Discovery could lead to mRNA therapeutic to reduce the risk of cardiac damage
Graphical Abstract summarising the key findings of the paper. The authors found that severe influenza damages the heart by exploiting a specific immune cells and engaging a type-I interferon response. The authors also show that therapeutic silencing of the response mitigates heart damage.
Researchers at Mount Sinai in the US have identified a cellular mechanism linking infections from influenza A viruses (IAVs) to cardiovascular disease, providing critical insights on how influenza can damage the heart and increase the risk of a heart attack or other major cardiovascular event.
Through its work with mouse models and human data, the team also provided evidence that a cutting-edge modified mRNA treatment that dampens an interferon signalling pathway in the heart can significantly mitigate cardiac damage following viral infection while preserving the protective antiviral response of the immune system. The study was published in the February 9 issue of Immunity.
“We have known for years that the frequency of heart attacks increases during flu season, yet outside of clinical intuition, scant evidence exists of the underlying mechanisms of that phenomenon,” says senior author Filip Swirski, PhD, Director of the Cardiovascular Research Institute at the Icahn School of Medicine at Mount Sinai.
“Studies like ours are now shedding valuable light on immune system pathways, like the antiviral cytokine type 1 interferon (IFN-1), that factor into damage to the heart following severe influenza infection. These findings offer great promise for the development of new therapies, which are desperately needed since there are currently no viable clinical options to prevent cardiac damage.”
Influenza A viruses are responsible for an estimated 1 billion infections globally each year, ranging from seasonal flu outbreaks locally to pandemics globally. While most infections are mild and self-resolving, in some cases they can become severe or even fatal, particularly when the virus travels to the heart and triggers the death of cardiomyocytes, specialized muscle cells that are responsible for the rhythmic contraction and relaxation of the heart.
The Mount Sinai team studied autopsies of 35 hospitalised patients who died of influenza and found that more than 85% had at least one significant cardiovascular comorbidity, such as hypertension, and that the majority had multiple comorbidities, including atherosclerosis and cardiac fibrosis, underscoring cardiovascular disease as a major driver of influenza mortality.
The research team also uncovered the mechanism by which cardiac damage occurs. They learned, for example, that a novel subset of white blood cells, known as pro-dendritic cell 3, becomes infected in the lung and, after traveling to the heart, produces large amounts of type 1 interferon. This, instead of fulfilling its mission of clearing the virus from the heart, triggers the death of cardiomyocytes, impairing cardiac output.
“We found that the pro-dendritic cell 3 acts as the ‘Trojan horse’ of the immune system during influenza infection, becoming infected in the lung, trafficking the virus to the heart, and disseminating it to cardiomyocytes. This process causes production of the damaging type 1 interferon that comes with considerable collateral damage to the heart,” explains Jeffrey Downey, PhD, a member of Dr Swirski’s laboratory who served as lead author of the study. “The hopeful news for patients is that by injecting a novel mod-RNA therapeutic that modulates the IFN-1 signaling pathway, we reduced levels of cardiac damage, as evidenced by lower troponin, and improved cardiac function, as measured by higher left ventricular ejection fraction.”
As part of its ongoing research, Dr Swirski’s team is collaborating with Lior Zangi, PhD, Associate Professor of Medicine (Cardiology), and Genetics and Genomic Sciences, at the Icahn school of Medicine at Mount Sinai, to investigate the use of a safe and effective systemic delivery method of the mod-RNA therapeutic to the heart’s muscle cells, instead of the direct injection method used in its proof-of-concept study. Additional work is focused on the pro-dendritic cell 3 itself: why is it so susceptible to influenza and how could its protective capacity be fully harnessed to potentially minimize heart damage exacerbated by cardiovascular disease?
“Pathogens are constantly emerging and evolving, which means our strategies to combat them must evolve as well,” says Dr Swirski. “Better understanding of influenza pathogenesis and immune pathways that are activated throughout the body will help fuel the next stage of advanced care.”
Researchers at the Icahn School of Medicine at Mount Sinai, in collaboration with other leading institutions across the country, have published an innovative study that provides radiation oncologists with practical guidance to identify and protect female sexual organs during pelvic cancer treatment.
Published in the latest issue of Practical Radiation Oncology, this study addresses a long-standing gap in cancer care by bringing key female sexual anatomy into consideration during routine radiotherapy planning and survivorship research.
The study, “Getting c-literate: Bulboclitoris functional anatomy and its implications for radiotherapy,” synthesises current scientific knowledge and pairs it with original anatomic dissection, histology, and advanced imaging analysis. The work focuses on the bulboclitoris, a female erectile organ (consisting of the clitoris and the vestibular bulbs) that plays a central role in sexual arousal and orgasm and can be exposed to radiation during treatment for pelvic cancers.
“Pelvic radiotherapy can be life-saving, but it can also affect sexual function and quality of life,” said Deborah Marshall, MD, MAS, Assistant Professor, Departments of Radiation Oncology and Population Health Science and Policy at the Icahn School of Medicine at Mount Sinai; Division Chief of Women’s Health, Department of Population Health Science and Policy; and senior author of the study. “Compared to male sexual anatomy, female erectile structures have been largely invisible in standard radiation workflows. Our goal was to provide clinicians with a practical anatomy-grounded way to change that.”
Using detailed anatomic and radiologic correlation, the research team demonstrates how the bulboclitoris and related neurovascular structures can be identified on standard CT and MRI scans and consistently outlined (or “contoured”) for radiotherapy planning. This step-by-step guidance makes it feasible for clinicians to measure radiation dose to these tissues and begin linking exposure to patient-reported outcomes related to arousal and orgasm.
“This work builds upon our previous knowledge that the clitoris is not just an external structure,” Dr. Marshall said. “It includes an entire internal organ comprised of erectile tissues located just outside the pelvis, and those tissues matter for sexual health and, in particular, for female sexual pleasure. Once clinicians can reliably see and measure them, we can begin to ask better questions, have better conversations with patients, and ultimately deliver better care.”
Sexual function outcomes after pelvic radiotherapy have historically been understudied in women, limiting counselling, toxicity prevention strategies, and equitable survivorship care. By establishing a shared, standardised approach to identifying the bulboclitoris, the study lays the groundwork for future research to develop dose-volume constraints and mitigation strategies, as other organs at risk are managed in radiation oncology.
For clinicians, the framework enables routine contouring and dose reporting using CT alone when necessary, with MRI improving soft-tissue visualization when available. In the absence of prospective dose-response data, the authors recommend minimising radiation dose to the bulboclitoris when oncologically appropriate, using an “as low as reasonably achievable” approach.
For patients, the work supports more informed conversations about potential sexual side effects of pelvic radiotherapy, including changes in arousal, sensation, orgasm, lubrication, or pain. This research also promotes more personalized treatment planning that considers female sexual health and pleasure as a legitimate and important component of cancer survivorship.
Next steps include prospective research through Mount Sinai’s STAR program, deeper mapping of neurovascular anatomy relevant to sexual function, expanded educational resources for oncology and radiology teams, and improved patient-reported outcome measures that reflect diverse sexual practices and experiences.
Gliobastoma (astrocytoma) WHO grade IV – MRI sagittal view, post contrast. 15 year old boy. Credit: Christaras A.
The brain and spinal cord is made up of billions of neurons connected by synapses and managed and modified by glial cells. When neurons die, this communication network is disrupted and since this loss is irreversible, neuron death causes sensory loss, motor impairment and cognitive decline.
An interdisciplinary team of researchers from the University of Notre Dame is investigating the mechanisms of neuron death caused by chronic compression – such as the pressure exerted by a brain tumour – to better understand how to prevent neuron loss.
Published in the Proceedings of the National Academy of Sciences, their study found that chronic compression triggers neuron death by a variety of mechanisms, both directly and indirectly. The research is helping lay the groundwork for identifying therapies to prevent indirect neuron death.
“The impetus for this project was to figure out those underlying mechanisms. In cancer research, most researchers are focused on the tumour itself, but in the meantime, while the tumour is sitting there and growing, it’s damaging the organ that it’s living in,” said Meenal Datta, the Jane Scoelch DeFlorio Collegiate Professor of Aerospace and Mechanical Engineering at Notre Dame and co-lead author of the study. “We fully believe that these growth-induced mechanical forces of the tumor as it expands is part of the reason we see damage in the brain.”
As an engineer who leads the TIME Lab, Datta studies the mechanics of tumors and the microenvironment, specifically for glioblastoma, an incurable brain cancer. She had found in prior work that tumors damage the surrounding brain. But to understand the mechanisms by which tumors kill neurons from compression alone, Datta needed a “hardcore neuroscientist.”
Imaging of neurons from an experiment with the control group neurons on the left and the neurons impact by chronic compression on the right. (Provided by the Patzke lab.)
That neuroscientist is Christopher Patzke, the John M. and Mary Jo Boler Assistant Professor in the Department of Biological Sciences at Notre Dame and co-lead author of the study. Patzke utilises induced pluripotent stem cells (iPSCs), which are either obtained from external sources or generated directly in his lab. These cells function like embryonic stem cells and can be differentiated or changed in the lab into any cell type in the body, including neurons.
For this study, iPSCs were used to create neural cells and develop a model system of neurons and glial cells that behave as a neuronal network would in the brain. Researchers grew the cells and then applied pressure to the system to mimic the chronic compression of a glioblastoma tumour.
After compressing the cells, graduate students Maksym Zarodniuk and Anna Wenninger, from Datta and Patzke’s labs respectively, compared how many neurons and glial cells died versus lived.
“For the neurons that are still alive, many of them have this programmed self-destruction signaling activated,” Patzke said. “We wanted to understand which molecular pathway was responsible for this; is there a way to save neurons from going down the drain to this cell death mechanism?”
By sequencing and analysing all messenger RNA from the living neuronal and glial cells, the researchers found an increase in HIF-1 molecules, signalling for stress adaptive genes to improve cell survival, which leads to inflammation in the brain. The compression also triggered AP-1 gene expression, a type of neuroinflammatory response.
Both neurological reactions are indicators that neuronal damage and death is underway.
An analysis of data from the Ivy Glioblastoma Atlas Project shows that glioblastoma patients also reflect these compressive stress patterns and gene expression changes as well as synaptic dysfunction in line with the experiment’s results. The researchers confirmed these results by mimicking force via a live compression system applied to preclinical models of brains.
Overall, the findings may help explain why glioblastoma patients experience cognitive impairments, motor deficits and elevated seizure risk. Additionally, the signalling pathways offer opportunities for researchers to explore as drug targets to reduce neuronal death.
“Our approach to this study was disease agnostic, so our research could potentially extend to other brain pathologies that affect mechanical forces in the brain such as traumatic brain injury,” Datta said. “I’m all in on mechanics. Whatever it is that you’re interested in when it comes to cancer, above your question of interest, mechanics is sitting there and many don’t even know they should be considering it.”
The mechanics of compression and its effect on neuron loss is key for future research.
“Understanding why neurons are so vulnerable and die upon compression is critical to prevent excessive sensory loss, motor impairment and cognitive decline,” Patzke said. “This is how we will help patients.”
Just over one in 10 deaths from a wide range of infectious diseases are associated with obesity worldwide, finds a major new study led by a UCL researcher.
People with obesity face a 70% higher risk of hospitalisation or death from an infection than those of a healthy weight, suggest the findings published in The Lancet.
Obesity is linked to an increase in the risk posed by many different infectious diseases, from flu and COVID to stomach bugs and urinary tract infections, and the researchers found that the higher the BMI, the greater the risk.
The study’s lead author, Professor Mika Kivimaki (UCL Faculty of Brain Sciences), said: “Obesity is well known as a risk factor for metabolic syndrome, diabetes, cardiovascular disease, and many other chronic conditions. Here we have found robust evidence that obesity is also linked to worse outcomes from infectious diseases, as becoming very ill from an infection is markedly more common among people with obesity.”
The researchers studied data from over 540 000 people who participate in large cohort studies in the UK (the UK Biobank dataset) and Finland, to look at the relationship between obesity and severe infectious disease. Participants had their body mass index (BMI) assessed when they entered the studies and were then followed up for an average of 13-14 years.
The researchers found that people with obesity (defined as a BMI of 30 or higher) had a 70% higher risk of hospitalisation or death from any infectious disease in the study period compared to people with a BMI between 18.5 to 24.9 (classified as a healthy weight).
The risk increased steadily as body weight increased. People with a BMI of 40 or higher had three times the severe infection risk compared to people with a healthy weight.
The link between obesity and severe infections was consistent regardless of the measure of obesity used (BMI, waist circumference, or waist-to-height ratio, where data was available) and for a wide range of infection types.
The study included data on 925 bacterial, viral, parasitic, and fungal infectious diseases, and the authors also honed in on 10 common infectious diseases in more detail. For most of these diseases, including flu, Covid-19, pneumonia, gastroenteritis, urinary tract infections, and lower respiratory tract infections, they found that people with obesity were more likely to be hospitalised or die than people with a healthy BMI. However, obesity did not appear to increase the risk of severe HIV or tuberculosis.
The analysis found that the link to severe infections was not explained by obesity-related chronic conditions, as the association was consistent in people with obesity who did not have metabolic syndrome, diabetes, or heart disease, while the association was also not explained by lifestyle factors such as physical activity.
While the study did not investigate the causes of the association, the researchers say that previous studies have suggested that obesity contributes to a general impairment of immune function, including immune dysregulation, chronic systemic inflammation, and metabolic disturbances.
Professor Kivimaki said: “Our findings suggest that obesity weakens the body’s defences against infections, resulting in more serious diseases. People may not get infected more easily, but recovery from infection is clearly harder.”
The researchers found evidence that losing weight can reduce the risk of severe infections as people with obesity who lost weight had a roughly 20% lower risk of severe infections than those who remained obese.
First author Dr Solja Nyberg (University of Helsinki) commented: “As obesity rates are expected to rise globally, so will the number of deaths and hospitalisations from infectious diseases linked to obesity.
“To reduce the risk of severe infections, as well as other health issues linked with obesity, there is an urgent need for policies that help people stay healthy and support weight loss, such as access to affordable healthy food and opportunities for physical activity. Furthermore, if someone has obesity, it is especially important to keep their recommended vaccinations up to date.”
The authors used infectious disease mortality data from the Global Burden of Diseases (GBD) Study to model the impact of obesity on infectious disease deaths for different countries, regions and globally.
The analysis suggested 0.6 million out of 5.4 million (10.8% or one in 10) infectious diseases deaths globally were linked with obesity in 2023.
The researchers estimated that in the UK, one in six (17%) infection-related deaths can be attributable to obesity, and 26% in the US.
Co-author Dr Sara Ahmadi-Abhari (Imperial College London), who conducted the Global Burden of Diseases (GBD) analyses, said: “Estimates of the global impact give a sense of how large the problem may be, but they should be interpreted with caution. Data on infection-related deaths and obesity in the GBD are not always accurate, particularly in low-resource countries.”
It has long been known that heart attacks occurring in the morning are typically more serious than those that happen at night. While daily variations in stress hormone levels and blood pressure affect cardiac health, these are only part of the picture. There is also the diurnal variation in immune response involved: neutrophils, the body’s ‘first responders’, cause more inflammatory damage in the morning, causing havoc even as they neutralise pathogens.
“They’re the first sentinel, but they come fully loaded,” said Douglas Mann, MD, professor at Washington University School of Medicine in St Louis. “They’re shooting at everything and dumping a lot of toxic granules on the environment. They are indiscriminate in terms of their ability to destroy, and they take out healthy cells in the process.”
But exactly why they are more damaging at night has been a mystery. Now, researchers have found the reason behind this diurnal difference in destructiveness, and also how to tweak the ‘internal clocks’ of these white blood cells so that they cause less damage during sterile inflammation while still protecting against pathogens. Their findings are reported in the Journal of Exploratory Medicine, and are summarised in JAMA news.
Finding the pattern
The researchers, from Spain and Yale University, discovered that the timing of heart attacks significantly affects their severity due to a ‘neutrophil clock’ controlled by circadian rhythms. Neutrophils are more active during the day (activated by the Bmal1 protein) and less active at night (inhibited by the CXCR4 receptor).
Analysing more than 2000 patients with ST-segment elevation myocardial infarction, the researchers found that those who had an MI in the morning suffered worse cardiac damage than those who had them at night. Mouse experiments confirmed this pattern and showed that genetically disabling the Bmal1 protein reduced daytime neutrophil activity, protecting against severe cardiac injury.
This suggests a treatment strategy of tricking neutrophils into remaining in their nighttime inactive state, allowing doctors to reduce inflammation and lessen heart attack damage during daytime hours without compromising the immune system’s ability to fight infections.
Reducing cardiac damage without compromising the immune system
Mice engineered to have high levels of CXCR4 were given a drug compound, ATI2341, which bound to CXCR4 receptors. When heart attacks were induced, the mice showed reduced tissue damage. To test the neutrophils’ pathogen-fighting ability, they were also infected with Staphylococcus aureus or Candida albicans, but the mice were able to overcome the infection – the treated mice even tolerated the Candida infection better than the controls.
Mann explained why controlling the neutrophils was a better option. “Prior trials have tried to neutralise neutrophils or reduce neutrophil numbers entirely,” Mann noted. “But when you get rid of neutrophils, you’re also handcuffing the immune system. Before, it was considered an inevitability that neutrophils killing off infection also meant damaging a lot of tissue.”
The crucial question is of course whether this research in mice can translate to humans.
Luigi Adamo, MD, PhD, director of cardiac immunology at Johns Hopkins University who was not involved in the study, said that the study, one of the first use immune circadian rhythms to modulate inflammation, “offers new insight into neutrophils and a new way to look at this cardiac damage that might even apply to other types of sterile inflammation.”
Adamo struck a note of caution: the extremely low success rate in animal-to-human translation in cardioimmunology. “Immune cells are not always the same when you go from mice to humans,” he said.
Treatment implementation is a major obstacle
Even if this neutrophil clock alteration could be applied to humans, it would be difficult to administer since heart attacks strike without warning.
“If everyone took one of these drugs in the morning when they woke up, maybe it would make heart attacks less severe, but ‘preventive’ means you’re giving it chronically, and I don’t know what would happen with long-term stimulation of that receptor and other cell types,” Mann said. “Their data support the acute application, but in the long term, that’s a whole different story.”
As systemic treatment, the off-target effects of ATI2341 would need to be explored. He also struggled to envision a potential therapeutic solution.
“Today, when you have a heart attack, in most places with hospitals and well-developed health care systems, the patient gets an angioplasty,” Mann said. “The only time this drug could be given would be at the time of reperfusion, when you’re blowing up the balloon and opening up the clot.” Typically, ideal reperfusion timing is within two hours – but neutrophils probably do their damage within a matter of 30 minutes, Mann explained. “It’s a race against time, and I’m curious if [the researchers] can demonstrate that.”
The newly launched, first of its kind, EthiQal Recognition Programme strives to acknowledge professional conduct that reflects a commitment to the delivery of excellent patient care and the reduction of medicolegal risk.
It is aimed at specialist clinicians in private practice and is based on a point system where defined activities qualify for set points that over time convert to premium refunds.
The Programme underpins EthiQal’s pledge to promoting high-quality healthcare, supporting practitioners in building successful, safe practices and managing their medicolegal risk, and aligning individual practitioners’ professional indemnity premiums with their unique insurance risk.
How the Programme works and which activities qualify for point collection are outlined in the Recognition Programme Benefit Guide, with the formal details of the Programme defined in the Terms and Conditions and Benefit Rules documents, which can all be viewed on the EthiQal website: https://ethiqal.co.za/
For more information about EthiQal, click here [https://ethiqal.co.za/contact/] complete the form, and an Advisor will call you back.
Credit: Darryl Leja National Human Genome Research Institute National Institutes Of Health
Because treatment of the whole prostate can lead to long-term side effects in patients with prostate cancer, interest in minimally invasive, focal treatment options has been growing for certain patients. A clinical trial published in BJU International generated promising results for a type of focal therapy, which directly targets the cancer and spares the remainder of the unaffected prostate gland.
The ProFocal Laser Therapy for Prostate Tissue Ablation (PFLT-PC) trial is the first pivotal trial of ProFocal®, a novel, cooled laser focal therapy device for prostate cancer treatment.
In the 100-participant trial, 84% of patients had no clinically significant prostate cancer on their 3-month post-treatment biopsy. The treatment provided similar cancer-related outcomes to those that have been reported for other focal therapy devices, but with an improved safety profile and low rates of incontinence.
“This new technology is very promising with excellent cancer control while preserving patients’ quality of life,” said corresponding author Jonathan Kam, MD, of Nepean Hospital, in Australia. “Traditional radical prostatectomy and radiotherapy for prostate cancer results in very high rates of incontinence and erectile dysfunction. With this new technology, patients can have their prostate cancer treated with very low risk of suffering the side effects associated with traditional prostate cancer treatments.”
Mouse brain section highlights amyloid plaques, seen as bright green flecks (due to staining). Credit: Shipley et al.
Memory dysfunction in Alzheimer’s disease may be linked to impairment in how the brain replays our recent experiences while we are resting, according to a new study in mice by UCL scientists. The researchers say their findings, published in Current Biology, could help scientists develop drug treatments targeting this impaired brain function, or help design new tests for early diagnosis.
Co-lead author Dr Sarah Shipley (UCL Cell & Developmental Biology) said: “Alzheimer’s disease is caused by the build-up of harmful proteins and plaques in the brain, leading to symptoms such as memory loss and impaired navigation – but it’s not well understood exactly how these plaques disrupt normal brain processes.
“We wanted to understand how the function of brain cells changes as the disease develops, to identify what’s driving these symptoms.
“When we rest, our brains normally replay recent experiences – this is thought to be key to how memories are formed and maintained. We found this replay process is disrupted in mice engineered to develop the amyloid plaques characteristic of Alzheimer’s, and this disruption is associated with how badly animals perform on memory tasks.”
The replay process, which occurs in the brain’s hippocampus, involves place cells firing in rapid sequences during rest. Place cells – discovered by Nobel prize-winning UCL neuroscientist Professor John O’Keefe – are neurons (brain cells) that represent specific locations. When we visit somewhere, particular place cells fire, and as we move the cells fire in a sequence. Later, when we rest, these cells reactivate in the same sequence, helping memories become ingrained.
For the study, the researchers were testing how well mice performed in a simple maze task, while monitoring their brain activity with sets of electrodes that could simultaneously track roughly 100 individual place cells.
In mice with amyloid pathology, the replay process was fundamentally altered. Surprisingly, replay events occurred just as frequently as in healthy mice, but their structure was disorganised. The normal, coordinated patterns of place cell activity that should reinforce memories were scrambled. The researchers also found that place cells in affected mice became less stable over time, with individual neurons no longer reliably coding the same locations, particularly after rest periods – precisely when replay should be strengthening these representations.
This disruption had consequences on memory tasks: affected mice performed worse in the maze, appearing to forget where they had already been and revisiting corridors that led nowhere.
Co-lead author Professor Caswell Barry (UCL Cell & Developmental Biology) said: “We’ve uncovered a breakdown in how the brain consolidates memories, visible at the level of individual neurons. What’s striking is that replay events still occur – but they’ve lost their normal structure. It’s not that the brain stops trying to consolidate memories; the process itself has gone wrong.
“We hope our findings could help develop tests to detect Alzheimer’s early, before extensive damage has occurred, or lead to new treatments targeting this replay process. We’re now investigating whether we can manipulate replay through the neurotransmitter acetylcholine, which is already targeted by drugs used to treat Alzheimer’s symptoms. By understanding the mechanism better, we hope to make such treatments more effective.”
Following a Mediterranean diet is associated with a lower risk of all types of stroke among women, according to a study published on February 4, 2026, in Neurology® Open Access, an official journal of the American Academy of Neurology. The study does not prove that the Mediterranean diet is the cause of the lower risk of stroke; it only shows an association.
The diet was associated with a lower risk of stroke overall, as well as ischaemic stroke and haemorrhagic stroke. The Mediterranean diet includes a high intake of vegetables, legumes, fruits, fish and healthy fats such as olive oil, and a low intake of dairy products, meats and saturated fatty acids.
“Our findings support the mounting evidence that a healthy diet is critical to stroke prevention,” said study author Sophia S. Wang, PhD, of City of Hope Comprehensive Cancer Center in Duarte, California. “We were especially interested to see that this finding applies to haemorrhagic stroke, as few large studies have looked at this type of stroke.”
The study involved 105 614 women with an average age of 53 at the start of the study who had no history of stroke. The participants filled out a questionnaire at the start of the study about their diet. Participants were given a score of zero to nine based on how closely they followed the Mediterranean diet. People received one point if they consumed above the overall average in the population in these categories: whole grain cereals, fruits, vegetables, legumes, olive oil and fish, plus drinking a moderate amount of alcohol.
They also received one point if they consumed a below-average amount of red meat and dairy products. A total of 30% of participants had scores of six to nine – the highest group. And 13% had scores of zero to two, the lowest group.
The participants were followed for an average of 21 years. During that time, 4083 strokes occurred, with 3358 ischaemic strokes and 725 haemorrhagic strokes. For ischaemic strokes, there were 1058 among the 31 638 people in the highest group compared to 395 cases among the 13 204 people in the lowest group.
For haemorrhagic stroke, there were 211 strokes among those in the highest group, compared to 91 among the lowest group. When researchers adjusted for other factors that could affect stroke risk, such as smoking, physical activity and high blood pressure, they found that those in the highest group were 18% less likely to have a stroke than those in the lowest group. They were 16% less likely to have an ischaemic stroke and 25% less likely to have a haemorrhagic stroke.
“Stroke is a leading cause of death and disability, so it’s exciting to think that improving our diets could lessen our risk for this devastating disease,” said Wang. “Further studies are needed to confirm these findings and to help us understand the mechanisms behind them so we could identify new ways to prevent stroke.”
A limitation of the study is that people reported their own diet information, so they may not have remembered correctly.
Under South African law, no one may practise medicine unless they have the proper training and are officially registered. Photo by Usman Yousaf on Unsplash
By Elna Schütz
Bogus medical practitioners threaten the health of patients and undermine trust in doctors. The problem might be growing, but so is the fight against it.
“If you’re in the hands of an unqualified person, you’re as well as dead, and we think it is not fair for the country,” Dr Magome Masike tells Spotlight.
He is the Registrar of the Health Professions Council of South Africa (HPCSA), which is responsible for the registration of medical doctors and other health professionals in South Africa.
The controversy over bogus doctors gained widespread attention in late 2023 when it was discovered that ‘TikTok doctor’ Matthew Lani lied about being a medical doctor. In his videos, Lani was often seen in scrubs and wearing a stethoscope, impersonating a medical doctor. Although he was arrested at Helen Joseph Hospital in Johannesburg, the National Prosecuting Authority eventually decided not to prosecute.
The term bogus doctor has become a shorthand for any medical practitioner who is working without being properly qualified or registered by the HPCSA. In practice, being “bogus” can also apply to physiotherapists, interns, or anyone else practising medicine.
The misrepresentation may include using fraudulent certificates, using another practitioner’s registration, or being suspended or erased from the register. It can involve someone who studied but did not fully qualify, or has not kept up to date with their registration. Masike gives the example of the child of a registered practitioner who decides to take on their parent’s practice after their death without themselves being registered.
It is an ongoing problem. In the beginning of February, the HPCSA says it facilitated the arrest of a woman working at a medical facility in Midrand, north of Johannesburg, allegedly without being correctly registered to practice medicine.
Bogus qualifications are part of the larger problem of healthcare fraud. According to research in a report by risk management services firm D-Finitive, it is estimated that this fraud overall costs African countries more than USD50 billion in 2012. In the South African private sector, that comes to about R22-28 billion a year. The report explains that beyond bogus practitioners, there is a problem with similar fraud, like doctors billing more clients than is realistic, manipulating diagnostic and procedural codes, or deceased doctors billing the government for decades after their death. At times, this type of fraud is reportedly executed by syndicates.
“While the majority of practitioners are honest and committed to patient care, it takes only a small number of bad actors, whether unregistered impostors or credentialed professionals abusing the system, to inflict widespread damage,” says Dr Katlego Mothudi, Managing Director of the Board of Healthcare Funders (BHF).
A substantial problem
Masike says that from March 2024 to February 2025, 49 bogus practitioners were caught and arrested. From April to December 2025, that number was at 17. Even though these numbers do not suggest a year-on-year increase, Masike says that overall, the numbers are increasing.
The HPCSA’s annual report for 2024/2025 shows that 589 investigations into unregistered persons were concluded in the year in question. Over the past five years, 3 708 complaints were received.
The majority of bogus practitioners who have been caught were operating in economic hubs of the Western Cape, Gauteng, and KwaZulu-Natal, Masike says. “Bogus people want money, so they go where there’s money,” he explains. However, while the trend tends urban, he says rural communities also fall prey to scammers.
“A notable pattern is that many of these individuals use or forge the details of legitimately registered practitioners,” Masike says.
It is, of course, unclear how many unlicensed practitioners are not yet caught. “We can tell you the problem is bigger than we think,” Masike says. The problem, he says, is sector-wide and stretches across different health professions, with most of these illegal practices occurring in the private sector. Masike adds that bogus doctors often work with a network of others, for example, those who supply unregistered or fake medicines.
Mothudi also says that the problem is growing. “Medical schemes are seeing a rise in suspicious provider activity picked up through claims analysis and credential verification processes,” he says. This may include practitioners misrepresenting their registration status, practising outside their approved scope, or using the registration details of legitimate practitioners to submit claims.
Risk to patients
Catching and prosecuting bogus practitioners is crucial because they can pose a direct danger to unsuspecting patients. “Unregistered medical doctors, like other health professionals, pose severe risks to patients, including serious physical harm, injury, and misdiagnosis which may lead to death, due to their lack of necessary training, ethical standards and relevant qualifications,” warns Foster Mohale, the spokesperson for the National Department of Health.
Dr Zanele Bikitsha, National Vice Chairperson of the South African Medical Association, cautions that if bogus doctors are performing procedures, it will likely be in settings that are not appropriate or sterile.
“They’re not going to go to a registered facility, because they know they’ll be caught, so this puts patients in danger as well.”
While some operate on a cash basis, Mothudi says that submitting claims to medical schemes is attractive because it allows for much larger and repeatable payouts. “In some cases, bogus practitioners submit claims using stolen, borrowed or fraudulently obtained practice numbers belonging to legitimately registered healthcare professionals,” he says. “In other instances, they collude with registered providers who allow their credentials to be misused in exchange for payment.”
Knowing the signs
While the HPCSA undertakes compliance inspections, there are some clear signs that might help the public spot a bogus practitioner. Firstly, it is a legal requirement to have registration information easily visible in a practitioner’s practice and on the letterhead of documents or prescription notes.
Members of the public can also look up a doctor’s credentials. All registered practitioners should be listed in the HPCSA’s digital register online, which is publicly searchable. With as little as the practitioner’s surname, the system lets users search for registered practitioners.
Masike points out that a trained doctor tends to take an extensive medical history and make a systemic or wide-reaching inquiry. He recommends that patients look out for how doctors speak and whether they use and are able to explain medical terminology.
Complaints can be filed with the HPCSA’s Inspectorate, including anonymously. Their call centre is at 0123389300/1 and they can be e-mailed at office@hpcsa.co.za. Suspicious practitioners may also be reported to hospitals, the Department of Health, SAMA or other medical organisations.
Processing the problem
Complaints typically lead to an investigation by the HPCSA Inspectorate, which works together with other entities, such as the South African Health Products Regulatory Authority (SAHPRA), the Office of Health Standards Compliance, the Special Investigating Unit (SIU), and the South African Police Service.
Masike explains that the investigation tends to lead to a clandestine operation and involves the police arresting the suspects. He adds that police recently assigned specific staff members to focus on these cases. He says that once the case goes to court, there is a conviction rate of around 77%, although this may have changed. “Many of the cases from 2023 to 2025 remain before the courts, and therefore updated conviction statistics are not yet available.”
Practising medicine without proper training and registration is in contravention of Section 17(1) of the Health Professions Act, 56 of 1974. Typical sentences for such fraud include fines, such as R12 000, or around two years imprisonment. In one 2017 case, a man who had treated almost a thousand patients over six years was sentenced to 20 years’ imprisonment by the Mahikeng High Court in the North West.
Bikitsha says there are other systemic changes that could help catch the problem earlier on. “If you are still paper-based, you are at risk,” she says, referring to the way that hospitals and institutes tend to verify the qualifications of most interns, locums and medical practitioners. She argues that upgrading to biometrics and digital systems would decrease the risk of fraud.
Another step forward is simply to increase public awareness and education, so that patients know the risks.
Masike concurs. “We need society to stand up to this,” he says. “We need a participating community to get rid of this malaise, otherwise it will continue forever.”
