Professor Thapar brings considerable authority to this assessment. She chaired the NHS England ADHD taskforce and co-chaired the Welsh Government Neurodivergence Ministerial Advisory Group, placing her at the heart of the policy debate about why referrals and treatment for ADHD are increasing across the United Kingdom and Europe even as the underlying prevalence in the population appears stable. Her session in Munich will focus primarily on UK data and evidence while drawing on findings relevant to other European countries, and it is designed as an open discussion about what is driving the surge in referrals and how healthcare systems can respond to rising demand while ensuring that people who may have ADHD receive appropriate assessment and support. The framing matters, because the answer shapes how governments allocate resources, how clinicians triage assessments, and how the public understands what is happening around them.

The technical distinction at the heart of the argument is between diagnosed prevalence and population prevalence. Diagnosed prevalence refers to the total number of clinically recognised cases recorded within health systems, while population prevalence describes the expected rate of the condition in the community, estimated through epidemiological research. Evidence cited in the presentation confirms that diagnosed prevalence of ADHD has increased significantly in recent years, yet the population rate itself is estimated at approximately five to seven per cent of children and two to three per cent of adults across Europe, figures that have remained broadly consistent across European countries. In some nations, the proportion of people with a recognised ADHD diagnosis now matches that population rate. In others, including the United Kingdom, diagnosed rates sit well below the expected population figure, which is precisely why researchers argue that the condition is still under-recognised and under-treated rather than over-diagnosed.

Professor Thapar argues that several converging factors explain the diagnostic surge. Diagnostic criteria for ADHD have changed over time, which means the threshold at which a diagnosis is made and treatment is indicated has also moved. Public and professional awareness has improved markedly, and research evidence on ADHD and its associated risks has accumulated to the point where the condition is now being recognised where in the past it was not. She draws a deliberate parallel with other medical conditions: high lipid levels and hypertension and their health risks were not widely recognised in the 1960s, yet nobody today interprets the routine identification and treatment of those conditions as evidence of an epidemic. The same logic, she contends, applies to ADHD. As she puts it, the rise in diagnoses seems to be due to changes in diagnostic criteria, improved awareness and research evidence on ADHD and its risks, rather than to an epidemic of ADHD itself.

Two groups whose ADHD was historically overlooked deserve particular attention. There is now much greater awareness that ADHD can affect adults, not only children, and far stronger evidence that the condition develops in women and girls, something that was neglected in the past because the classic hyperactive presentation seen in young boys dominated both research and clinical expectations. This shift has visible consequences in prescribing data. A recent publication reported increased ADHD medication use in Belgium, Germany, the Netherlands, Spain and the United Kingdom between 2010 and 2023. In the UK, the prevalence of medication use rose more than threefold over that period, from 0.12 per cent to 0.39 per cent of the population, with adult use increasing particularly sharply among women. That pattern is exactly what would be expected if long-missed cases in women and adults were finally being identified, rather than what would be expected from a sudden new environmental cause.

Another important technical point concerns the nature of the condition itself. Having ADHD is not a simple yes-or-no state. As with high blood pressure or high cholesterol, the degree of the condition varies along a spectrum within the population, and the point at which doctors intervene, meaning the diagnostic threshold at which treatment is indicated, can change over time in line with research evidence. Guidelines typically suggest starting with non-pharmacological support and then moving to ADHD medication if those other strategies prove insufficient. This spectrum model explains why small shifts in clinical guidance or public understanding can produce large shifts in recorded case numbers without any change in the underlying biology of the population. It also explains why different countries, applying the same broad diagnostic concept within different service structures, can report very different diagnosed rates.

Indeed, that international variation is one of the most telling pieces of evidence. Population prevalence estimates for ADHD are broadly consistent across European countries, but the number of people formally recognised or treated within health systems varies considerably depending on service provision, access to assessment and local clinical practice. In the United Kingdom, the rate at which ADHD is seen in clinics is lower than the true rate of ADHD in the population, which researchers interpret as a clear signal that the condition is under-recognised and under-treated rather than over-diagnosed. While some observers raise concerns about potential misdiagnosis as assessments multiply, Professor Thapar notes that the research evidence on that question is limited, and she cautions against drawing firm conclusions in either direction from the limited data available.

The stakes of getting this right extend beyond statistics. There is now evidence that treatment can reduce known risks associated with ADHD, including premature mortality and suicide, which reframes the diagnostic surge not as a fashionable trend but as the identification of a genuine health risk that carries real consequences when missed. Untreated ADHD is associated with substantial impairment across education, employment and relationships, and the accumulating evidence base on those risks is itself one of the drivers of improved recognition, as clinicians and policymakers take the condition more seriously. From this perspective, the rising number of referrals reflects a health system slowly catching up with the evidence rather than chasing a fad, even if the pace of that catch-up is straining assessment services.

The wider research community has welcomed the growing recognition while sounding a note of frustration about resources. Commenting on the presentation, Professor Barbara Franke of Radboud University in Nijmegen, the Netherlands, an independent commentator who was not involved in the work, said that for years ADHD researchers have done their best to raise awareness that ADHD is underdiagnosed in females and in adults in general, and that over recent years this knowledge has finally taken hold in the population, but with such speed that it feels like an epidemic. Despite the relatively high prevalence and the burden associated with the condition, however, she noted that funding for research into ADHD, from its causes to its treatment, is surprisingly hard to find, and that ADHD unfortunately remains one of the most under-researched conditions in medicine, a situation she sincerely hopes will change.

For the public, the message from Munich is likely to be one of reassurance tempered with realism. The explosion in ADHD diagnoses across the UK and Europe tells a story about medicine catching up, about women and adults finally being seen, and about diagnostic thresholds moving in line with better evidence, not about a mysterious new epidemic sweeping a generation. At the same time, the gap between the estimated five to seven per cent of children and two to three per cent of adults who have the condition and the far smaller numbers actually diagnosed and treated in countries like the UK means that demand for assessment will likely continue to grow as awareness spreads. The challenge for healthcare systems, as the ECNP discussion will explore, is to meet that rising demand with adequate services and funding, ensuring that people who may have ADHD receive timely and appropriate assessment and support, while sustaining the research effort needed to answer the questions that still remain about this long-overlooked condition.

Subject of Research: Rising ADHD diagnosis rates and population prevalence in the UK and Europe

Article Title: Is ADHD on the rise in children and adults in the UK and Europe?

Article References: Is ADHD on the rise in children and adults in the UK and Europe?. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: ADHD, diagnosis, prevalence, ECNP Congress, Anita Thapar, United Kingdom, Europe, medication use, under-diagnosis, women and girls, adult ADHD, Cardiff University

Imprinted genes are a peculiar subset of the genome. Most genes are expressed from both the maternal and paternal copies, but imprinted genes carry chemical tags laid down in the egg or sperm that silence one copy entirely, leaving only the maternal or paternal version active. In the placenta, these parent-of-origin effects are thought to reflect evolutionary conflict: paternal genes tend to push for greater extraction of maternal resources, while maternal genes restrain fetal demands to preserve the mother’s ability to sustain current and future pregnancies. Phlda2, formally known as Pleckstrin Homology-Like Domain Family A Member 2, is one of the maternal army’s foot soldiers, normally expressed only from the chromosome inherited from the mother.

Researchers at Cardiff University, led by R. M. John together with colleagues including A. R. Isles, had previously shown that elevated Phlda2 expression, a state mimicking loss of imprinting in which the gene’s dosage is effectively doubled, produces placentas that secrete fewer hormones, fetuses that grow poorly, and mothers that neglect their pups after birth. Their earlier work on the paternally expressed gene Peg3 had already demonstrated that imprinted genes can act as master regulators of placental endocrine lineages and that disrupting them can produce sexually dimorphic outcomes, with males suffering more. The natural question was whether a maternally expressed gene would show the same pattern, or whether the sexes would flip.

To find out, the team crossed wildtype C57BL/6 female mice with transgenic males carrying an extra bacterial artificial chromosome copy of Phlda2, generating embryos that overexpressed the gene and thus modelled loss of imprinting. They then dissected the placenta at embryonic day 14.5, a critical window when the placenta’s endocrine machinery is being established, and collected fetal and placental weights at embryonic day 18.5, near the end of gestation.

The team used RNAscope, a high-resolution in situ hybridization technique, combined with classical histology to map the placenta’s specialized cell populations. The mouse placenta is organized into two major compartments. The labyrinth zone handles nutrient and gas exchange, while the junctional zone is the endocrine heart of the organ, packed with hormone-producing cells including the spongiotrophoblast layer, glycogen cells, and parietal trophoblast giant cells. The spongiotrophoblast in particular churns out a vast repertoire of prolactin-related hormones and pregnancy-specific glycoproteins that remodel the mother’s physiology, directing blood flow, nutrient mobilization, and even priming her brain for maternal care.

What the researchers saw was unambiguous. In placentas carrying the Phlda2 overexpression, the junctional zone lost a significant number of spongiotrophoblast cells, and the depletion was substantially more severe in female placentas than in male ones. Glycogen cells and parietal trophoblast giant cells were also reduced in number, but those losses were even-handed between the sexes. The sexual dimorphism was confined specifically to the spongiotrophoblast compartment, the very cell population responsible for the placenta’s most powerful endocrine output.

Molecular measurements backed up the cellular picture. Using reverse-transcription quantitative PCR and bulk RNA sequencing, the team found that genes encoding placental hormones normally produced by the spongiotrophoblast were downregulated in the mutant placentas, and once again the reduction was biased toward females. Gene set enrichment analysis reinforced the conclusion: the female mutant placenta showed a more profound dampening of its hormone-producing program than the male, despite both sexes carrying the identical genetic modification.

The most consequential result, however, appeared in the growth curves. At embryonic day 18.5, late in gestation, female fetuses with elevated Phlda2 expression were significantly growth restricted compared with their wildtype female littermates. Male fetuses carrying the same transgene showed no comparable reduction in weight. In other words, the genetic perturbation narrowed the female placenta’s endocrine signalling capacity, and the female fetus paid the price by growing more slowly, while the male fetus maintained its growth trajectory despite the same molecular insult.

The authors interpret this asymmetry through the lens of evolutionary theory about parental resource allocation. Phlda2 is known to be responsive to maternal adversity: when the mother experiences nutritional deficiency or other forms of prenatal stress, placental Phlda2 expression rises, and the resulting restraint on hormone production lowers the fetus’s demands on her body. The new findings suggest that this demand-dampening system is not symmetrical. Female fetuses appear to reduce their claims on the mother when Phlda2 signalling rises, effectively shrinking their own growth to spare maternal reserves. Male fetuses, by contrast, hold their ground, continuing to extract resources even under adverse conditions. Such sex-specific strategies could reflect the different reproductive payoffs that sons and daughters offer under variable environmental conditions, with parent-of-origin imprinting serving as the molecular lever that mediates the negotiation.

The translational implications are hard to ignore. In human pregnancies, elevated placental PHLDA2 has repeatedly been associated with fetal growth restriction and low birthweight, yet these clinical studies have generally not accounted for the sex of the infant. If, as the mouse data suggest, the gene’s effects on growth are sex-specific, then pooling male and female pregnancies may have obscured important patterns and muddied the interpretation of biomarker studies. The Cardiff team argues that fetal sex deserves routine consideration in research on imprinted genes and pregnancy complications, from intrauterine growth restriction to the long-term metabolic and behavioural consequences of prenatal adversity. The work, funded by the Biotechnology and Biological Sciences Research Council, adds Phlda2 to a growing list of imprinted genes, alongside Peg3, whose disruption produces sex-dimorphic placental and offspring phenotypes, and it strengthens the broader hypothesis that the placenta is not merely a passive conduit for nutrients but an active, sexually differentiated endocrine organ that negotiates the terms of maternal investment on the fetus’s behalf.

Subject of Research: Sex-specific effects of loss-of-imprinting of the maternally expressed gene Phlda2 on placental endocrine development and fetal growth in mice

Article Title: Sex-specific consequences of loss-of-imprinting of the maternally expressed gene Pleckstrin Homology-Like Domain Family A Member 2 (Phlda2) on placental development and fetal growth

Article References: Chibnall, A., Harrison, D. J., Lysikova, E., Malinoshevska, M., Stoddart, A., Perry, I. A., Christofides, S., Isles, A. R., & John, R. M. (2026). Sex-specific consequences of loss-of-imprinting of the maternally expressed gene Pleckstrin Homology-Like Domain Family A Member 2 (Phlda2) on placental development and fetal growth. Biology of Sex Differences. https://doi.org/10.1186/s13293-026-00972-z

Image Credits: AI Generated

DOI: 10.1186/s13293-026-00972-z

Keywords: genomic imprinting, Phlda2, placenta, placental hormones, fetal growth restriction, sexual dimorphism, spongiotrophoblast, junctional zone, prenatal adversity, parent-of-origin effects, Biology of Sex Differences, Cardiff University

The research, published in the journal Society and Animals under the title The Origins of Bear Baiting: Evidence from Medieval England and France, represents the first detailed synthesis of archaeological and documentary evidence for bears in medieval Britain. Its central conclusion is striking: the practice of importing live bears and exhibiting them in fights with dogs appears to have intensified dramatically in the wake of the Norman Conquest of 1066. Before that date, the archaeological record for live bears in England is essentially empty. Immediately afterwards, bear remains begin to appear at sites in London and North Yorkshire, suggesting that the new Norman elite brought with them both the animals and the appetite for spectacle that had characterised aristocratic entertainments on the continent.

Brown bears were once native to Great Britain, but the species had already disappeared from the island by the Roman period. Every bear that appeared in a medieval English arena, market square or royal court therefore had to be transported from continental Europe, at considerable expense. The logistics alone are remarkable. Captured animals would have needed to be moved across hundreds of kilometres, ferried across the Channel, and then sustained on journeys that could take them as far as Colchester in the south of England or Carlisle near the Scottish border, both of which have yielded confirmed medieval bear remains. The costs of importation, travel and ongoing sustenance imply that bears were valuable commodities, owned and displayed by people with significant resources.

Dr Liam Lewis of Cardiff University’s School of Global Humanities, who led the research, explained that the convergence of different strands of evidence is what makes the new findings so conclusive. The combination of literary, archival, archaeological and visual analysis allows researchers to state definitively that bear baiting was an established activity in England by the twelfth century. Lewis noted that the absence of bear remains from live animals in England prior to the Norman Conquest, and their sudden appearance in London and North Yorkshire in its immediate aftermath, points to a real increase in the importation of live bears following the conquest. The timing is too consistent to be coincidental, and it reframes the blood sport not as a Tudor novelty but as a Norman import that took root and spread.

What emerges from the study is a picture of bears circulating widely through medieval English society. Literary works, sermons and chronicles frequently mention baiting in connection with marriages, aristocratic pastimes and rowdy public festivities, and historians had generally assumed these references described elite entertainments or literary conveniences. The archaeological evidence tells a different story. Bear bones indicative of live animals have been recovered from a number of English towns, indicating that ordinary townspeople encountered bears regularly and that baiting functioned as popular entertainment for the general public, not merely as a diversion of the nobility. For a town to host a bear, someone had to pay for the animal’s transport, feeding and upkeep, and someone had to profit from exhibiting it, a commercial dynamic that anticipates the professional bear gardens of the later middle ages.

Material evidence for the earliest phase of this trade comes from a network of ten sites across England and France where bear bones from the medieval period have been identified. Among the most significant new results is a radiocarbon date obtained on a bear shoulder blade, or scapula, recovered from Richmond in North Yorkshire. The bone, found in 1864 and held in the collections of the Yorkshire Museum, was sampled in collaboration with the museum and dated by Dr Thibaut Devièse at the University of Oxford as part of the Natural Environment Research Council funded Decline of the Bear project, led by Professor Hannah O’Regan of the University of Nottingham. The result was unexpectedly late, placing the animal firmly in the medieval period and demonstrating that bears were present in northern England immediately after the Norman Conquest.

Professor O’Regan emphasised the wider significance of the finding. Bear baiting was an important social and economic activity in early modern England, and the study demonstrates that it has much longer roots than scholars had appreciated. According to O’Regan, this is the first study of the medieval origins of the practice, and the new radiocarbon date on the Richmond bear shows that bears were widespread very early in the medieval period. The research team also surveyed documents such as the Domesday Book, along with other historical records and medieval manuscripts, for references to bears, building a documentary dataset that complements the skeletal evidence and allows the movements and ownership of the animals to be traced through the centuries.

One of the most evocative documentary discoveries concerns Richmond itself. The town appears in one of the earliest known references to a named medieval bearward, the professional keeper responsible for the care and exhibition of a performing bear. The record names Spenellus, a bearward who lived at Richmond in the early 1200s, providing a rare human face for a trade that must otherwise be reconstructed from bones and passing mentions. Bearwards appear increasingly often in later medieval records, leading dancing and fighting bears through towns and fairs, and the Richmond reference shows that this profession, with its distinctive title and its itinerant economy, was already established within a century and a half of the Conquest. For Lewis, the discovery underscores the richness of the documentary record once it is read alongside the archaeology.

The visual record adds a further dimension. Historians have long puzzled over images of dancing and performing bears sketched into the margins of medieval manuscripts, wondering how often ordinary people actually encountered these animals. The new study is the first to combine such imagery systematically with archaeological and documentary sources, and it identifies an even earlier and more famous image: a bear baiting scene depicted in the lower margin of the Bayeux Tapestry, the eleventh century embroidery that narrates the Norman conquest of England. That a baiting scene should appear in a work produced for the Norman elite is consistent with the study’s broader argument that the spectacle arrived in England with the conquerors, embedded in their culture of aristocratic display and public festivity.

The Richmond scapula also carries a lesson about the value of museum collections. The bone lay in storage for more than a century and a half before modern radiocarbon dating revealed its significance, and Lewis argues that the case demonstrates the importance of keeping samples and re-examining old collections, because there is still much more to learn from material gathered by antiquarians in the nineteenth century. As the AHRC funded Box Office Bears project, through which Lewis and O’Regan are jointly investigating the medieval roots of baiting culture, continues, the team expects more bones in museum drawers across Britain and France to yield dates and isotopic signatures that could map the trade in live bears in still finer detail. What is already clear, however, is that the chained bears of Shakespeare’s Bankside had ancestors in the England of William the Conqueror, transported across the sea, carried along the roads of a newly conquered kingdom, and fought before crowds who found in the spectacle a shared, enduring and very medieval form of entertainment.

Baiting spectacles of this kind were not unique to bears. Medieval England also hosted bull baiting and cock fighting, and the same towns that accommodated travelling bears often staged other animal contests, suggesting a broader culture of blood sports in which the bear occupied a particularly prestigious place because of its exotic origins. The need to import every animal from the continent meant that each bear represented a substantial investment, and its survival in the pit mattered economically as well as morally to its keeper.

The study also illustrates how radiocarbon dating can overturn long held assumptions about museum specimens. Bones recovered by antiquarians were frequently catalogued with only vague provenance, and without scientific dating many medieval bear remains could easily have been misassigned to earlier periods when bears were still native to Britain. A precise date on a single scapula was enough to anchor the entire northern distribution of the evidence to the decades following the Conquest.

For archaeologists, the distinction between bones from live animals and those from imported meat or hides is crucial. Remains showing signs of captivity, such as those found in urban contexts far from any plausible wild population, indicate living animals kept for display rather than carcasses traded for their pelts. It is this distinction that allows the ten sites in the study to be read as evidence of a trade in performing bears rather than simply a commerce in animal products, and that gives the documentary references to bearwards their material confirmation.

Subject of Research: The medieval origins of bear baiting and the importation of live brown bears into Norman and later medieval England

Article Title: Bear baiting became more common following Norman invasion

Article References: Bear baiting became more common following Norman invasion. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: bear baiting, Norman Conquest, medieval England, brown bears, radiocarbon dating, Bayeux Tapestry, Domesday Book, bearward, Richmond scapula, Cardiff University, University of Nottingham, medieval archaeology