Discovery Health has recently abandoned its efforts to reclaim roughly R170 million from 16 507 members following a widespread administrative error in processing medical claims. This happened after the successful intervention of the advocacy group MediCheck, which argued that the affected members were being unfairly penalised for a technical glitch which they had nothing to do with.
The glitch, which happened last year, resulted in over-reimbursement of certain medicine costs that occurred throughout 2025. Several specific technical and procedural issues were involved which caused the problem to grow undetected for nearly a year, as detailed by Moonstone.
The main error was that certain claims were incorrectly reimbursed at 100% of the Discovery Health Rate, regardless of the specific benefit limits that should have applied to those categories, when they should have been reimbursed at a lower rate.
Because these claims were incorrectly reimbursed at higher rates, they were inaccurately accumulated towards members’ benefit thresholds. This caused members who had Above-Threshold Benefit (ATB) as part of their plan to reach it prematurely. Upon reaching the ATB, subsequent medical claims were funded by the scheme. Normally, these claims would have been covered by the members’ medical savings accounts or out-of-pocket contributions.
Delayed detection allowed the problem to grow. The error was particularly difficult to identify because it was a “second-order impact”. The systemic failure only became apparent late in the year when members began reaching the ATB and the financial discrepancies were finally flagged.
This snowballing error eventually affected some 16 507 members on specific Executive, Comprehensive, and Priority plans. While Discovery Health initially sought to recover these funds, ranging from thousands of rand to as much as R80 000 per member, the Council for Medical Schemes stepped in to exert pressure amid widespread media coverage of the situation. Discovery gave in and committed to refunding any recovered funds and absorbing the total financial loss itself – estimated between R130 million and R170 million.
An analysis of genetic data over nearly one million individuals shows that certain stretches of DNA, made up of short sequences repeated over and over, become longer and more unstable as we age. The study found that common genetic variants can speed up or slow down this process by up to fourfold, and that certain expanded sequences are linked to serious diseases including kidney failure and liver disease.
Why it matters
More than 60 inherited disorders are caused by expanded DNA repeats: repetitive genetic sequences that grow longer over time. These include devastating conditions like Huntington’s disease, myotonic dystrophy, and certain forms of ALS. Most people carry DNA repeats that gradually expand throughout their lives, but this instability and what genetic factors control it hadn’t been fully analysed within large biobanks. This study demonstrates that DNA repeat expansion is far more widespread than previously recognised and identifies dozens of genes that regulate this process, opening new avenues for developing treatments that could slow disease progression.
What the study did
Researchers from UCLA, the Broad Institute, and Harvard Medical School analysed whole-genome sequencing data from 490 416 UK Biobank participants and 414 830 All of Us Research Program participants. They developed new computational methods to detect and measure DNA repeat lengths and instability from standard sequencing data. The team examined 356 131 polymorphic repeat locations across the genome, tracking how repeat lengths changed with age in blood cells and identifying genetic variants that influenced expansion rates. They also searched for links between repeat expansions and thousands of disease outcomes to discover previously unknown disease associations.
What they found
Common DNA repeats in blood cells expand as people age. The researchers identified 29 genetic locations where inherited variants modified DNA repeat expansion rates, with effects varying up to fourfold between individuals with the highest and lowest genetic risk scores. Interestingly, the same DNA repair genes had opposite effects on different repeats: variants that stabilised some repeats destabilised others. The study also discovered that expansions in the GLS gene, which have a prevalence of around 0.03%, were associated with 14-fold higher risk of severe kidney disease and 3-fold higher risk of liver diseases, representing a newly recognised repeat expansion disorder.
What’s next
The findings establish blood-based DNA repeat measurements as potential biomarkers for testing future therapies aimed at slowing repeat expansion in diseases like Huntington’s. The research team’s computational tools can now be applied to other large biobank datasets to discover additional unstable repeats and disease associations. Understanding why the same genetic modifiers have opposite effects on different repeats will require detailed mechanistic studies of how DNA repair processes vary across cell types and genetic contexts. The discovery of GLS repeat-associated kidney and liver disease suggests additional unrecognised repeat expansion disorders may be lurking in biobank data, waiting to be found.
From the experts
“We found that most human genomes contain repeat elements that expand as we age,” said Margaux L. A. Hujoel, PhD, lead author of the study and assistant professor in the Departments of Human Genetics and Computational Medicine at the David Geffen School of Medicine at UCLA. “The strong genetic control of this expansion, with some individuals’ repeats expanding four times faster than others, points to opportunities for therapeutic intervention. These naturally occurring genetic modifiers show us which molecular pathways could be targeted to slow repeat expansion in disease.”
A Scottish patient has become the first person in the world to receive a pioneering therapy aimed at improving outcomes for those having heart bypass surgery. The treatment involves precisely editing DNA in veins to be used during heart bypass surgery to boost the production of a protective protein.
The treatment could help extend the lifespan of blood vessels used during the surgery and significantly improve patient health, experts say.
Cause of failures in bypass surgery
Heart bypass surgery – an operation to improve blood flow to the heart – is a life-saving treatment for patients with coronary heart disease.
The process typically uses one artery and two or more veins as bypass grafts – healthy blood vessels used to bypass a narrowed or blocked artery – creating a new route for blood to flow.
Vein grafts used in this type of surgery can fail because they are not naturally designed to withstand the high pressure of blood flow from the heart.
Protecting vein grafts
The PROTECT study, led by NHS Greater Glasgow and Clyde and the University of Glasgow in collaboration with NHS Golden Jubilee and the University of Edinburgh, is trialling a new gene therapy designed to support newly grafted blood vessels.
The treatment will introduce a gene, which produces a protein called TIMP-3, into the vein to be grafted.
TIMP-3 is involved in tissue remodelling. Higher levels of the protein could help to prevent thickening and blockage of the blood vessel over time, scientists say.
Exciting milestone
The research team has developed a way to treat the graft directly at the time of surgery, safely and efficiently delivering the gene therapy to the affected tissue before grafting into the heart.
It is hoped the treatment will help to extend a patient’s healthy life expectancy and reduce the need for further surgeries, experts say.
Depiction of multiple myeloma. Credit: Scientific Animations
Patients with relapsed or refractory (R/R) multiple myeloma who received a combination of teclistamab, a bispecific monoclonal antibody, and daratumumab, a CD38-directed monoclonal antibody, were 83% more likely to be alive without disease progression compared with those who received standard second-line therapies at a median of nearly 35 months of follow-up, according to the results of a new trial presented at the 67th American Society of Hematology (ASH) Annual Meeting and Exposition.
The trial is the first to test a bispecific monoclonal antibody as early as the first relapse after initial treatment for multiple myeloma. Based on the findings, researchers suggest the combination of teclistamab and daratumumab, known as Tec-Dara, could represent a new standard of care for R/R multiple myeloma.
“We were surprised by the efficacy data because we didn’t expect such a magnitude of benefit,” said lead study author María-Victoria Mateos, MD, PhD, physician in the haematology department and professor of medicine at the University of Salamanca in Spain. “These are the best data we’ve seen in patients with R/R multiple myeloma after one line of therapy. Patients will live longer overall and with no worsening of quality of life.”
Multiple myeloma is a cancer that causes excessive production of plasma cells, crowding out the production of other types of blood cells and harming the body’s ability to fight infections. It is most common in older adults. Patients who relapse or experience an incomplete response to initial treatment often have their cancer return after subsequent therapies, pointing to a need for improved second-line treatments.
Teclistamab is approved by the U.S. Food and Drug Administration for R/R multiple myeloma after at least four prior lines of therapy. Daratumumab is a therapy targeting the CD38 protein that has been approved for use in combination with other therapies for newly diagnosed and R/R multiple myeloma. Laboratory studies have suggested that teclistamab and daratumumab may work synergistically to eradicate cancer to a greater extent than either agent individually.
To test this hypothesis, researchers randomized 587 patients with R/R multiple myeloma to receive either Tec-Dara or standard second-line therapies. For patients in the control arm, treating physicians chose between two standard three-agent combination therapies which included daratumumab with dexamethasone plus either pomalidomide or bortezomib (known as DPd or DVd, respectively).
Study participants had a median age of 64 with a range of 25-88, and all patients were R/R after one to three prior lines of therapy. Participants remained on their assigned treatment regimen unless they experienced intolerable adverse events, and were followed for a median of nearly 35 months.
The 36-month rate of progression-free survival, the study’s primary endpoint, was achieved in 83.4% of participants who received Tec-Dara and 29.7% of those receiving DPd/DVd, a substantial improvement in favor of Tec-Dara. This benefit was consistent across subgroups of patients by age, prior treatment, tumor genetics, and other factors.
In addition to being a highly efficacious treatment for R/R multiple myeloma as early as the first relapse, researchers noted that the Tec-Dara combination could be more accessible than other second-line therapies for multiple myeloma as it could be delivered in community settings, not just academic centers.
Tec-Dara outperformed DPd/DVd in terms of the trial’s secondary efficacy endpoints as well as quality of life outcomes and had a safety profile comparable to the control arm. Patients receiving Tec-Dara were significantly more likely to achieve a complete response or better, which occurred in 81.8% of patients receiving Tec-Dara and 32.1% among the control arm. They were also more likely to test negative for minimal residual disease (MRD), a sensitive test for remaining cancer cells, with 58.4% of those in the Tec-Dara arm achieving MRD-negativity compared with 17.1% in the control arm. Overall survival was also higher in the Tec-Dara arm, with 83.3% of patients in this group being alive at 36 months compared with 65.0% in the control arm.
The results showed comparable rates of treatment-emergent adverse events, with 95.1% of patients in the Tec-Dara arm and 96.6% of those in the control arm experiencing grade 3-4 adverse events. Rates of serious adverse events and discontinuations due to adverse events were also comparable between groups, researchers reported.
The rate of infections was higher among those receiving Tec-Dara, with 96.5% of patients in this group experiencing infections compared with 84.1% in the control group. The onset of higher-grade infections decreased over time, and researchers noted that strategies for managing infections also improved over the course of the study. Low-grade cytokine release syndrome (CRS) was also common, with grade 1-2 CRS occurring in 60.1% of those receiving Tec-Dara.
One limitation of the study is that patients refractory to daratumumab were not included in the trial. However, some patients (5%) had received daratumumab as part of their first-line therapy and benefited equally from the Tec-Dara combination.
Dr. Mateos noted that future studies could help clarify how doctors might select which patients would benefit most from the Tec-Dara combination in comparison to other therapies. Trials involving other bispecific antibody combinations are also underway and could shed additional light on the optimal use of such combinations as early as the first relapse.
New paper challenges old notions of ‘glitched brain’ idea of delusions and instead focuses on physical experiences of strong and deeply held emotion.
Photo by Alex Green on Pexels
People experiencing delusions during an episode of psychosis may be ‘living out’ a deeply held emotion, according to new research that provides a ‘radically different perspective’ on one of the most puzzling elements of psychosis.
About 2–3% of the UK and Australian population will experience psychosis at some point in their lives, with people commonly experiencing their first psychotic episode between the ages of 16 and 30 years old. Delusions are often described as fixed or false beliefs, understood to be reasoning or cognitive deficits and usually portrayed as incomprehensible and bizarre in popular culture.
New research by the University of Birmingham, University of Melbourne, and the University of York, in collaboration with the Australian youth mental health research institute Orygen, offers the first-known study of how delusions in psychosis are shaped by emotions and language, leading those experiencing delusions to ‘live in metaphor.’
Our research provides a radically different perspective on psychotic delusions, demonstrating how they emerge from the emotional, bodily, and linguistic fabric of people’s lives.Dr Rosa Ritunnano, University of Birmingham
Conducted with young adults receiving care from Early Intervention in Psychosis services, the research combines clinical assessment, phenomenological interviews, and life-story narratives to explore how people’s sense of self and their perception of reality change during psychosis.
Dr Rosa Ritunnano, from the Institute for Mental Health at the University of Birmingham, consultant psychiatrist and author of the study, said: “Our research provides a radically different perspective on psychotic delusions, demonstrating how they emerge from the emotional, bodily, and linguistic fabric of people’s lives.
“For a long time, clinicians have struggled to understand where delusions come from and how they take shape. Our research offers new insight by showing how delusions are grounded in emotional experiences that involve great bodily turmoil.”
Strong emotions
The findings reveal that delusions are not isolated ideas produced by ‘glitches in the brain,’ but they reflect distinctive patterns of the body reacting to strong emotions or experiences of dissociation.
Participants described alternating states of intense emotional embodiment, such as feeling exposed, powerful, or connected to God, and disembodiment, such as feeling unreal or detached from one’s body, other people, and the world.
Before the delusions started, people often went through upsetting or traumatic experiences that triggered the same intense feelings they later felt during the delusions, especially being shamed.
Repeated negative experiences such as being publicly mocked and shamed by bullies could induce the bodily perception of being surveilled by others when no one is present (so-called ‘reference delusions’). These turn into persecutory beliefs that others are out to get them, and that an audience can literally see what they are doing or hear what they are thinking at all times — leaving no space for privacy (delusions of ‘thought broadcasting’).
Importantly, delusional experiences were not always negative. For some participants, they involved powerful feelings of awe, love, and spiritual connection, fostering a positive sense of identity and a renewed sense of hope about the future.
Figurative language
A striking feature of participants’ accounts was their use of figurative and metonymic language (expressions linking bodily sensations with complex emotions or abstract ideas). This helps explain why delusional content can appear unusual or bizarre. For instance, feeling ‘exposed’ or ‘tainted’ might be expressed through the beliefs of being watched by cameras or being contaminated (as in delusions of parasitosis).
As a result of having endured strong (often negative) emotional experiences, which are then responded to by the body, and shaped by everyday language use, people experiencing psychotic delusions really are living in metaphor. People may feel delighted and say they are so happy they can ‘touch the sky’; this could lead them to experience the delusion of thinking they can fly.Professor Jeannette Littlemore, University of Birmingham
The language reflects how emotion concepts take shape in bodily experiences, establishing fundamental cognitive links between, for instance, the emotion of parental love and the physical sensation of warmth, or the emotion of shame and the physical sensation of being ‘seen’ by others.
Jeannette Littlemore, Professor of Linguistics and Communication at the University of Birmingham and co-author of the paper, said: “We all use metaphors and narratives to understand our experiences and make sense of our lives. But psychosis patients do so more intensely. As a result of having endured strong (often negative) emotional experiences, which are then responded to by the body, and shaped by everyday language use, people experiencing psychotic delusions really are living in metaphor. People may feel delighted and say they are so happy they can ‘touch the sky’; this could lead them to experience the delusion of thinking they can fly.”
The study argues that better insight into how delusions come about can be used to create more effective care for people experiencing psychosis. Participants felt that there was no space to talk about the meaning of their delusions in the context of their treatment and recovery from psychosis, which led to more shame and increased the sense of being dismissed and marginalised.
The researchers highlight the importance of attending to people’s bodily and emotional worlds, and how they express them, when developing compassionate, effective approaches to psychosis care.
The paper concludes that delusions are not simply beliefs gone wrong, but embodied attempts to restore meaning and emotional balance when life becomes overwhelming. The metaphors and narratives people use are keys to understanding their suffering and are not signs of irrationality.
Hyundai Automotive South Africa reaffirmed its commitment towards embedding disability inclusion into its operations, through continuous disability-related employee training, improving dealership layouts and vehicle modifications.
The aim is to foster a culture that recognises disability as part of human diversity rather than a limitation. “Mobility is not just about getting from one point to another, rather, about access and dignity,” said Stanley Anderson, CEO of Hyundai Automotive South Africa.
“Our commitment is to ensure our vehicles and dealerships are adequately prepared to support the needs of all customers, including those with disabilities. More importantly, we want to empower our customer-facing employees with deeper understanding of disability, dismantle misconceptions. By so doing, we will ensure that customers with disabilities feel welcomed, respected and supported when visiting any Hyundai dealership.”
It has also implemented a range of practical measures to ensure its dealerships are physically accessible and welcoming to persons with disabilities. This includes improving dealership layouts for ease of movement, ensuring wheelchair-friendly access points.
The company works closely with a range of specialised suppliers who modify some of its vehicles to suit the mobility needs of persons with disabilities. “These partnerships ensure that more South Africans can access safe, reliable and custom-adapted mobility solutions suited to their lifestyles and independence,” stated Christine Masinga, Human Resources Director at Hyundai Automotive South Africa.
The national disability prevalence rate in South Africa is estimated at around 7.5%. Despite national government targets for 2% representation of persons with disabilities in workplaces, recent reports indicate that they comprise less than 1% of the total employees across both government and private companies.
According to the Department of Employment and Labour, eight out of ten disabled persons are unemployed nationally, which is significantly higher than the general unemployment rate.
McGill researchers studying printed stickers on packaged food find some chemicals now used instead of bisphenol A can disrupt human ovarian cell function, and warn that ‘BPA-free’ does not necessarily mean safe
Chemicals used to replace bisphenol A (BPA) in food packaging can trigger potentially harmful effects in human ovarian cells, according to McGill University researchers.
A new study examined several chemicals commonly used in price stickers on packaged meat, fish, cheese and produce found early signs of potential toxicity.
The findings, published in the journal Toxicological Sciences, raise concerns about the safety of BPA-free packaging and whether current regulations go far enough to protect consumers.
BPA substitutes disrupt gene expression
The research began with the 2023 discovery by Stéphane Bayen, Associate Professor in McGill’s Department of Food Science and Agricultural Chemistry, that label-printing chemicals like bisphenol S (BPS), a BPA replacement, were leaching through plastic wrap into the food. He teamed up with colleagues in reproductive toxicology to investigate what these substances could be doing inside the body.
Lab-grown human ovarian cells were exposed to four commonly used BPA substitutes: TGSA, D-8, PF-201 and BPS. Several of the chemicals, particularly TGSA and D-8, caused a buildup of fat droplets in the cells and changed the activity of genes that help cells grow and repair their DNA.
“These are major cellular functions,” said Bernard Robaire, co-senior author of the study and James McGill Professor in McGill’s Departments of Pharmacology & Therapeutics and Obstetrics & Gynecology. “Disrupting them doesn’t prove harm in humans, but it gives us a strong signal that these chemicals should be further investigated.”
Unregulated replacements under the radar
BPA is a chemical that can interfere with the body’s hormones, and has been linked to problems with fertility, early development and metabolism. Because of these risks, it has been banned in baby bottles and restricted in some products in Canada.
Many of the chemicals used to replace BPA are not regulated or routinely tested, the researchers explained.
“‘BPA-free’ is an incredibly misleading label,” said Robaire. “It usually means one bisphenol has been swapped for another, and there are more than 200 of them. Some may be just as harmful, or even worse. We need to test these compounds before they’re widely adopted, not after.”
Health Canada has now added all four substances to a list of chemicals requiring further investigation.
For consumers looking to err on the side of caution, Robaire suggests removing labels and plastic wrap from fresh foods before storing. He also recommends choosing items from the top of store display piles rather than the bottom, where pressure from stacking may push chemicals more deeply into the packaging and food.
Many people stop taking cholesterol-lowering statins because they experience muscle aches, weakness, and fatigue. A new study by Columbia researchers now suggests that at least for some people, the side effects arise when statins bind to a protein in muscle cells and cause a leak of calcium ions inside the cells.
“It is unlikely that this explanation applies to everyone who experiences muscular side effects with statins, but even if it explains a small subset, that’s a lot of people we could help if we can resolve the issue,” says Andrew Marks, chair of the Department of Physiology and Cellular Biophysics at the Vagelos College of Physicians and Surgeons.
About 10% of adults taking statins experience these muscular side effects.
“I’ve had patients who’ve been prescribed statins, and they refused to take them because of the side effects. It’s the most common reason patients quit statins, and it’s a very real problem that needs a solution,” says Marks.
Electron microscopy pinpoints statin-muscle interaction
Statins’ muscular side effects have puzzled researchers since the drugs hit the market in the late 80s. Statins are designed to lower cholesterol by binding to an enzyme involved in cholesterol synthesis. But statins also bind to other “off-target” molecules, and some previous studies have suggested that muscular side effects occur when statins bind to a specific protein in muscle.
With cryo-electron microscopy, a technique that can image molecules down to individual atoms, the researchers of the new study documented this binding and uncovered the precise details of the interaction.
Simvastatin molecules bind to two locations on a muscle protein, called the ryanodine receptor, which opens a channel in the receptor. The flow of calcium through the open channel could explain the muscular side effects of statins.
The images revealed two locations on the muscle protein, called the ryanodine receptor, where a statin called simvastatin binds, opening a channel in the receptor and allowing calcium to flow through.
The calcium leak could explain the muscular side effects of statins, Marks says, by weakening the muscle directly or by activating enzymes that degrade muscle tissue.
Building a better statin
The new images also suggest that statins could be redesigned so they do not bind the ryanodine receptor but retain their cholesterol-lowering ability.
Marks is now collaborating with chemists to create such a statin.
Plugging the calcium leak could be another option: Statin-induced calcium leaks in mice can be closed, the researchers showed, with an experimental drug developed in the Marks lab for other conditions involving calcium leaks.
These drugs are currently being tested in people with rare muscle diseases. If it shows efficacy in those patients, we can test it in statin-induced myopathies,” Marks says
This is a pseudo-colored image of high-resolution gradient-echo MRI scan of a fixed cerebral hemisphere from a person with multiple sclerosis.
Credit: Govind Bhagavatheeshwaran, Daniel Reich, National Institute of Neurological Disorders and Stroke, National Institutes of Health
The immune system’s reaction to the common Epstein-Barr virus can ultimately damage the brain and contribute to multiple sclerosis (MS). This is shown by new research from Karolinska Institutet, published in Cell. The study provides new insight into the long-suspected link between Epstein-Barr virus (EBV) and MS.
Multiple sclerosis is a chronic inflammatory disease in which the immune system attacks the central nervous system and causes nerve damage. It has long been known that everyone who develops MS has had an infection with the Epstein-Barr virus (EBV) – a common virus that often infects young people, sometimes causing glandular fever but often without any obvious symptoms.. Exactly how this virus contributes to MS has long been unclear.
The new study shows that when the immune system fights EBV, certain T cells – which normally attack the virus – can also react to a protein in the brain called Anoctamin-2 (ANO2). This phenomenon is called molecular mimicry – immune cells mistaking the body’s own proteins for those of the virus.
The researchers found that these cross-reactive T cells are significantly more common in people with MS than in healthy controls. The study builds on previous research showing that misdirected antibodies after EBV infection may play a role.
“Our results provide mechanistic evidence that immune responses to EBV can directly damage the brain in MS. It is a complex neurological disease, and it may be that the molecular mechanisms vary between patients,” says the study’s first author, Olivia Thomas, assistant professor at the Department of Clinical Neuroscience at Karolinska Institutet.
The study is based on analyses of blood samples from people with MS and compared with healthy controls. The researchers were able to isolate T cells that react to both the EBV protein EBNA1 and ANO2 from people with MS. In addition, experiments in a mouse model showed that these cells can exacerbate MS-like symptoms and cause damage to the brain.
According to the researchers, the results may help explain why some people develop MS after an EBV infection while others do not.
“The discovery opens up new treatments that target these cross-reactive immune cells. Since several EBV vaccines and antiviral drugs are now being tested in clinical trials, the results may be of great importance for future preventive and therapeutic efforts,” says Professor Tomas Olsson, who led the study together with Associate Professor Andre Ortlieb Guerreiro-Cacais at the same institution.
Rates of multiple myeloma (MM), the second most common blood cancer in the United States, are increasing and are twice as high in men than in women. A new study published by Wiley online in CANCER, a peer-reviewed journal of the American Cancer Society, provides insights that may help to explain this disparity.
To investigate the sex difference in MM, researchers analyzed data on 850 patients with newly diagnosed MM enrolled in the Integrative Molecular And Genetic Epidemiology (IMAGE) study at the University of Alabama at Birmingham.
Compared with female patients, male patients were more likely to have advanced (International Staging System stage III) disease at the time of diagnosis. Males were also more likely to have high myeloma load—serum monoclonal protein (an abnormal protein produced by cancerous blood cells), more organ failure (especially kidney failure), and bone damage. Men were less likely than women to have low bone mineral density, and myeloma-defining features tended to differ between the two sexes. These differences were apparent even after taking numerous factors into account – including race, age, body mass index, education, income, smoking, and alcohol use.
Analyses suggested that certain chromosomal abnormalities that lead to initiation of myeloma occurring more often in younger males may help to explain some of the differences seen in this study.
“This research suggests that sex-specific mechanisms promote multiple myeloma pathogenesis, which may account for the excess risk seen in men,” said lead author Krystle L. Ong, PhD, of the O’Neal Comprehensive Cancer Center at the University of Alabama at Birmingham. “These findings may be used to improve risk stratification, diagnosis, and tailored treatments for both men and women with newly diagnosed multiple myeloma or related early precursor conditions.”
