control (ECDC) is now calling for measures to be taken. Until polio is eradicated, all children worldwide will need to be vaccinated. But, just as the future of this disease is once again in the spotlight, so too questions are being asked about its past.
The church in Hagby parish, Sweden. Excavations here revealed a disturbed burial dating to between AD 1200 and 1800. The individual interred there seemingly suffered from a case of severe paralysis, and it has been wondered if this could have been caused by polio.
A dangerous disease
Polio is an infection, a viral disease that is mainly spread via contaminated water, although it can also be passed on by close contact between people. Three subtypes of the poliovirus are known to have existed. While Type 2 and Type 3 have been eradicated following extensive vaccination programmes, Type 1 is still present.
Around 95% of individuals infected with poliovirus will display no outward signs of the disease. Others will only experience flu-like symptoms: fever, headache, nausea, and vomiting. In many cases, the disease stops at this stage. If the course of the disease is not interrupted, though, after three or four days the virus will enter the bloodstream and reach bodily organs. After this, a range of serious outcomes can occur, including paralysis of the arms, legs, and respiratory muscles, and even death. About one in 200 people infected by the virus will suffer from paralysis, which often affects some parts of the body, rather than all of it. Sadly, children are particularly susceptible to polio.
For reasons that remain unclear, the disease tends to be most prevalent during the autumn months. When poliovirus has manifested in populations where hygienic conditions were poor – a situation that is frequently associated with the Middle Ages – children would often be exposed to the disease during the first year of their life. Antibodies from their mother would, though, suppress the spread of the virus from the infected gut to other parts of the body. Thanks to this protection, while occasional cases of paralysis could occur, they were not common.
It was during the 19th century that polio became far more prevalent and visible as a disease. This occurred against a backdrop of striking demographic change, which saw the human population nearly quadruple over 200 years, between 1750 and 1950, alongside a marked growth in urban living. Compared to the Middle Ages, this was also a period of increasingly hygienic conditions and rising living standards for many – a marked difference from the circumstances usually associated with epidemics becoming more common. Indeed, despite having comparatively good levels of sanitation, Scandinavia was one of the first areas to experience epidemics of polio, with Sweden very heavily affected. There, epidemics recurred again and again between 1881 and 1965. It was only after vaccination began in 1957 that the incidence of polio was drastically reduced.
A stele dating to 1403-1365 BC and depicting an ancient Egyptian who is standing with the help of a crutch. Image: AEIN 134 Ny Carlsberg Glyptotek, foto: Ole Haupt
As we will see, there are grounds to believe that polio has been afflicting humanity for thousands of years, but it is not until the 18th century that definite descriptions of the disease can be found. One example concerns the famous writer Sir Walter Scott, who was born in 1771. At the age of one and a half, he suffered paralysis in the leg after contracting polio, and was left with impaired movement. In the decades that followed, Michael Underwood became the first person to give a clinical description of polio in 1789, while the Italian surgeon Giovanni Battista Monteggia provided the first clear medical description of the disease in 1813. It was a little over two decades later, in 1835, that John Badham documented four cases of polio in Nottinghamshire, Britain, during what may well have been the first epidemic outbreak of the virus in the world.
Tracing incidences of polio before these 18th- and 19th-century outbreaks remains fraught with uncertainty. Even so, a candidate for the oldest indication of the disease is provided by an ancient Egyptian stele dating to 1403-1365 BC, which depicts a man called Roma. He is shown standing with the help of a crutch, because one leg is much thinner and shorter than the other. This leg also has a foot that points downwards, with just the toes touching the ground, which can be caused by a form of paralysis that is consistent with polio. A thousand years later, in around 400 BC, examples of feet displaying comparable traits were noted by the ancient Greek physician Hippocrates. The Roman physician Galen, who practised in the 2nd and 3rd centuries AD, describes isolated cases of paralysis, too, which may have been caused by polio.
Above & below: Leg bones from the individual buried at Åhus, Sweden. The two femurs appear narrow compared to one from a younger individual, which is shown to the left of them (above). The child’s tibias are straight, while the fibulas are curved (below).
A challenging diagnosis
Despite the prevalence of polio in recent centuries, and intermittent occurrences of possible examples in the ancient sculptural and literary records, traces of the disease are seldom identified in skeletal material, regardless of the time period in question. This raises questions about whether polio was simply absent from these populations, or sufferers were buried elsewhere, or if the disease is one that is difficult to identify correctly in the archaeological/palaeopathological record.
This last possibility is supported by a discovery in 1995, at the Dominican Convent Cemetery in Åhus, Sweden. It concerns the skeleton of a child aged between 9 and 12, who was suffering from an affliction that initially seemed impossible to diagnose. This was because his or her leg bones (that is, the femurs, tibias, and fibulas) were slighter than would be expected, but while the shin bones (tibias) were straight, the calf bones (fibulas) were bent. Most conditions, such as rickets, would result in both bones becoming curved. At the same time, the changes to the calf bones were symmetrical, with both the right and left legs affected, making it virtually impossible that they could be caused by healed fractures. An intensive search for disease diagnoses was conducted, with experts in the field consulted around the world. As a result, some very rare disorders were considered, but these were always proposed with reservations, because in all cases the tibia should also have been affected.
It was only when another case was discovered 500km north of Åhus, in the cemetery of a Franciscan monastery and hospital at Linköping, that the picture became clearer. On this occasion, the attention of the specialists was drawn to not only the bent calf bones, but also the appearance of the deceased child’s entire lower limbs and their position within the grave. Instead of lying with his or her legs straight like everyone else who was buried in this cemetery, the left leg was bent at both the hip and knee, leaving it resting on the right leg. At the same time, the left foot was pointing downwards, as if the individual only had his or her toes on the ground. An additional factor was that, just like the first individual, the child’s leg bones were much thinner than would be expected of people who were the same size.
The child buried in Linköping is visible in the lower part of the photograph. Note that he or she was buried with bent legs, with the left foot pointing downwards.
Examining the leg bones of the child from Linköping revealed that he or she had narrow femurs, straight tibias, and curved fibulas.
Considering the gracile nature of this child’s legs brought another case to light, involving another child who had probably died at a similar age. This individual had been buried in Hagby Church, which lies in a small village near Kalmar in southern Sweden. This child’s burial had previously been disturbed, leaving the skeleton not only incomplete, but also mixed in with other bones. On this occasion, the leg bones were even thinner – with those on one side smaller than the other – perhaps indicating that this individual had suffered from severe paralysis. It was this possibility that prompted the suspicion that the cause could be polio. Although X-ray images showing the skeletons of individuals affected by polio paralysis are rare, a skeleton in an anatomical collection at the Pathological Museum in Vienna has femurs that are bent, while the tibias remain straight. Despite this similarity to the leg bones from Sweden, it should be noted that other causes remain possible – one that has been considered is a serious condition known as Guillain-Barré syndrome, which can affect children.
Top, Above & below: The bones from the disturbed burial at Hagby Church. Top: In this photograph the femur is narrow in comparison to another femur from a younger individual. Above: This picture shows both of the femurs from the Hagby burial. Below: The shins were also affected, with this image showing one alongside a bone of nearly the same length from another individual.
Medieval polio?
All three of the children described here died between 9 and 12 years old, but in no case is their sex known. The child from Åhus was buried during the medieval period (AD 1200-1536), while radiocarbon dating of the child from Linköping indicates that he or she died AD 1440-1640. Due to the disturbance of the grave from Hagby, it is more difficult to date the burial, but it certainly occurred before AD 1800, although not earlier than AD 1200.
Based on what is known about the virus, it was probably very common at these times. Even so, serious cases are likely to have been unusual, because most people would have been protected by the antibodies from their mother. As a result, cases of paralysis seem likely to have been rare. Perhaps it is examples of the unfortunate individuals who contracted such occasional cases that have been found here.
Polio became epidemic… against the backdrop of improving living conditions.
Given that polio first became epidemic at the end of the 19th century, against the backdrop of improving living conditions, it is notable that two of these children were buried in cemeteries associated with better-off members of medieval society. Although we can only speculate, it is conceivable that they had lived in more protected environments, and so had only contracted the disease later on in childhood, when they were able to move around by themselves. Alternatively, could the higher status of the household have increased the chance of the children becoming infected, without the mother being affected, meaning she did not have antibodies to pass on?
Whatever the truth, we can conclude from the skeletal changes that for several years – perhaps even most of their short lives – these three children would have had enormous difficulty getting around without help. In the case of the child from Linköping, it is apparent that his or her arm bones weigh considerably more than the respective tibia and fibula combined. This is especially true on the left side, which could indicate that the child used some form of crutches for support. The child from Hagby must also have had considerable difficulty walking, as the leg bones indicate an almost total absence of developed muscles.
Part of the skeleton of a man who died in 1880, at the age of 24. According to documentary information, he suffered from polio. It is noticeable that the fibulas curve close to the tibias.
All of this raises questions about how children with comparable conditions coped with life in the medieval period. They must have been heavily dependent on the assistance of adults or older children for activities as everyday as going to the bathroom. Even with such help, life was probably much more sedentary than it was for their peers. Study of several thousand well-preserved skeletons from the Middle Ages shows that it is rare to identify children who suffered injuries or illnesses that resulted in a disability during this era. Perhaps this is one of the reasons why adults with disabilities are more often described and discussed in studies of past societies. These three cases present a poignant glimpse of the day-to-day realities for children with physical impairments in medieval societies.
If these children did contract polio, then their circumstances remain highly relevant today, as sufferers of a disease that still exists, despite the potential for its eradication.
All Images: courtesy of Caroline Arcini and Emma Karlsson, unless otherwise stated
Point-of-care ultrasound (POCUS) can accurately identify clinically significant pneumothorax (PTX) in emergency trauma patients, suggest findings published July 17 in the Journal of Emergency Medicine.
Researchers led by Daniel Singer, MD, from Stony Brook University in New York, found that POCUS outperformed supine chest x-ray in finding PTX, whether it was used by experts or less-trained physicians. POCUS also led to faster exam times over x-ray and CT.
“These results highlight the necessity for ongoing real-time quality improvement,” Singer and colleagues wrote.
While CT is the standard for diagnosing PTX, the researchers noted that this can be time-consuming due to transferring patients to imaging, especially if they are unstable. And while chest x-ray is another modality used for PTX detection, previous reports suggest that it can miss up to half of PTX cases.
POCUS has become a useful emergency imaging tool that can be used at the bedside for trauma assessment. Previous studies showed the modality’s effectiveness for PTX, including high sensitivity and specificity.
Singer and colleagues compared the sensitivities of POCUS and portable chest x-ray in detecting all cases of PTX, including cases with clinically significant PTX.
The researchers reviewed retrospective data over a three-year period at a level I trauma center, focusing on high-severity trauma patients. They determined the presence or absence of PTX by either CT findings or a clinician’s description of a “rush of air” on tube thoracostomy placement. They also defined PTX as clinically significant if the patient needed tube thoracostomy within 2.5 hours of triaging.
Final analysis included 924 patients, 40 of whom had clinically significant PTX. POCUS outperformed plain chest x-ray, whether it was used by fellowship-trained or less-trained physicians.
Comparison between POCUS, chest x-ray for PTX detection
Measure
Plain chest x-ray
POCUS (less-trained physicians)
POCUS (fellowship-trained physicians)
Sensitivity
48.1%
68%
84%
Specificity
99%
100%
100%
POCUS also achieved a positive predictive value of 100% for both novice and experienced users and a negative predictive value of 14.3% for less-trained users and 25% for fellowship-trained users.
Finally, the time to acquisition of a POCUS exam was 9.9 minutes compared with 16.9 minutes for chest x-ray and 76.6 minutes for CT.
The study authors highlighted that thoracic POCUS can be performed accurately by non-fellowship trained emergency department providers with greater attention to technique.
“There may be a need for more supervision, recurrent hands-on practice, and establishment of a consensus protocol on location for scanning,” they wrote.
Prior vaccination against COVID-19 may play a critical role in improving renal outcomes and overall survival in patients with chronic kidney disease (CKD) and COVID-19, according to findings from a recent study.1
Leveraging real-world data from the TriNetX database, the global retrospective cohort study found prior vaccination against COVID-19 reduced the risks of major adverse kidney events (MAKEs) and all-cause mortality in those with CKD and COVID-19 infection, especially with ≥ 3 vaccine doses.1
“There is a critical gap in understanding the potential renal implications of COVID-19 vaccination, particularly in CKD patients,” I-Ning Yang, of the division of nephrology at Chi Mei Medical Center and the Institute of Clinical Pharmacy and Pharmaceutical Sciences at National Cheng Kung University, and colleagues wrote.1 “To the best of our knowledge, no research has specifically addressed this critical issue.”
While COVID-19 was initially recognized for its respiratory manifestations, emerging evidence indicates SARS-CoV-2 infection can lead to long-term complications affecting multiple organ systems, including the kidneys. Recent research has linked severe COVID-19 infection to kidney damage, even in patients who had no underlying kidney problems before they were infected with the coronavirus.2 However, less is known about the impact of COVID-19 vaccination on outcomes in patients with kidney disease.1
To assess the real-world impact of prior COVID-19 vaccination on MAKEs and mortality in CKD patients with COVID-19, investigators examined data for adults ≥18 years of age with CKD enrolled in the TriNetX network from January 2020 to May 2024 who were diagnosed with COVID-19 based on ICD-10-CM codes or a positive polymerase chain reaction test result. Of note, they excluded individuals undergoing dialysis and those with a history of transplantation due to their potentially different immune responses.1
The study cohort was divided into 2 groups based on COVID-19 vaccination status. The vaccinated group encompassed CKD individuals who received ≥ 1 dose of the mRNA vaccines, BNT162b2 (Pfizer/BioNTech) and mRNA-1273 (Moderna), within 1 year to 7 days before the index date. Conversely, the unvaccinated group included CKD individuals with no documented history of COVID-19 vaccination.1
Investigators used propensity score matching accounting for demographics, lifestyles, comorbidities, medication usage, and laboratory data to create a 1:1 cohort of 8520 vaccinated and 8520 unvaccinated CKD patients with COVID-19.1
The primary outcome was a composite endpoint of MAKEs or all-cause mortality. MAKEs were defined by the first occurrence of any of the following procedure and diagnostic codes: dialysis services and procedures, dialysis procedure other than hemodialysis, dependence on renal dialysis, hemodialysis, hemodialysis access, intervascular cannulation for extracorporeal circulation, shunt insertion procedures on arteries and veins, or hemodialysis procedures. Both groups were followed from the first day to 30 days after the index date to estimate the risk of incident MAKEs or mortality.1
During the 30-day follow-up period, compared with the unvaccinated group, investigators noted the vaccinated group exhibited a significantly reduced risk of development of MAKEs or all-cause mortality (8.85% vs 13.29%; hazard ratio [HR], 0.637; 95% CI, 0.581–0.689) and an increased probability of event-free survival at 30 days (log-rank test, P <.0001). Additionally, those receiving vaccination had a lower risk of MAKEs (HR, 0.792; 95% CI, 0.698–0.898) and all-cause mortality (HR, 0.549, 95% CI, 0.484–0.622), respectively.1
Of note, the beneficial effects of COVID-19 vaccination on the primary outcome were consistent across subgroup analyses for sex, age, CKD status, and diabetes status.1
Investigators also called attention to a statistically significant reduced risk of MAKEs or all-cause mortality among individuals with vaccination status of > 3 doses (HR, 0.449; 95% CI, 0.397–0.508). A significant interaction was observed in patients receiving ≥ 3 doses (P <.0001), a trend that was similarly significant in the analysis of MAKEs and all-cause mortality (P = .0208 and P <.0001).1
“Our findings suggested that prior vaccination against COVID-19 might play a critical role in reducing the incidence of MAKEs and all-cause mortality in this vulnerable population and provided important real-world insights for clinicians concerning the post-vaccination risks of subsequent kidney diseases,” investigators concluded.1
References
Huang CY, Wu JY, Lin GY, et al. Impact of prior COVID-19 vaccination on major adverse kidney events in patients with non-dialysis dependent chronic kidney disease: a global retrospective study. Expert Rev Vaccines. doi:10.1080/14760584.2025.2536077
Brooks A. COVID-19 Infection Linked to Faster Kidney Function Decline Than Pneumonia. HCPLive. January 1, 2025. Accessed July 21, 2025. https://www.hcplive.com/view/covid-19-infection-linked-faster-kidney-function-decline-than-pneumonia
Anemia, fatigue, nausea, edema peripheral, and constipation were the most common adverse effects across both treatments.
Patients with advanced renal cell carcinoma had statistically significant and clinically meaningful improvement of quality-adjusted survival when treated with belzutifan (Welireg) vs everolimus (Afinitor), per a quality-adjusted time without symptoms or toxicity (Q-TWiST) analysis of the phase 3 LITESPARK-005 trial (NCT04195750) presented at the 2025 Kidney Cancer Research Summit.1
Based on the main analysis, in which toxicity accounted for grade 3/4 adverse effects (AEs), the mean Q-TWiST was 17.47 months among patients who received belzutifan (n = 374) vs 14.81 months among those who received everolimus (n = 372; difference, 2.66; 95% CI, 1.06-4.49). The relative gain in Q-TWiST with belzutifan, defined as the absolute Q-TWiST difference divided by mean overall survival (OS) for the everolimus arm, was 11.32% (range, 4.49%-19.09%) in the main analysis.
The sensitivity analysis, which included grade 1 to 4 serious AEs, showed a mean Q-TWiST of 17.50 months in the belzutifan arm vs 15.03 months in the everolimus arm (difference, 2.47; 95% CI, 0.81-4.28). Data highlighted a relative Q-TWiST gain of 10.50% (range, 3.44%-18.18%) in the sensitivity analysis.
“In conclusion, belzutifan outperformed everolimus from a response and a progression-free-survival [PFS] perspective. The toxicity profile was distinct, the quality of life was better, and so was the TWiST and the Q-TWiST analysis,” lead study investigator, Thomas Powles, MBBS, MCRP, MD, stated in the presentation.1 “This [Q-TWiST analysis] does help patients and doctors make decisions. I quite like this type of exploratory analysis, and I’m happy to be involved in future projects with it.”
Powles is a professor of genitourinary oncology, lead for Solid Tumor Research, and director of Barts Cancer Institute at St. Bartholomew’s Hospital, Queen Mary University of London.
As part of this analysis, investigators divided patient survival time following randomization into 3 mutually exclusive states: investigator-assessed time with grade 3/4 toxicity before disease progression (TOX), time without symptoms and progression of grade 3/4 toxicity (TWiST), and time from progression until death (REL). Investigators calculated Q-TWiST as the sum-product of restricted mean time spent in the individual states and state-specific utility weights. Additionally, standard utility weights used in literature—1 for TWiST as well as 0.5 for TOX and REL—were considered, and threshold utility analysis was performed to determine the impact of the differing health state utility.
The study authors summarized the treatment effects as differences in restricted mean time spent in each state; the difference in Q-TWiST; and the relative gain in Q-TWiST, or the absolute Q-TWiST difference divided by mean OS in the everolimus arm. Use of nonparametric bootstrapping method was involved for generating 95% confidence intervals for the treatment differences related to the health states and Q-TWiST.
In the multicenter, open-label phase 3 LITESPARK-005 trial, patients were randomly assigned 1:1 to receive belzutifan at 120 mg or everolimus at 10 mg orally once daily until progressive disease or unacceptable toxicity.2
The trial’s dual primary end points were PFS based on blinded independent central review (BICR) per RECIST v1.1 criteria and OS. Secondary end points included the objective response rate per RECIST v1.1 guidelines, duration of response, and safety.
Patients 18 years and older with stage IV clear cell RCC, a Karnofsky performance status of 70 or higher, and at least 1 measurable lesion per RECIST v1.1 guidelines, and disease progression after prior treatment with a PD-(L)1 inhibitor and a VEGFR tyrosine kinase inhibitor were eligible for enrollment on the trial. Having 3 or fewer prior lines of systemic therapy were required for study entry.
In the main analysis, the mean TOX time was 1.45 months in the belzutifan arm vs 1.22 months in the everolimus arm (difference, 0.23; 95% CI, –0.29 to 0.76). Despite a numerically longer time in TOX among those in the belzutifan arm, data showed significantly longer time in TWiST with belzutifan at a mean of 10.73 months vs 6.07 months with everolimus, which was driven by prolonged periods without progression (difference, 4.66 months; 95% CI, 3.28-6.02).
Prior safety data showed that the most common any-grade AEs in the belzutifan and everolimus arms, respectively, included anemia (83.1% vs 57.2%), fatigue (32.3% vs 25.8%), nausea (18.5% vs 12.2%), edema peripheral (17.2% vs 18.1%), and constipation (16.9% vs 8.3%).
References
Powles T, de Velasco G, Choueiri TK, et al. Quality-adjusted time without symptoms or toxicity (Q-TWiST) analysis of belzutifan versus everolimus in previously treated advanced renal cell carcinoma (RCC): LITESPARK-005 (LS-005). Presented at the 2025 Kidney Cancer Research Summit; July 17-18, 2025; Boston, MA. Abstract 13.
Choueiri TK, Powles T, Peltola K, et al. LITESPARK-005 Investigators. Belzutifan versus everolimus for advanced renal-cell carcinoma. N Engl J Med. 2024;391(8):710-721. doi:10.1056/NEJMoa2313906.
FDA panel convenes on SSRIs and pregnancy amid ongoing debate over risk, efficacy | Image credit: Contemporary OB/GYN
The US Food and Drug Administration (FDA) convened a public expert panel to discuss the use of selective serotonin reuptake inhibitors (SSRIs) during pregnancy, highlighting a contentious and complex issue that affects millions of women in the United States. The panel brought together perinatal psychiatrists, developmental biologists, epidemiologists, obstetricians, and mental health experts to assess the current state of evidence on SSRIs, including their risks, benefits, and regulatory implications.
FDA Commissioner Marty Makary, MD, MPH, opened the session by acknowledging that “nearly 1 in 4 middle-aged women are on an antidepressant, and up to 5% of women in pregnancy are on an antidepressant.” While recognizing the potential benefit of SSRIs, he cautioned that the broader picture of mental health in the United States has not improved despite increasing prescriptions. “The more antidepressants we prescribe, the more depression there is,” he said, adding, “We have to start talking about root causes.”
Anick Bérard, PhD, professor of Perinatal Epidemiology, University of Montreal, faculty of Pharmacy, and CHU Ste-Justine in Montreal, and adjunct professor at the Faculty of Medicine, Université Claude Bernard, stated that depression and anxiety in pregnancy are prevalent and require treatment. “Untreated depression and anxiety during pregnancy has been shown to be associated with an increased risk of postpartum depression,” she said. She emphasized the complexity of risk-benefit analysis for antidepressant use in pregnancy and noted that the absolute risk of outcomes such as miscarriage or autism remains low, even if relative risk appears elevated in some studies.
Jay Gingrich, MD, PhD, director, Institute for Developmental Sciences, and professor of Developmental Psychology (in Psychiatry), Columbia University Irving Medical Center, presented findings from large-scale studies linking in utero SSRI exposure to increased rates of adolescent depression. “Until recently, there’s really never been any attempt to study whether this treatment of the mother actually improves outcomes in the offspring,” he noted. Gingrich also emphasized that serotonin plays a different developmental role in utero than in adults, acting as a neuromodulator that influences organ and neural development.
Adam Urato, MD, chief of Maternal-Fetal Medicine at MetroWest Medical Center, called for stronger FDA warnings. “Patients regularly tell me that essentially the only counseling they received is that SSRIs don’t affect the baby or cause complications. This is simply not accurate,” he said. He cited data from animal studies and human imaging studies to assert that SSRIs alter fetal brain development. “The SSRIs can be very difficult to get off of, so the time to think about these things is long before pregnancy,” he added.
Some panelists, such as Kay Roussos-Ross, MD, took a different position. “One in 5 women will have a perinatal mood disorder,” she said. “Psychotherapy and SSRIs are tools that we have… Treating mental illness in pregnancy is not a luxury. It’s a necessity.” Roussos-Ross cited guidelines from multiple professional societies and argued that the risks of untreated mental illness often outweigh those of SSRI exposure, especially when factoring in increased rates of preterm birth, poor prenatal care, and maternal suicide.
Roussos-Ross is a professor and chief in the Division of Academic Specialists in General Obstetrics and Gynecology, and director of the Perinatal Mood Disorders Program in the Department of Obstetrics and Gynecology and Psychiatry at the University of Florida College of Medicine.
However, several participants questioned the foundational premise of SSRI efficacy. Joanna Moncrieff, MD, professor of Critical and Social Psychiatry at University College London and practising psychiatrist, stated, “There is very little evidence that antidepressants have actual benefits in depression.” She argued that perceived improvements may stem from nonspecific psychoactive effects rather than the correction of a biochemical imbalance.
Multiple speakers also criticized the prevailing “chemical imbalance” narrative. Jeffrey Lacasse,PhD, MSW, associate professor, College of Social Work, Florida State University, noted, “88% of Americans believe that antidepressants correct chemical imbalances, despite no conclusive scientific basis.” He suggested this belief contributes to overprescribing, including among women of reproductive age.
Michael Levin, PhD, distinguished professor, Department of Biology and Director of the Allen Discovery Center at Tufts University, provided evidence that serotonin signaling plays a critical role in early embryonic patterning and organ asymmetry. “Manipulating its use by cells with SSRIs is very, very likely to cause certain kinds of defects,” he said, referencing experiments in frogs and chicks.
In addressing regulatory implications, a psychiatrist at Taperclinic and former FDA medical officer Josef Witt-Doerring, MD, highlighted that even known risks like neonatal withdrawal and cardiac malformations are inconsistently addressed across SSRI drug labels. He proposed more accessible patient education, such as QR codes on prescription bottles linking to FDA-approved risk summaries.
The panel did not reach consensus on new regulatory action, but many agreed that greater transparency, improved labeling, and expanded access to nonpharmacologic interventions are needed. “The key is information,” said Urato. “Never before in human history have we chemically altered developing babies like this… without any real public warning.”
The FDA has not yet announced whether it will revise current SSRI labeling or issue new guidance. However, the agency indicated it would consider the panel’s input in evaluating potential policy updates.
Reference:
FDA. FDA Expert Panel on Selective Serotonin Reuptake Inhibitors (SSRIs) and Pregnancy. FDA July 21, 2025. Accessed July 21, 2025. https://www.youtube.com/watch?v=2Nha1Zh63SA
The latest edition of Medicines, Ethics and Practice (MEP) includes new sections on gender incongruence and dysphoria, and pharmacy services at a distance, which are aimed to show “the growing complexity of pharmacy practice”, the Royal Pharmaceutical Society (RPS) has said.
This iteration of MEP, published on 21 July 2025, marks the 48th edition of the professional guide for pharmacists.
The new material on gender incongruence and dysphoria includes guidance aimed to help pharmacists decide whether a supply of gonadotrophin-releasing hormone analogues for children and young people would be appropriate or not. It also includes information to help pharmacists signpost to support provided by other organisations.
The MEP sets out guidance on pharmacy services at a distance — including online — that provides signposting to, and information on, the General Pharmaceutical Council’s (GPhC) guidance for registered pharmacies providing these services.
Existing sections of the MEP have also been updated, including information about the RPS’s position statement on facilitated self-selection of Pharmacy (P) medicines, guidance on new legislation for original pack dispensing, and guidance around emergency supply at the request of a patient, to help pharmacists ensure duplicate supplies of a medicine are not provided.
Rakhee Amin, senior professional standards pharmacist at the RPS and editor of MEP, said: “This edition reflects the continuing evolution of pharmacy practice. We’ve worked closely with colleagues and expert contributors to ensure that MEP remains a valuable, relevant and trusted resource.
“We encourage all members to explore the easy-to-use digital MEP for up-to-date information wherever you practise.”
The digital MEP is free to access for all RPS members, and all foundation trainee members receive a free print copy.
A new study of Ukrainian refugees reveals how the country’s war with Russia may be helping promote the spread of multidrug-resistant (MDR) bacteria throughout Europe, researchers reported today in Clinical Microbiology and Infection.
In what they say is the largest cohort study to date on the topic, researchers from Helsinki University Hospital in Finland assessed MDR bacterial carriage among 166 Ukrainian refugees treated at the hospital in the 2 years after the Russian invasion of Ukraine in February 2022. They found that significant proportions of previously hospitalized Ukrainians, especially those who had been treated for war wounds, carried MDR strains. Previously hospitalized patients also had the highest rates of MDR infections.
Previous research has indicated a significant increase in MDR organisms in Ukrainian hospitals since the invasion, primarily linked to traumatic war wounds. But the war in Ukraine has also resulted in the transfer of thousands of hospital patients to hospitals in Finland and elsewhere in Europe. The authors of the letter say these findings suggest European hospitals need to focus on the antimicrobial resistance (AMR) threat posed by those patients.
“Our findings highlight that war-related hospitalisations represent a distinct and urgent AMR risk,” the authors wrote.
High rate of MDR infection in war-wounded patients
The 166 Ukrainian patients treated at the hospital from February 24, 2022, to May 31, 2024, were screened for carriage of several MDR pathogens, including methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant Enterococcus (VRE), extended-spectrum beta-lactamase-producing Enterobacterales (ESBL-PE), carbapenemase-producing Enterobacterales (CPE), multiresistant Acinetobacter baumannii (MRAB), and multiresistant Pseudomonas aeruginosa (MRPA). They were grouped based on hospitalization abroad in the prior year: No hospitalization (102 patients, 61.4%), hospitalization without war-related injuries (50, 30.1%), and hospitalization with war injuries (14, 8.4%).
While only 17.6% of the non-hospitalized patients carried MDR bacteria (primarily ESBL-PE and MRSA), MDR bacterial carriage was found in 46% of those hospitalized without war injuries and 78.6% of those hospitalized with war injuries.
Our findings highlight that war-related hospitalisations represent a distinct and urgent AMR risk.
The MDR bacteria carried by previously hospitalized patients included the most highly-resistant pathogens. Among the war-injured, carriage rates for CPE, MRAB, and MRPA were 35.7%, 28.6%, and 21.4%, respectively. In those hospitalized without war injuries, 16% harbored CPE, 4% carried MRAB, and 2% carried MRPA.
“All MRAB and MRPA carriers had recently experienced ICU [intensive care unit] care admission or surgery abroad, suggesting significant transmission in conflict-affected healthcare systems,” the researchers wrote.
Two patients with war-related injuries carried VRE. In contrast, no CPE, MRAB, VRE, or MRPA isolates were identified in non-hospitalized patients.
Although most of the MDR carriage was asymptomatic, more than 1 in 5 (21.2%) developed clinical MDR infections, a rate the authors say is significantly higher than observed in a previous study of refugees/asylum seekers conducted before the war in Ukraine. Most of the infections were wound-related. The MDR infection rate was 45.5% among MDR carriers with war wounds and 17.4% among those hospitalized without war injuries.
“We strongly recommend targeted MDR screening and strict contact precautions for patients hospitalised in conflict zones,” the authors concluded. “War-injured patients should be considered as a high-priority group for infection control across Europe and beyond.”
KAMPALA, July 21 (Xinhua) — Health experts, policymakers, and researchers on Monday began a three-day meeting in Kampala, the Ugandan capital, to accelerate the elimination of mother-to-child transmission of HIV, syphilis, and hepatitis B across Africa.
The event, held under the theme “Unifying Actions, Transforming Futures: Achieving Triple Elimination in Africa by 2030,” is dubbed as Africa’s first-ever high-level conference focused on the triple elimination of mother-to-child transmission of HIV, syphilis, and hepatitis B.
Ugandan President Yoweri Museveni, represented by Vice President Jessica Alupo, emphasized the importance of unity and innovation in tackling the continent’s health challenges, especially in the face of shifting global health priorities and diminishing funding.
“As Africa, and as a global community, we must act with unity, innovation, and purpose to advance maternal and child health and eliminate mother-to-child transmission of HIV, syphilis, and hepatitis B,” said Museveni.
He noted that the interconnected epidemics of HIV, syphilis, and hepatitis B pose a significant burden to public health, particularly through mother-to-child transmission during pregnancy, childbirth, and breastfeeding.
Uganda’s Minister of Health Ruth Aceng told the gathering that while progress has been made in HIV prevention, care, and treatment, major challenges persist, particularly in addressing syphilis and hepatitis B.
She said that by the end of 2024, Africa had approximately 26.3 million people living with HIV, accounting for 65 percent of the global total. Meanwhile, syphilis cases are rising worldwide, with eight million adults infected, 700,000 congenital cases, and 230,000 deaths annually.
While Africa has recorded the highest increase in syphilis cases globally, with only Botswana and Namibia currently on track to eliminate mother-to-child transmission, 65 million people across the continent are chronically infected with hepatitis B, contributing 63 percent of the world’s new infections, the minister added.
“Integration is the way to go now, especially in this era of unprecedented funding challenges, where we are already seeing a reduction in funding from development partners,” said Aceng.
According to the event organizers, the conference aligns with the World Health Organization’s 2030 disease elimination targets and the African Union’s Agenda 2063, both of which envision a healthier, more resilient Africa. ■
Scientists use a precise form of gene editing called prime editing to correct the most common genetic mutations that cause alternating hemiplegia of childhood, a rare and severe neurological disorder that begins in infancy.
By the time they are a few months old, infants born with alternating hemiplegia of childhood (AHC) begin experiencing terrifying episodes of paralysis and seizures, and will soon show developmental delays and intellectual disability. There is no cure or effective treatment for this rare genetic disease, but new research suggests a potential path to one.
Researchers at the Broad Institute and The Jackson Laboratory have used prime editing, a precise and versatile form of gene editing, to correct the root cause of AHC in mice. The team used a scalable approach to develop prime editing treatments that directly repaired five different AHC-causing genetic mutations. Mice that received the treatment had far fewer and less severe symptoms of AHC, and survived more than twice as long as untreated mice.
The new study, published in Cell, is the first time prime editing has been used to treat a neurological disease in animals, offering hope for treating people with AHC and other genetic brain disorders. Prime editing was developed in 2019 by the lab of David Liu, a Broad core institute member and co-senior author of the new paper. The technology has already been successfully tested in a clinical trial for another rare genetic disease.
This study is an important milestone for prime editing and one of the most exciting examples of therapeutic gene editing to come from our team. It opens the door to one day repairing the underlying genetic causes of many neurological disorders that have long been considered untreatable.”
David Liu, Richard Merkin Professor and director of the Merkin Institute of Transformative Technologies in Healthcare at the Broad
Liu is also a Howard Hughes Medical Institute investigator and a professor at Harvard University.
The ability to precisely edit DNA directly in the brain has important implications for neurological diseases, said Cathleen Lutz, vice president of the Rare Disease Translational Center at The Jackson Laboratory and co-senior author of the study. “This level of editing efficiency in the brain is really quite remarkable.”
The team’s patient partner is RARE Hope (formerly Hope for Annabel), a non-profit focused on accelerating research on AHC and developing scalable, patient-centric research platforms to benefit the larger rare disease community. RARE Hope initiated the collaboration and was closely engaged throughout the project.
“This study is a win not just for our community but for all rare neurological conditions, and a breakthrough moment in expanding access to a broader cohort of potential patients,” said Nina Frost, founder and president of RARE Hope, a co-author of the study, and mother of a daughter with AHC. “It’s been a privilege to collaborate on such a scientifically significant effort with a team that has kept patients at the center of proof-of-concept research – engaging the patient community, modeling the patient experience, and integrating patient priorities into experimental design. This is a model for patient-relevant, patient-centered research because the team included us as true partners.”
Brain gene editing
The vast majority of AHC cases are caused by one of four mutations in ATP1A3, a gene essential for brain cell function. In the new work, Liu’s team set out to simultaneously develop prime editing treatments that could fix five ATP1A3 mutations, including the four most common – a scale rarely attempted in therapeutic gene editing research. Most other gene editing treatments, such as one recently used to treat baby KJ Muldoon, are designed to correct one mutation at a time. The scientists worked on correcting all five mutations, streamlining experiments, saving resources, and testing the robustness of the underlying science.
“We developed a robust framework to correct multiple mutations in parallel,” said Alexander Sousa, a postdoctoral fellow in the Liu lab and one of three co-first authors along with Holt Sakai of the Liu lab and Markus Terrey of The Jackson Laboratory. “This effort was really about creating a blueprint that could be rapidly applied to other rare diseases too.”
The researchers first tested their strategies in cultured cells from patients with AHC. They demonstrated that they could correctly repair AHC mutations in up to 90 percent of treated cells, with minimal changes to other stretches of DNA.
Next, the group collaborated with Jackson Lab researchers to test their treatments in two mouse models of AHC, which carry Atp1a3 mutations similar to those in patients with AHC. Without treatment, the mice developed seizures, movement problems, and died prematurely. When the scientists injected their editing system into the brains of the animals, their symptoms disappeared or were substantially reduced. Treated mice survived more than twice as long as untreated animals. Moreover, the function of their Atp1a3 protein was restored in the brain, and their motor and cognitive deficits were ameliorated. The scientists delivered the prime editors to cells in mice using clinically validated viruses called AAVs, which are already used in FDA-approved gene therapies targeting brain cells.
“The results really exceeded our expectations,” said Sakai. “It was incredibly exciting to see that data.”
The team also tested traditional gene therapy, which delivered an extra, healthy copy of the ATP1A3 gene to cells, and found that symptoms did not improve in animals. This finding highlights the unique advantage of using gene editing to directly correct a mutation that results in a malfunctioning, disease-causing protein, the researchers said.
“Before this study, we didn’t even know if we could intervene in AHC after birth in an animal,” said Sousa. “Now we know you can.”
A template for rare diseases
Because the treatment required direct injection into the brain shortly after birth, the team is now exploring less invasive delivery methods, and whether treatment later in life could still be effective.
Beyond AHC, the team sees their approach as a template for tackling other rare genetic diseases – especially those that affect the brain. With the ability to rapidly design and test multiple gene editing treatments at once, they hope to bring the same precision and speed to many other conditions.
“This is a powerful proof of concept,” said Sakai. “It shows that we can use prime editing to treat genetic brain diseases, and it lays the groundwork for translating this approach to the clinic.”
Support for the study was provided by the National Institutes of Health, the Chan-Zuckerberg Initiative, RARE Hope, the Alternating Hemiplegia of Childhood Foundation, the For Henry AHC Foundation, the Davis Family Foundation, the Toolbox Foundation L2C Initiative, the Cure AHC Foundation, the Howard Hughes Medical Institute, and the National Science Foundation.
Source:
Broad Institute of MIT and Harvard
Journal reference:
Sousa, A. A., et al. (2025). In vivo prime editing rescues alternating hemiplegia of childhood in mice. Cell. doi.org/10.1016/j.cell.2025.06.038.
