This website is intended for healthcare professionals only.
Take a look at a selection of our recent media coverage:
24th February 2020
The Berlin Prehospital Or Usual Delivery (B_PROUD) trial investigated if prehospital treatment in a mobile stroke unit could improve patient outcomes compared to usual care, which was emergency transportation in a conventional ambulance and in-hospital treatment. Patients (total 749, average age 73, 46% females) were assigned to treatment based on the availability of three mobile stroke units in the metropolitan area of Berlin, Germany, and compared with patients (total 794, average age 74, 48% females) who received conventional care.
Mobile stroke units are ambulances staffed with emergency medicine neurologists and equipped with a CT scanner and a lab designed to enable specific stroke treatment at the scene. Timing is key because alteplase should be administered within 4.5 hours of stroke symptoms.
Researchers found that:
60% of patients assigned to the mobile stroke unit received clot-busting treatment with alteplase if a mobile stroke unit was available, compared with 48% of patients who received conventional treatment in the hospital;
the time to treatment was shortened by an average of 20 minutes when a mobile stroke unit was dispatched; and
the use of a mobile stroke unit reduced the likelihood and severity of disability and death at three months by 26%.
“While we had anticipated better outcomes in the patients treated in the mobile stroke units, we are amazed by the magnitude of the effects,” said lead study author Heinrich Audebert, MD, professor in the department of neurology and Center for Stroke Research at Charité Universitätsmedizin in Berlin. “It is obvious that clot-busting treatment is most effective if it is applied in the ultra-early phase of stroke – ideally within the first or ‘golden hour’ of symptom onset.”
Since treatment within the first hour of symptom onset happens rarely in conventional care, Audebert said health care providers should consider ways to optimize treatment so it can begin while in route to the hospital.
“Stroke treatment is more effective the earlier it starts,” he said. “Just waiting until the patient arrives at the hospital is not enough anymore.”
The findings, published in the Journal of Neurology, Neurosurgery, and Psychiatry, suggest that measures of brain iron might eventually help predict which people with Parkinson’s will develop dementia.
“Iron in the brain is of growing interest to people researching neurodegenerative diseases such as Parkinson’s and dementias. As you get older, iron accumulates in the brain, but it’s also linked to the build-up of harmful brain proteins, so we’re starting to find evidence that it could be useful in monitoring disease progression, and potentially even in diagnostics,” said the study’s lead author, Dr Rimona Weil (UCL Queen Square Institute of Neurology, London).
The study involved 97 people with Parkinson’s disease, who had been diagnosed within the last 10 years, along with 37 people without the condition, as a control group. They were tested for their thinking and memory as well as for their motor function.
Currently there are no reliable measures to track Parkinson’s progression in the brain, so clinicians rely on monitoring symptoms. Conventional brain imaging fails to track progression until quite a late stage, when large-scale brain volume loss can be detected.
Iron accumulates in people’s brains as part of the normal ageing process, partly due to increased permeability in the blood-brain barrier. Excess iron can have toxic effects leading to proteins being irreversibly modified. Recent studies have found that when proteins linked to Alzheimer’s disease (amyloid and tau, which are also linked to Parkinson’s dementia) build up, iron also accumulates in the affected brain areas.
In the current study, researchers used a new technique, called quantitative susceptibility mapping, to map iron levels in the brain based on MRI scans. They found that iron accumulation in the hippocampus and thalamus brain regions was associated with poor memory and thinking scores. Iron in the putamen brain region was associated with poor movement scores, suggesting a more advanced stage of the disease.
In Parkinson’s disease, the hippocampus and thalamus are known to be associated with thinking and memory, and the putamen with movement scores, so the researchers say it’s very promising that iron deposition was specifically detected in those areas.
The findings suggest that iron deposition could be valuable to track if a treatment is working in a clinical trial, and might eventually be helpful for early diagnosis of Parkinson’s or other neurodegenerative diseases.
Dr Weil has previously found in a 2019 study that a suite of vision tests may be helpful to predict cognitive decline in Parkinson’s. She and her colleagues hope that further research will determine if the vision tests and iron measures could be helpful to predict which people with dementia are likely to develop dementia.
First author, PhD student George Thomas (UCL Queen Square Institute of Neurology), said: “It’s really promising to see measures like this which can potentially track the varying progression of Parkinson’s disease, as it could help clinicians devise better treatment plans for people based on how their condition manifests.”
Co-author Dr Julio Acosta-Cabronero (Tenoke Ltd. and Wellcome Centre for Human Neuroimaging, UCL) added: “We were surprised at how well the iron levels measured in different regions of the brain with MRI were correlated with cognitive and motor skills. We hope that brain iron measurement could be useful for a wide range of conditions, such as to gauge dementia severity or to see which brain regions are affected by other movement, neuromuscular and neuroinflammatory disorders, stroke, traumatic brain injury and drug abuse.”
The researchers are now following up the same study participants to see how their disease is progressing, whether they develop dementia, and how such measures correlate with changes in iron levels over time.
Even when experiencing jaundice, a life-threatening condition, only 61% of people would go to the GP.
The survey showed that that 27% of people are too embarrassed to go to the doctors with 31% worrying what the doctor might find.
Pale and smelly stools, one of the symptoms linked to being ‘embarrassing’, is a sign of pancreatic cancer, which has one of the lowest survival rates of all common cancers. In the survey, only 27% of people answered that they were ‘very likely’ to go to the GP if they had a change in bowel habit.
Even though 61% agreed that they should visit a GP sooner if they have symptoms that concern them, people are clearly putting off going to the doctors which is a cause for concern.
Dr Ellie Cannon says, “Early diagnosis of cancer is so important – if people are not visiting their GP with symptoms then they could be missing out on early diagnosis which often saves lives, particularly for pancreatic cancer.”
“People should never be embarrassed of going to the doctors, regardless of the problem, doctors will never judge and are there to help you.”
The survey, commissioned by Pancreatic Cancer Action, also revealed that 24% say they are too busy to go to the doctor, 19% have too many other things to worry about and 37% are worried about wasting a doctor’s time.
Dr Ellie Cannon continues, “A lot of doctors surgeries do more convenient phone consultation which can save time and a lot of surgeries have early/late appointments for people who work full time.”
Ali Stunt, Founder and CEO of Pancreatic Cancer Action and 12-year survivor says, “We need to get the message out to the public not to be embarrassed or worried what the doctor might find and to put their health first.”
“With pancreatic cancer survival rates being under 8%, early diagnosis is vital. People need to go to their doctors if they are experiencing symptoms that are persistent and not normal to them.”
21st February 2020
Antiphospholipid syndrome (APS) is a systemic autoimmune disorder manifesting as venous and/or arterial thrombosis or obstetric complications, secondary to elevated production of antiphospholipid antibodies (aPL).
APS can occur in a primary form (primary APS, PAPS), in combination with other autoimmune diseases such as systemic lupus erythematosus (SLE) or in the rare, fulminant, form of catastrophic APS (CAPS) leading to multiorgan failure. The three types of aPL included in the most recent classification criteria for APS are the anticardiolipin (aCL) and anti-beta2 glycoprotein (anti-β2GPI) antibodies, as well as the lupus anticoagulant (LA).1
Due to the rarity of the syndrome, its wide clinical spectrum involving several thrombotic and pregnancy morbidity complications, and the lack of high-quality, randomised clinical trials, the formulation of guidelines for the management of APS has been both a dire necessity and a difficult task.
EULAR recommendations for the management of APS in adults were developed to address this issue, aiming to provide evidence-based recommendations for APS stemming from a combination of expert opinion and a systematic review of the relevant literature.
A task force comprised of specialists from 11 European countries tackled four pivotal questions regarding the prevention and treatment of different forms of APS. These were risk stratification and modification in asymptomatic individuals with positive aPL; primary and secondary prevention of thrombosis in APS; management of obstetric APS; and CAPS treatment.2
The qualitative and quantitative characterisation of aPL such as their type, single-, double- or triple-positivity, titre, and persistence of positivity in repeat measurements formulate the ‘aPL profile’. Stratification of patients into those having low- and high-risk aPL profiles is considered as one of the main pillars on which the varying recommendations are based.
High-risk aPL profile was defined as the presence of LA or double or triple aPL positivity (any combination of the three aPL or all three aPL) or of high aPL titres. Isolated aCL or anti-β2GPI antibodies at low-medium titres, particularly if transiently positive, are defined as low-risk aPL. Proposed risk attenuation measures are comprised of lifestyle modifications, emphasising the importance of treatment adherence and eliminating cardiovascular and venous thrombosis risk factors.2
As far as pharmacological treatment of APS is concerned, different substances including low-dose aspirin (LDA), vitamin K antagonists (VKA), heparin, hydroxychloroquine (HCQ) or immunosuppressive agents can be used variably in accordance to each different clinical scenario.
Administration of LDA was recommended for asymptomatic aPL carriers, patients with SLE without history of thrombotic or obstetric APS, and non-pregnant women with prior obstetric APS, if high-risk aPL profiles are present. Patients with first unprovoked venous thrombosis should receive VKA with a target international normalised ratio (INR) of 2–3, while in those with first arterial thrombosis VKA treatment of a target INR of 2–3 or 3–4 can be considered, according to each individual bleeding/thrombosis risk. In patients with recurrent thrombotic events despite an appropriate treatment, either adding LDA to the treatment regimen, increasing the target INR to 3–4 or using low molecular weight heparin are effective alternatives.2,3
Based on current evidence from the recent TRAPS randomised controlled trial that showed a higher percentage of thrombotic relapses in APS patients with triple aPL positivity treated with rivaroxaban versus those treated with warfarin,4 use of rivaroxaban is not recommended in patients with a history of vascular thrombosis and triple aPL positivity, especially in those with arterial thrombosis history. New evidence from ongoing trials on direct oral anticoagulants is anticipated that will help to better understand their efficacy and safety in thrombotic APS.
In pregnant women with a history of foetal loss after the 10th week, or delivery before the 34 weeks of gestation due to eclampsia or severe pre-eclampsia or placental insufficiency, a prophylactic dose of heparin should be considered in conjunction with LDA. In women with recurring pregnancy complications despite a combination treatment with prophylactic dose heparin and low dose aspirin, therapeutic dose of heparin plus LDA, or add-on therapy with either HCQ or low-dose prednisone during the first trimester, are appropriate treatment options.2,3 First-line treatment of CAPS includes a combination therapy with glucocorticoids, heparin and plasma exchange or intravenous immunoglobulins.
Following the formulation of the current recommendations for APS in adults, an emerging need for more high-quality studies is evident. To this end, a plan in the form of a research agenda has been drafted by the task force, underlining the main points on which future studies should be focused.
Further clarification of the pathogenetic mechanisms of APS along with studies focusing on how the different phenotypes of the syndrome may respond to various treatment types are necessary in order to facilitate the expansion and improvement of the current recommendations so as to achieve better quality of care for individuals with APS.
Maria Tektonidou MD PhD
Associate professor of rheumatology, head of the Rheumatology Unit, First Department of Propaedeutic Internal Medicine, School of Medicine, National and Kapodistrian University of Athens, Greece
18th February 2020
Researchers from the University of Helsinki found that molecule BT13 has the potential to both boost levels of dopamine, the chemical that is lost in Parkinson’s, as well as protect the dopamine-producing brain cells from dying.
The results from the study, co-funded by Parkinson’s UK and published online today in the journal Movement Disorders, showed an increase in dopamine levels in the brains of mice following the injection of the molecule. BT13 also activated a specific receptor in the mouse brains to protect the cells.
Typically, by the time people are diagnosed with Parkinson’s, they have already lost 70-80% of their dopamine-producing cells, which are involved in coordinating movement.
While current treatments mask the symptoms, there is nothing that can slow down its progression or prevent more brain cells from being lost, and as dopamine levels continue to fall, symptoms get worse and new symptoms can appear.
Researchers are now working on improving the properties of BT13 to make it more effective as a potential treatment which, if successful, could benefit the 145,000 people living with Parkinson’s in the UK.
The study builds on previous research on another molecule that targets the same receptors in the brain, glial cell line-derived neurotrophic factor (GDNF), an experimental treatment for Parkinson’s which was the subject of a BBC documentary in February 2019. While the results were not clear cut, GDNF has shown promise to restore damaged cells in Parkinson’s.
However, the GDNF protein requires complex surgery to deliver the treatment to the brain because it’s a large molecule that cannot cross the blood-brain barrier.
BT13, a smaller molecule, is able to cross the blood-brain barrier – and therefore could be more easily administered as a treatment, if shown to be beneficial in further clinical trials.
Professor David Dexter, Deputy Director of Research at Parkinson’s UK, said: “People with Parkinson’s desperately need a new treatment that can stop the condition in its tracks, instead of just masking the symptoms.
“One of the biggest challenges for Parkinson’s research is how to get drugs past the blood-brain barrier, so the exciting discovery of BT13 has opened up a new avenue for research to explore, and the molecule holds great promise as a way to slow or stop Parkinson’s.
“More research is needed to turn BT13 into a treatment to be tested in clinical trials, to see if it really could transform the lives of people living with Parkinson’s.”
Dr Yulia Sidorova, lead researcher on the study, said: “We are constantly working on improving the effectiveness of BT13. We are now testing a series of similar BT13 compounds, which were predicted by a computer program to have even better characteristics.
“Our ultimate goal is to progress these compounds to clinical trials in a few coming years.”
An international team of scientists, brought together by an ambitious £20 million Grand Challenge award from Cancer Research UK, has developed intricate maps of breast tumour samples, with a resolution smaller than a single cell.
These maps show how the complex cancer landscape varies between and within tumours, depending on their genetic makeup.
This technique could one day provide doctors with an unparalleled wealth of information about each patient’s tumour upon diagnosis, allowing them to match each patient with the best course of treatment for them.
In the future, it could also be used to analyse tumours during treatment, allowing doctors to see in unprecedented detail how tumours are responding to drugs or radiotherapy. They could then modify treatments accordingly, to give each patient the best chance of beating the disease.
Dr Raza Ali, lead author of the study and junior group leader at the Cancer Research UK Cambridge Institute, said: “At the moment, doctors only look for a few key markers to understand what type of breast cancer someone has. But as we enter an era of personalised medicine, the more information we have about a patient’s tumour, the more targeted and effective we can make their treatment.”
The researchers studied 483 different tumour samples, collected as part of the Cancer Research UK funded METABRIC study, a project that has already revolutionised our understanding of the disease by revealing that there are at least 11 different subtypes of breast cancer.
The team looked within the samples for the presence of 37 key proteins, indicative of the characteristics and behaviour of cancer cells. Using a technique called imaging mass cytometry, they produced detailed images, which revealed precisely how each of the 37 proteins were distributed across the tumour.
The researchers then combined this information with vast amounts of genetic data from each patient’s sample to further enhance the image resolution. This is the first time imaging mass cytometry has been paired with genomic data.
These tumour ‘blueprints’ expose the distribution of different types of cells, their individual characteristics and the interactions between them.
By matching these pictures of tumours to clinical information from each patient, the team also found that the technique could be used to predict how someone’s cancer might progress and respond to different treatments.
Professor Carlos Caldas, co-author of the study from the Cancer Research UK Cambridge Institute, said: “We’ve shown that the effects of mutations in cancer are far more wide-ranging than first thought.
“They affect how cancer cells interact with their neighbours and other types of cell, influencing the entire structure of the tumour.”
The research was funded by Cancer Research UK’s Grand Challenge initiative. By providing international, multidisciplinary teams with £20 million grants, this initiative aims to solve the biggest challenges in cancer.
Dr David Scott, director of Grand Challenge at Cancer Research UK said: “This team is making incredible advances, helping us to peer into a future when breast cancer treatments are truly personalised.
“There’s still a long way to go before this technology reaches patients, but with further research and clinical trials, we hope to unlock its powerful potential.“
The guidelines are being presented at the SCCM 49th Critical Care Congress.
The new guidelines assemble recommendations for critical care specialists managing the wide range of conditions and complications posed by liver failure – a serious organ derangement that carries a high risk of death, and for which liver transplantation may be the only definitive treatment. Rahul Nanchal, MD, MS, FCCM, of Medical College of Wisconsin, Milwaukee, and Ram Subramanian, MD, FCCM, of Emory University Hospital were Co-Chairs of the Guidelines Committee.
Recommendations on liver failure in five key areas
As for all SCCM guidelines, the multidisciplinary, international expert Committee followed a rigorous approach to reviewing the best available evidence and developing consensus guidelines to answer a defined set of clinical questions. Two forms of hepatic failure are addressed. Acute liver failure (ALF) is a life-threatening condition associated with rapid loss of liver function – over a period of days or weeks – in a previously healthy person. Acute- on -chronic liver failure (ACLF) develops in a patient with pre-existing chronic liver disease.
Critically ill patients with liver disease are at risk of unique manifestations affecting various organ systems. “Strategies used to manage organ complications in general critical illness are not always applicable to the care of the patient with liver failure,” according to the guideline statement. Through a formal review and guideline development process, the Committee approved 29 evidence-based recommendations in five areas.
Cardiovascular. Patients with ALF or ACLF are at risk of circulatory abnormalities leading to inadequate blood flow (shock). Recommendations address the choice of resuscitation fluid and use of vasopressor drugs in patients ALF/ACLF in shock. The guidelines also include recommendations for blood pressure monitoring, including the use of invasive haemodynamic monitoring.
Haematology. Recommendations address the risks of bleeding and venous thromboembolism (VTE) associated with ALF and ACLF. The guidelines address prevention and treatment of VTE and assessment of bleeding risk before invasive procedures.
Pulmonary. Several recommendations address preferred strategies for mechanical ventilation in patients with ALF/ACLF. The guidelines also discuss the management of some unique complications of chronic liver failure, including hepatopulmonary syndrome (low oxygen levels due to abnormal blood flow to the lungs) and hepatic hydrothorax (excess fluid around the lungs).
Renal. Issues related to decreased kidney function in patients with ALF/ACLF are analysed. Due to lack of evidence, no recommendation is made for renal replacement therapy (RRT, or dialysis) during liver transplant surgery. Early RRT is recommended for patients with acute kidney injury, a common complication of ALF. Other recommendations address hepatorenal syndrome, a distinct type of kidney injury occurring in patients with cirrhosis.
Endocrine and nutrition. The guidelines include recommendations for monitoring and control of blood glucose levels in patients with ALF/ACLF; the role of stress-dose steroids in patients with septic shock; and the use of enteral feeding. Recommendations call for drug screening to identify the wide range of potential causes of ALF/ACLF and medication dose adjustment for patients with decreased liver function.
Although the guidelines reflect the latest research on each topic, most of the recommendations are based on “low-quality indirect evidence” – for a few clinical questions, no evidence-based recommendation could be made. The Committee highlights areas in need of further research to better inform clinical practice. While acknowledging the limitations of the recommendations regarding the complex challenges in critically ill patients with ALF/ACLF, the Guideline authors conclude: “Our approach led to the generation of a contemporary document that can be used as a reference for clinicians.”
13th February 2020
The London Borough of Sutton and The Institute of Cancer Research, London, have together secured £8.4 million in funding to prepare land for development and put in place the infrastructure required for the first wave of commercial life-science buildings.
The funding comes from the Strategic Investment Pot, which is administered by the City of London on behalf of all London Boroughs to support projects that will help promote future economic growth.
The London Cancer Hub will be a global centre for cancer innovation – a vibrant community of scientists, doctors and innovative companies, which will deliver major benefits for cancer patients and the UK economy. The project will create around 13,000 jobs – around 7000 in life sciences and supporting activities, and 6200 in the site’s construction.
The project is jointly led by the ICR and the London Borough of Sutton – which has already invested more than £30 million to acquire 4.8 hectares of land on the site, to accommodate up to 100,000 square metres of new life-science facilities and commercial space.
The new funding award represents an important step in the development of the project. It will be used to put in place the infrastructure requirements for initial buildings including a flagship Knowledge Centre, hosting labs, offices, business engagement activities, and collaboration and events space.
The London Cancer Hub is already home to the Sutton sites of the ICR and The Royal Marsden NHS Foundation Trust – which together are ranked as one of the world’s top four centres for cancer research and treatment.
The Knowledge Centre will form one of the first new developments on The London Cancer Hub site, along with the ICR’s £75m Centre for Cancer Drug Discovery – which is currently under construction – The Royal Marsden’s planned £70m Oak Cancer Centre, and the completed Maggie’s Cancer Centre and Harris Federation secondary school.
The Knowledge Centre will host labs, offices, collaboration and events space – and bring together academic researchers, clinicians, technology transfer specialists and innovative companies in one shared space to create a vibrant melting pot of ideas that will accelerate progress in cancer research and treatment.
Professor Paul Workman, Chief Executive of The Institute of Cancer Research, London, said: “We’re extremely pleased to receive this important boost to our plans for The London Cancer Hub. The new funding will catalyse development and underpin the creation of a flagship Knowledge Centre that will further enhance our already excellent collaborations with industry partners.
“This new investment represents a big step forward for our plans to create the world’s leading cancer-focused life-science district, and will help to accelerate our research discoveries and their development for patients.”
10th February 2020
The research team, made up of scientists from Queen Mary University of London, the University of Manchester, Cardiff University, and Radboud University Medical Center, Nijmegen, found significantly higher levels of a protein called factor H-related protein 4 (FHR-4) in the blood of AMD patients.
Further investigation, using eye tissue donated for medical research, showed the presence of the FHR-4 protein within the macula – the specific region of the eye affected by the disease.
The results of this study open up new routes for early diagnosis, by measuring FHR-4 levels in the blood, and suggests therapies targeting this protein could provide promising future treatment options for the disease.
FHR-4 regulates the complement system, part of the immune system, which plays a critical role in inflammation and the body’s defence against infection.
Previous studies have linked the complement system to AMD showing that genetically inherited faults in key complement proteins are strong risk factors for the condition.
In this study, the researchers used a genetic technique, known as a genome-wide association study, to identify specific changes in the genome related to the increased levels of FHR-4 found in AMD patients.
They found higher blood FHR-4 levels were associated with changes to genes that code for proteins belonging to the factor H family, which clustered together within a specific region of the genome. The identified genetic changes also overlapped with genetic variants first found to increase the risk of AMD over 20 years ago.
Together, the findings suggest that inherited genetic changes can lead to higher blood FHR-4 levels, which results in uncontrolled activation of the complement system within the eye and drives disease.
Blood levels of FHR-4 were measured in 484 patients and 522 age-matched control samples using two independent, established collections of AMD patient data. These were the Cambridge AMD study, led by Professor Anthony Moore from Moorfields Eye Hospital and UCL Institute of Ophthalmology (now at the University of California San Francisco) and Professor John Yates from Cambridge University, and the European Genetic Database (EUGENDA), led by Professor Anneke den Hollander and Professor Carel Hoyng from Radboud University Medical Center.
There are two main types of AMD – ‘wet’ AMD and ‘dry’ AMD. Whilst some treatment options exist for ‘wet’ AMD, there is currently no available treatment for ‘dry’ AMD.
Dr Valentina Cipriani, who jointly led the statistical data analysis with Dr. Laura Lorés-Motta from the Radboud University Medical Center and is an expert in ophthalmic statistical genetics at Queen Mary University of London, and member of the International AMD Genomics Consortium (IAMDGC), said: “By unveiling FHR-4 as a novel, key molecular player for AMD, our study was able to dissect further the genetic disease predisposition at the factor H region. This is one of the most established genetic associations in the field of complex genetics. We hope our findings will accelerate interest from the wider research community in the involvement of the complement system in AMD, with the ultimate goal of uncovering the role of the whole ‘complementome’ in the disease.”
Professor Simon Clark, a specialist in the regulation of the complement system in health and disease at the University of Manchester, said: “This study really is a step-change in our understanding of how complement activation drives this major blinding disease. Up until now, the role played by FHR proteins in disease has only ever been inferred. But now we show a direct link and, more excitingly, become a tangible step closer to identifying a group of potential therapeutic targets to treat this debilitating disease.”
Professor Paul Bishop, an ophthalmologist and AMD expert at the University of Manchester, said: “The combined protein and genetic findings provide compelling evidence that FHR-4 is a critical controller of that part of the immune system which affects the eyes. Apart from improving understanding of how AMD is caused, this work also provides a way of predicting risk of the disease by simply measuring blood levels of FHR-4 and also provides a new route to treatment by reducing the blood levels of FHR-4 to restore immune system function in the eyes.”
Professor Paul Morgan, an expert in complement biology at Cardiff University, and leader in the development of the antibodies and assays that underpinned this work said: “The collaboration between experts in complement biology, eye disease and genetics across Europe has enabled the accumulation of a robust body of evidence that genetically dictated FHR-4 levels in plasma are an important predictor of risk of developing AMD. The unique antibodies and assays we have developed have potential not only for contributing to risk prediction but also to new ways of treating this common and devastating disease.”
Children with ADHD from the poorest areas are significantly more likely to receive medication as children with ADHD from the most affluent areas, according to the first UK study of its kind.
Previous research has shown that children in poorer areas are more likely to be diagnosed with ADHD. This new research in BJPsych Open, is the first UK study to show an association between deprivation and the likelihood of receiving medication for ADHD.
The finding is unlikely to have a single, simple explanation, but suggests that children from poorer areas are less able to benefit from treatments which don’t involve medication, such a behavioural management classes for parents. Parents in poorer areas may find it more difficult to attend these regular classes, because of economic insecurity, for example working multiple jobs.
Dr Samuel Nunn, junior doctor at Leeds Teaching Hospitals NHS Trust and lead author of the paper, said: “This finding is important because it has implications for those in clinical practice and for policymakers. Further research would inform development of possible interventions to tackle the effects of social deprivation, though progress may be difficult unless the broader social determinants of health are addressed.”
Researchers investigated a sample of 1354 young people with a diagnosis of ADHD in the Sheffield area. Household postcodes were used to derive a standard measure of socioeconomic deprivation.
Statistical analysis showed that higher deprivation was associated with a higher likelihood of receiving medication, after controlling for age, sex, religion, ethnicity and the presence of other diagnoses.
IMPORTANT LINKS
MORE FROM COGORA
© Cogora 2025
Cogora Limited. 1 Giltspur Street, London EC1A 9DD
Registered in the United Kingdom. Reg. No. 2147432
