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COVID Lockdowns Found to Set Back Children’s Development by Years

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Even when controlling for age and family background, COVID’s impact was evident

Photo by Kelly Sikkema on Unsplash

The COVID pandemic disrupted children’s ability to self-regulate, according to research from three UK universities just published in the journal Child Development.

The study by Lancaster University, East Anglia and Durham reveals that the pandemic hampered children’s ability to regulate their behaviour, stay focused and adapt to new situations – skills known collectively as executive functions.

The greatest impact was seen among pupils who were in reception when the first lockdowns began – a crucial stage at four or five when youngsters normally learn to socialise, follow routines and navigate the busy world of the classroom. Primary school in the UK then begins at Grade 1, starting at age five or six.

These children showed less growth in their self-regulatory and cognitive flexibility scores over time compared to a second group of children who were in preschool when the pandemic started.

The research team say these children may still be feeling the effects years later.

How the research happened

Scientists were already running a long-term study tracking youngsters from toddlerhood to early school years when the COVID pandemic hit.

They followed 139 children aged between two-and-a-half and six-and-a-half years old over several years, including 94 families who joined the study before Covid struck.

This meant that they had a rare baseline of children’s abilities before the pandemic began, which allowed them to track exactly how development changed during and after the lockdowns.

Using a standardised assessment called the Minnesota Executive Function Scale, they were able to measure the same cognitive skills at regular intervals.

Dr Eleanor Johns from Lancaster University’s Department of Psychology said: “We began this study to understand how children’s executive function develops across early childhood, and we saw clear, steady growth between 2.5 and 6.5 years of age. However, because our longitudinal study spanned the COVID-19 pandemic, we also had a unique opportunity to examine how this unprecedented disruption affected the children we were already following.

“We found that children who had just started school when the first lockdown began showed a slower rate of growth in executive function compared to those who were preschool age. Starting school is a major developmental transition, as children learn new routines, adapt to classroom rules, and develop self-regulation alongside their peers. When schools closed almost overnight, those opportunities were suddenly removed.”

The research revealed that:

  • Individual differences in executive function abilities were remarkably stable. Children who had stronger skills at two-and-a-half years old tended to remain ahead at six-and-a-half years.
  • Children from lower socio-economic households consistently scored lower, echoing long-standing research on the impact of maternal education and home environment.
  • Even when controlling for age and family background, COVID’s impact was evident. Children who were in reception at the start of the pandemic made more modest improvements in executive function compared to those still in preschool.

Dr Johns said: “Our findings suggest that the structured school environment and regular interaction with peers play a crucial role in supporting the development of executive function. When those experiences were disrupted, children’s executive function developed more slowly than that of younger children who were still in preschool.”

The researchers say their work highlights a generation of children who may need more support from teachers, schools and health services in coming years.

Sources: Lancaster University and University of East Anglia

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Active Ingredient from Red Foxglove Helps with Heart Failure

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Foxglove helps with heart failure: Cardiologists Professor Dr Udo Bavendiek (left) and Professor Dr Johann Bauersachs have scientifically proven the life-prolonging effect of digitoxin for the first time. Copyright: pixabay, Karin Kaiser/MHH

A multicentre study has demonstrated a clear positive effect of digitoxin in heart failure, which is derived from the red foxglove plant. Results from ten years of research involving more than 1200 participants have clearly confirmed the safety and efficacy of the cardiac glycoside in people diagnosed with heart failure with reduced ejection fraction.

Digitalis has been used to treat heart failure for more than 200 years. The drug digitoxin also belongs to this group of active ingredients known as cardiac glycosides. Although there were indications that digitalis was beneficial in heart failure, it has only now been scientifically proven that digitoxin has a significant positive effect in heart failure due to reduced pumping function and insufficient emptying of the left ventricle – known in medical terms as HFrEF (heart failure with reduced ejection fraction). For ten years, researchers led by Professor Dr Johann Bauersachs, Director of the Department of Cardiology and Angiology at Hanover Medical School (MHH), and senior physician Professor Dr Udo Bavendiek thoroughly investigated the safety and efficacy of the active ingredient in a clinical study involving more than 1200 participants.

The large-scale DIGIT-HF study coordinated by them, involving more than 50 centres in Germany, Austria and Serbia, has now been completed and delivers a clear result: adjunctive therapy with digitoxin reduces mortality and the number of hospitalisations for heart failure in patients with advanced HFrEF. The results have been published in the New England Journal of Medicine. At the same time, they were presented at the end of August 2025 at the European Society of Cardiology Congress in Madrid in the so-called Hot Line Session, where new clinical studies that promise significant changes in patient outcomes are presented.

No proof of effectiveness according to scientific standards to date

Our heart is a high-performance engine. It beats around 70 times per minute, pumping around five litres of blood through our vessels. In doing so, it supplies the body with vital oxygen and nutrients. If this pumping capacity is permanently reduced, physicians refer to this as chronic heart failure or cardiac insufficiency. Around four million people in Germany are affected. Symptoms include shortness of breath, low exercise tolerance, water retention, immobility and severe arrhythmia. The condition is one of the most common reasons for hospitalisation and even death. Until around 2020, digitalis preparations were still on the production list of major pharmaceutical companies. Currently, digitoxin is only produced as a generic drug. ‘However, it remains the most commonly used digitalis preparation in Germany – so far, however, without any scientifically proven evidence of its effectiveness,’ notes Professor Bavendiek.

Can also be used in cases of impaired kidney function

This has now been proven. ‘In the DIGIT-HF study, we examined patients who had exhausted all conventional treatment options,’ says Professor Bauersachs. ‘We were surprised ourselves that we were able to achieve such a significant improvement with the additional digitoxin treatment in these very well-treated study participants.’ The usual medications for heart failure include beta blockers and inhibitors of the renin-angiotensin-aldosterone system, which inhibit excessively activated hormone cascades and thus relieve the heart, as well as diuretics. Defibrillators, which are implanted in the patient’s body, also help against acute arrhythmias. Since 2021, so-called SGLT-2 inhibitors have also been used in Germany. These were originally approved for the treatment of type 2 diabetes, but also have positive effects in all forms of heart failure. Thanks to the DIGIT-HF study, digitoxin could now become another mainstay in the treatment of people diagnosed with HFrEF.

Previous clinical studies have been conducted almost exclusively with digoxin, another cardiac glycoside. However, digoxin can only be used to a limited extent in patients with impaired kidney function, which is often the case in patients with advanced heart failure, as it is excreted almost exclusively via the kidneys. ‘With digitoxin, however, the situation is different,’ explains Professor Bavendiek. This is because digitoxin is excreted via the liver and intestines to a greater extent in patients with impaired kidney function. The already approved drug is therefore also suitable for use in patients with pre-existing kidney weakness.

Safe and cost-effective

In addition, the results of the DIGIT-HF study dispelled fears that digitoxin is dangerous for certain groups of patients with heart failure and could lead to death. ‘When dosed correctly, digitoxin is a safe treatment for heart failure and is also suitable for controlling heart rate in atrial fibrillation when beta blockers alone are not sufficient,’ emphasises Professor Bavendiek. Another advantage of the drug sounds trivial, but is certainly interesting in view of rising healthcare costs: digitoxin costs just a few pence and is drastically cheaper than other drugs for heart failure. Based on the study data available to date, heart specialists have already developed recommendations for simple and safe dosing. Whereas 0.1 milligrams of digitoxin were often prescribed in the past, the current recommendations are 0.07 milligrams per day or even less. The DIGIT-HF study showed that this dosage reduced mortality and hospital admissions due to heart failure without any safety issues.

Source: Hannover Medical School (in German)

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New Study Reveals that Sex Hormones Reset Circadian Clocks

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Photo by Cottonbro on Pexels

The findings may shed new light on disruptions to the circadian clocks during menstruation, pregnancy and menopause

Disruptions to circadian clocks can lead to a wide range of health problems, from sleep disturbances to diabetes and cancer. But there has been no certainty about the identity of the body’s substances that can “shift” these clocks forward or backward and, when altered, potentially cause such disruptions.

A new study from Prof Gad Asher’s lab at the Weizmann Institute of Science, now published in Nature Communications, reveals that sex hormones play a central role in aligning the cellular clocks with one another and with the environment. The research team, led by Drs Gal Manella, Saar Ezagouri and Nityanand Bolshette, showed that female sex hormones – especially progesterone – together with the stress hormone cortisol, have a dramatic effect on the clocks.

It is already known that circadian clocks are affected not only by external signals such as sunlight but also by signals carried through the bloodstream. Until now, however, these blood-borne signals had not been fully mapped, and there was no certainty about the component within the clock that serves as their “point of entry.” The reason: Researchers lacked a precise method for tracking the clock’s response to different signals over a full 24-hour cycle.

In recent years, Prof Asher’s lab – an international leader in studying the molecular mechanisms of circadian clocks – developed an ingenious method that uses an array of human cells each representing a different “time of day.” It resembles a wall lined with clocks showing the current time in major cities around the world. The new approach enabled the researchers, for the first time and with unprecedented precision, to map how the cellular clocks are synchronized by blood-borne signals.

In addition to uncovering the influence of sex hormones, the study revealed that the clock component receiving these signals is the protein Cry2, rather than Per2, as previously believed.

The “ticking” of a circadian clock inside a human cell over the course of 24 hours. A fluorescent marker allows scientists to tell “what time it is” at any given moment

“The levels of sex hormones change throughout life – during menstrual cycles, pregnancy, hormone therapy, contraceptive use and various disease states. These conditions are also known to be associated with disturbances to circadian clocks,” Asher notes. “Our new findings suggest that these disturbances are linked to interactions between sex hormones and the mechanisms that synchronize circadian clocks.”

Source: Weizmann Institute of Science

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Review Finds Rapid Rebound from Weight Loss Medications

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Photo by I Yunmai on Unsplash

Obesity is a chronic, repeating disease: those who lose weight tend to put it back on after a time. In order to understand the impact of stopping weight management medications (WMMs), researchers conducted a systematic review and meta-analysis on the effect of these drugs on long-term health and body mass.

The research indicates that individuals typically experience rapid weight regain after treatment ends, with many returning to their original weight within approximately 1.7 years. Furthermore, cardiometabolic improvements, including blood pressure and glucose levels, were found to typically reverse and return to baseline shortly after the drugs are discontinued.

Notably, weight is regained significantly faster after pharmacological treatment than after finishing behavioural weight management programmes. Listen to our podcast for a summary of the paper published in The BMJ, along with the researchers’ conclusions.

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A Key Marker that Links Coronary Artery Disease to Cognitive Decline

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A new model combining a dozen metrics measures differences in white matter structure between older CAD patients and healthy controls

Source: Wikimedia CC0

Although coronary artery disease (CAD) increases the risks of strokes, cognitive impairment and dementia, the link between CAD and cognitive function is not fully understood. A new study led by Concordia researchers looks at how the disease affects the brain’s white matter, the network of nerve fibres that connects different regions of the brains and is critical to transmitting information efficiently.

The study, published in the Journal of Neuroscience, applied a novel multivariate approach using 12 separate metrics. The researchers compared test results and MRI scans of 43 patients with CAD to those of 36 healthy individuals. All participants were over age 50.

The researchers found that individuals with CAD had widespread structural changes in their white matter compared to their healthy counterparts. The changes were particularly noticeable in the parts of the brain fed by the middle cerebral (MCA) and anterior cerebral arteries. Both regions are key for cognitive and motor functions.

“This makes sense because those regions, especially the MCA territory, are most prone to strokes,” says PhD candidate Zacharie Potvin-Jutras, the study’s co-lead author. “We made sure that there was no history of strokes in our CAD cohort.

“Our goal is to examine conditions at the onset of a heart disease, before there has been any significant impact on the brain,” he says.

Stéfanie Tremblay, a 2023 Concordia Public Scholar now a postdoctoral researcher at McGill University, is the study’s other co-lead author.

Small measurements provide a bigger picture

The multivariate approach of bundling individual white matter metrics into one overarching metric provides advantages over past univariate studies. It allows the researchers to simplify complex aspects of brain health into a single metric that can be compared to the same metric in healthy controls. While individual metric variations between CAD patients and healthy controls may be very small, when seen together, they can provide significant indicators of early stages of cognitive impairment.

“The metrics are often overlapping, meaning they measure things that are related to each other,” says corresponding author Claudine Gauthier, an associate professor in the Department of Physics. “Having one single metric that captures many aspects of brain health allows us to identify differences between patients and controls that reflect a complex combination of changes in a single analysis. Then we can unpack it and see which aspects of white matter health drove the difference more than the others.”

The researchers found that the changes were mainly linked to reduced myelin content, the fatty envelope surrounding nerve fibres. Myelin loss can slow communication between brain cells and is often an early sign of cognitive ageing.

Interestingly, participants with higher measures of myelin integrity (specifically, in a marker called R1) performed better on tests of processing speed, a key aspect of thinking and attention. However, no significant differences were observed between groups in overall cognitive scores, suggesting that brain changes may precede noticeable symptoms.

“This study adds mechanistic insight into our understanding of how CAD affects white matter health,” says Gauthier. “Now that we know that myelin content is a good biomarker for coronary heart disease, the next step is to focus on potential interventions. If we have a preventive lifestyle intervention, we can optimize the intensity to improve myelin health and maintain cognitive function.”

The Canadian Institutes of Health Research, the Heart and Stroke Foundation of Canada and Brain Canada supported this research.

Read the cited paper: “Multivariate White Matter Microstructure Alterations in Older Adults with Coronary Artery Disease”

Source: Concordia University

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Boy Given World-first Gene Therapy for Hunter Syndrome Is ‘Thriving’

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Ollie Chu with his father, Ricky.

A young boy born with a devastating, rare genetic condition has been given a new lease of life thanks to a team of UCL scientists who manufactured a pioneering gene therapy for him.

Ollie Chu was born with Hunter syndrome – or MPSII – an inherited, life-limiting genetic condition which causes progressive damage to the body and brain.

In the most severe cases, patients with the disease usually die before the age of 20. The effects are sometimes described as a type of childhood dementia.

Due to a faulty gene, before the treatment Ollie was unable to produce an enzyme crucial for keeping cells healthy.

But in a world first, scientists at UCL have altered Ollie’s cells using gene therapy in a bid to halt the disease.

His parents are thrilled at Ollie’s progress which they say they has been “exponential” since his transplant. He is being treated in hospital in Manchester.

Dr Karen Buckland (UCL Great Ormond Street Institute of Child Heath) said: “It’s really heart-warming to hear how well Ollie is doing – his progress is amazing.

“It’s also really, really rewarding for the team here. A lot of hard work has gone into manufacturing this new gene therapy. As well as the core team of five, around 50 staff were involved in total including all the clinical trial co-ordinators, project managers and quality assurance staff.

“It took two years just to check that the manufacturing process worked correctly. We then had to get regulatory approval before we could even begin treating Ollie’s cells.”

Dr Buckland and three other of her UCL Institute of Child Heath colleagues were directly involved with manufacturing his cells: Dr Winston Vetharoy, Edward Morgan and Raymond Nguyen. The fifth member of the team was Agrim Mahajan, from Great Ormond Street Hospital.

Dr Buckland said the project came about because she and colleagues had worked successfully on a previous project with the same Manchester team on a treatment for a similar condition called Mucopolysaccharidosis type III (MPS III) or San Filippo Syndrome.

In 2019 the Manchester team, then led by Professor Brian Bigger, approached Dr Buckland and her team again and asked them to manufacture the treatment for Hunter’s Syndrome.

In 2021 the UCL team began the process of checking the manufacturing process worked correctly.

That process, which is the first outside-of-the-body gene therapy to treat the condition, involves purifying a patient’s white blood cells to retrieve their stem cells, which are then added to a specialist growth medium.

A working copy of the gene is then added to a viral vector, which is used to transport the healthy copy of the gene into the patient’s own stem cells.

The cells are then washed and frozen and stored at -130 degrees C, in a process known as cryopreservation.

The cells are checked using several quality control tests to make sure they’re safe to be given back to the patient.

Having confirmed, in 2022, that the process worked correctly the University of Manchester applied successfully to the UK medicines regulator, the Medicines and Healthcare products Regulatory Agency (MHRA), for approval. They could then use the process on a patient.

Ollie, from California, is the first of five boys around the world to receive the treatment.

The team treating him at Royal Manchester Children’s Hospital (RMCH) sent Dr Buckland and her colleagues some of his white blood cells.

Dr Vetharoy, who led the manufacture of the gene therapy product for Ollie, said: “Every stage of the process required meticulous attention to detail. We needed to maintain absolute control over contamination risks and ensure that all reagents and materials met the highest-quality standards.

“Seeing how well Ollie is thriving after such a short time is incredibly fulfilling for the entire team, and we wish him continued progress and good health in the years to come.”

In November 2024, the UCL manufacturing team made the altered cells for him, using the validated manufacturing process. In February 2025, those altered cells were transplanted into Ollie’s body.

Nine months on, his father, Ricky, says the improvement in his son’s condition is remarkable.

He said: “I don’t want to jinx it, but I feel like it’s gone very, very well. His life is no longer dominated by needles and hospital visits. His speech, agility and cognitive development have all got dramatically better.

“It’s not just a slow, gradual curve as he gets older, it has shot up exponentially since the transplant.”

Currently the only licensed treatment that can help to improve life for children with Hunter syndrome is Elaprase – a weekly enzyme replacement therapy that takes approximately three hours to administer, that children must take for their whole life. 

Dr Buckland and her colleagues manufactured the new gene therapy treatment at the specialist Cell and Gene Therapy Manufacturing Facility in The Zayed Centre for Research (ZCR) into Rare Diseases in Children, a facility jointly run by UCL and GOSH.

The clinical trial at RMCH is being done in collaboration with University of Manchester and the Manchester Centre for Genomic Medicine at Saint Mary’s Hospital.

Source: University College London

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Bird Flu Viruses Are Resistant to Fever – Making Them a Major Threat to Humans

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Photo by Karol Klajar on Unsplash

Bird flu viruses are a particular threat to humans because they can replicate at temperatures higher than a typical fever, one of the body’s ways of stopping viruses in their tracks, according to new research led by the universities of Cambridge and Glasgow.

In a study published in Science, the team identified a gene that plays an important role in setting the temperature sensitivity of a virus. In the deadly pandemics of 1957 and 1968, this gene transferred into human flu viruses, and the resulting virus thrived.

Human flu viruses cause millions of infections every year. The most common types of these viruses, which cause seasonal flu, are known as influenza A viruses. They tend to thrive in the upper respiratory tract, where the temperature is around 33°C, rather than deep in the lungs in the lower respiratory tract, where the temperature is around 37°C.

Unchecked, a virus will replicate and spread throughout the body, where it can cause illness, occasionally severe. One of the body’s self-defence mechanisms is fever, which can cause our body temperature to reach as high as 41°C, though until now it has not been clear how fever stops viruses – and why some viruses can survive.

Unlike human flu viruses, avian influenza viruses tend to thrive in the lower respiratory tract. In fact, in their natural hosts, which include ducks and seagulls, the virus often infects the gut, where temperatures can be as high as 40-42C.

In previous studies using cultured cells, scientists have shown that avian influenza viruses appear more resistant to temperatures typically seen in fever in humans. Today’s study uses in vivo models – mice infected with influenza viruses – to help explain how fever protects us and why it may not be enough to protect us against avian influenza.

An international team led by scientists in Cambridge and Glasgow simulated in mice what happens during a fever in response to influenza infections. To carry out the research, they used a laboratory-adapted influenza virus of human origin, known as PR8, which does not pose a risk to humans.

Although mice do not typically develop fever in response to influenza A viruses, the researchers were able to mimic its effect on the virus by raising the ambient temperature where the mice were housed (elevating the body temperature of the mice).

The researchers showed that raising body temperature to fever levels is effective at stopping human-origin flu viruses from replicating, but it is unlikely to stop avian flu viruses. Fever protected against severe infection from human-origin flu viruses, with just a 2C increase in body temperature enough to turn a lethal infection into a mild disease.

The research also revealed that the PB1 gene of the virus, important in the replication of the virus genome inside infected cells, plays a key role in setting the temperature-sensitivity. Viruses carrying an avian-like PB1 gene were able to withstand the high temperatures associated with fever, and caused severe illness in the mice. This is important, because human and bird flu viruses can ‘swap’ their genes when they co-infect a host at the same time, for example when both viruses infect pigs.

Dr Matt Turnbull, the first author of the study, from the Medical Research Council Centre for Virus Research at the University of Glasgow said: “The ability of viruses to swap genes is a continued source of threat for emerging flu viruses. We’ve seen it happen before during previous pandemics, such as in 1957 and 1968, where a human virus swapped its PB1 gene with that from an avian strain. This may help explain why these pandemics caused serious illness in people.

“It’s crucial that we monitor bird flu strains to help us prepare for potential outbreaks. Testing potential spillover viruses for how resistant they are likely to be to fever may help us identify more virulent strains.”

Senior author Professor Sam Wilson, from the Cambridge Institute of Therapeutic Immunology and Infectious Disease at the University of Cambridge, said: “Thankfully, humans don’t tend to get infected by bird flu viruses very frequently, but we still see dozens of human cases a year. Bird flu fatality rates in humans have traditionally been worryingly high, such as in historic H5N1 infections that caused more than 40% mortality.

“Understanding what makes bird flu viruses cause serious illness in humans is crucial for surveillance and pandemic preparedness efforts. This is especially important because of the pandemic threat posed by avian H5N1 viruses.”

The findings may have implications for the treatment of infections, though the team stresses that more research is needed before changes are considered for treatment guidelines. Fever is often treated with antipyretic medication, which include ibuprofen and aspirin. However, there is clinical evidence that treating fever may not always be beneficial to the patient and may even promote transmission of influenza A viruses in humans.

Professor Wendy Barclay, Chair of the Medical Research Council (MRC) Infections and Immunity Board, said: “This elegant study builds on the very simple observation that different animals have different body temperatures, and shows how this may impact the way that viruses replicate in new hosts as they cross species barriers. The authors show that replication of human-adapted influenza virus is attenuated when temperatures are increased, such as in a fever. But avian influenza viruses, whose natural hosts have higher body temperatures, are not controlled by the fever response when they cross into mammals.

“They link their findings to one particular gene of the virus, called PB1, which is often carried over from birds when a new pandemic virus emerges. These findings have important implications for when and how to use drugs to control the fever that is associated with an influenza infection, and may also help us to understand why the disease from some influenza outbreaks is more severe.”

The research was funded primarily by the Medical Research Council, with additional funding from the Wellcome Trust, Biotechnology and Biological Sciences Research Council, European Research Council, European Union Horizon 2020, UK Department for Environment, Food & Rural Affairs, and US Department of Agriculture.

Reference

Turnbull, ML et al. Avian-origin influenza A viruses tolerate elevated pyrexic temperatures in mammals. Science; 27 Nov 2025; DOI: 10.1126/science.adq4691

Republished from Cambridge University under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

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Release of Useful Health Statistics: 2015 to 2025

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Mycobacterium tuberculosis drug susceptibility test. Photo by CDC on Unsplash

By Marcus Low and Nathan Geffen

The National Health Laboratory Service has provided HIV, TB, syphilis and cholesterol data, which Spotlight and GroundUp obtained through the Promotion of Access to Information Act.

Earlier this year, we made a request for data to the National Health Laboratory Service (NHLS) using the Promotion of Access to Information Act. In October, we were provided with the data we requested (and more).

We are grateful and impressed that the NHLS provided the data without fuss and without the need to go to court. Other state institutions could learn from this.

We used the data to analyse HIV viral load data in light of the withdrawal of US aid. It led to us publishing this article: Withdrawal of US aid has hurt South Africa’s HIV programme.

From the outset, we’ve intended to make the data public. No information on patients is recoverable from this data as the finest detail is at the monthly provincial level. We are therefore publishing this data, as an open document format spreadsheet, today. We are of the view that the data provided is useful for scientists and journalists and we hope the NHLS will regularly publish updates to it.

The spreadsheet contains monthly tallies per province of viral load tests, CD4 counts, TB tests, syphilis tests, full blood counts and cholesterol tests. The period covered is January 2015 to September 2025.

Download the spreadsheet

Much of the data is not straightforward to interpret. For example, after we puzzled over the decline in cholesterol tests, one expert pointed out to us that the decrease is probably due to changes in the standard second-line HIV treatment used in the public sector (some older HIV medicines had potential side effects that made cholesterol tests necessary). Similarly, changes in the number of TB tests conducted will have been impacted by guidelines that expanded eligibility for TB testing.

The NHLS informed us of the following caveats:

  1. All counts reflect the number of tests captured on the NHLS TrakCare (LabTrak) Laboratory Information System (LIS) as at the time the counts were performed (21 October 2025).
  2. A system-generated date from the time a sample was captured onto the LIS was used to total counts per month/year.
  3. There may be anomalies in counts for a few months from July 2024 because of disruptions caused by a cyber-attack.
  4. As test counts were requested, rejected tests and unreviewed results were included.
  5. As test counts were requested, the counts provided reflect the number of tests done, not the number of patients tested, as multiple tests may be performed on one patient sample. For example, for a full blood count, each individual test was counted.
  6. The “Pregnant or postnatal women” group was identified according to the NHLS maternal eGK (electronic gatekeeping) codes.

(We have amended the NHLS spreadsheet by inserting a new sheet with the above caveats and a link to this article. No other material changes have been made to the spreadsheet.)

This article was jointly produced by Spotlight and GroundUp.

Republished from Spotlight under a Creative Commons licence.

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Hidden Genetic Risk Could Delay Diabetes Diagnosis for Black and Asian Men

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Photo by Wes Dissy on Unsplash

A common but often undiagnosed genetic condition may be causing delays in type 2 diabetes diagnoses and increasing the risk of serious complications for thousands of Black and South Asian men in the UK – and potentially millions worldwide.

The new study is conducted by the University of Exeter, in collaboration with Queen Mary University of London (QMUL). The findings, published in Diabetes Care, show that around one in seven Black and one in 63 South Asian men in the UK carry a genetic variant known as G6PD deficiency. Men with G6PD deficiency are, on average, diagnosed with type 2 diabetes four years later than those without the gene variant. But despite this, fewer than one in 50 have been diagnosed with the condition

G6PD deficiency does not cause diabetes, but it makes the widely used HbA1c blood test – which diagnoses and monitors diabetes – appear artificially low. This can mislead doctors and patients, resulting in delayed diabetes diagnosis and treatment.

Professor Inês Barroso from the University of Exeter said: “Our findings highlight the urgent need for changes to testing practices to tackle health inequalities. Doctors and health policy makers need to be aware that the HbA1c test may not be accurate for people with G6PD deficiency and routine G6PD screening could help identify those at risk. Addressing this issue is not only crucial for medicine, but for health equity.”

G6PD deficiency is a genetic condition that affects more than 400 million people worldwide, and is especially prevalent among those with African, Asian, Middle Eastern, and Mediterranean backgrounds. It is more common in men and usually goes undetected because it rarely causes symptoms. The World Health Organization recommends routine screening for G6PD deficiency in populations where it is common, but this is not widely implemented in the UK or many other countries.

This new study, supported by the National Institute for Health and Care Research Exeter Biomedical Research Centre, has found men with G6PD deficiency are at a 37% higher risk of developing diabetes-related microvascular complications, such as eye, kidney, and nerve damage, compared to other men with diabetes.

The HbA1c blood test is the international standard for managing type 2 diabetes and is used in 136 countries worldwide to diagnose diabetes, including being the routine test for diagnosis in the UK. However, for people with G6PD deficiency, this test may underestimate their blood sugar levels, causing significant medical delays and increasing their risk of serious complications.

Dr Veline L’Esperance, a GP and Senior Clinical Research Fellow at QMUL, said: “These findings are deeply concerning because they show how a widely used diagnostic tool may be failing communities that are already disproportionately affected by type 2 diabetes. Too many people are being left undiagnosed until it is too late to prevent serious complications. We need greater awareness among healthcare professionals and stronger policies to ensure equitable screening and diagnosis. That is why we are launching ‘Black Health Legacy’, which aims to be the largest health research programme focused on tackling diseases that disproportionately affect people from Black backgrounds. This is about saving lives and tackling long-standing inequalities in our healthcare system.”

The findings are based on genetic and health data from over half a million people in UK Biobank and Genes & Health studies. The research was conducted by a multidisciplinary team of clinicians and scientists, with the support of community partners, who linked the genetic data from each participant to their medical information. By doing this the team found men with the G6PD deficiency genetic variant were diagnosed at an older age compared to those without the condition. In addition, those with G6PD deficiency and diabetes also had more diabetes related complications. Researchers say further studies in more diverse populations are now needed to confirm these findings globally.

More information about Black Health Legacy can be found at https://blackhealthlegacy.org

Source: Exeter University

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Prediabetes Remission Possible Without Dropping Pounds, Our New Study Finds

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Photo by Kenny Eliason on Unsplash

Andreas L. Birkenfeld, University of Tübingen and Reiner Jumpertz-von Schwartzenberg, University of Tübingen

There’s a long-held belief in diabetes prevention that weight loss is the main way to lower disease risk. Our new study challenges this.

For decades, people diagnosed with prediabetes – a condition affecting up to one in three adults depending on age – have been told the same thing by their doctors: eat healthily and lose weight to avoid developing diabetes.

This approach hasn’t been working for all. Despite unchanged medical recommendations for more than 20 years, diabetes prevalence continues rising globally. Most people with prediabetes find weight-loss goals hard to reach, leaving them discouraged and still at high risk of diabetes.

Our latest research, published in Nature Medicine, reveals a different approach entirely. We found that prediabetes can go into remission – with blood sugar returning to normal – even without weight loss.

About one in four people in lifestyle intervention programmes bring their blood sugar back to normal without losing any weight. Remarkably, this weight-stable remission protects against future diabetes just as effectively as remission achieved through weight loss.

This represents a significant shift in how doctors might treat overweight or obese patients at high risk for diabetes. But how is it possible to reduce blood glucose levels without losing weight, or even while gaining weight?

The answer lies in how fat is distributed throughout the body. Not all body fat behaves the same way.

The visceral fat deep in our abdomen, surrounding our internal organs, acts as a metabolic troublemaker. This belly fat drives chronic inflammation that interferes with insulin – the hormone responsible for controlling blood sugar levels. When insulin can’t function properly, blood glucose rises.

In contrast, subcutaneous fat – the fat directly under our skin – can be beneficial. This type of fat tissue produces hormones that help insulin work more effectively. Our study shows that people who reverse prediabetes without weight loss shift fat from deep within their abdomen to beneath their skin, even if their total weight stays the same.

Subcutaneous fat can be beneficial. Photo by Andres Ayrton on Pexels

We’ve also uncovered another piece of the puzzle. Natural hormones that are mimicked by new weight-loss medications like Wegovy and Mounjaro appear to play a crucial role in this process. These hormones, particularly GLP-1, help pancreatic beta cells secrete insulin when blood sugar levels rise.

People who reverse their prediabetes without losing weight seem to naturally enhance this hormone system, while simultaneously suppressing other hormones that typically drive glucose levels higher.

Targeting fat redistribution, not just weight loss

The practical implications are encouraging. Instead of focusing only on the scales, people with prediabetes can aim to shift body fat with diet and exercise.

Research shows that polyunsaturated fatty acids, abundant in Mediterranean diets rich in fish oil, olives and nuts, may help reduce visceral belly fat. Similarly, endurance training can decrease abdominal fat even without overall weight loss.

This doesn’t mean weight loss should be abandoned as a goal – it remains beneficial for overall health and diabetes prevention. However, our findings suggest that achieving normal blood glucose levels, regardless of weight changes, should become a primary target for prediabetes treatment.

This approach could help millions of people who have struggled with traditional weight-loss programmes but might still achieve meaningful health improvements through metabolic changes.

For healthcare providers, this research suggests a need to broaden treatment approaches beyond weight-focused interventions. Monitoring blood glucose improvements and encouraging fat redistribution through targeted nutrition and exercise could provide alternative pathways to diabetes prevention for patients who find weight loss particularly difficult.

The implications extend globally, where diabetes represents one of the fastest-growing health problems. By recognising that prediabetes can improve without weight loss, we open new possibilities for preventing a disease that affects hundreds of millions worldwide and continues rapidly expanding.

This research fundamentally reframes diabetes prevention, suggesting that metabolic health improvements – not just weight reduction – should be central to clinical practice. For the many people living with prediabetes who have felt discouraged by unsuccessful weight-loss attempts, this offers renewed hope and practical alternative strategies for reducing their diabetes risk.

Andreas L. Birkenfeld, Professor, Diabetology, Endocrinology and Nephrology, University of Tübingen and Reiner Jumpertz-von Schwartzenberg, Professorship for Clinical Metabolism and Obesity Research, University Hospital and Medical Faculty, University of Tübingen

This article is republished from The Conversation under a Creative Commons license. Read the original article.