In an Arthritis & Rheumatology analysis of data on 60 980 US adults with autoimmune rheumatic conditions who developed COVID between December 2020 and August 2024, those who received booster or updated (2023-2024) COVID vaccines were less likely to be hospitalised for COVID compared to those who received only the initial series vaccines or who were unvaccinated.
Compared with no vaccination, completion of the initial series, booster vaccination, and updated vaccination were associated with 41%, 71%, and 69% lower adjusted odds of COVID-related hospitalisation, respectively. Among patients who had received only the initial vaccine series versus booster/updated vaccine, the absolute risk reduction was 5.6%.
“Our findings provide important real-world evidence that updated vaccines continue to offer substantial protection in this medically vulnerable population,” said corresponding author Maria I. Danila, MD, MSc, MSPH, of the University of Alabama at Birmingham. “These results underscore the need for continued efforts by clinicians, policymakers, and patient advocacy groups to help ensure that these patients remain current with updated COVID vaccines,” added first author Lesley E. Jackson, MD, MSPH, also of the University of Alabama at Birmingham.
Exposure to light during the nighttime is linked to important and potentially harmful changes to the structure and function of the heart, according to a study of more than 11 000 people published in the European Heart Journal today (Thursday).
The research was led by Professor Lu Qi from Tulane University, New Orleans, USA. He said: “Previous observational studies have linked nighttime light exposure with a higher risk of cardiovascular disease, but little is known about the related cardiac structure and functional changes. We carried out this research to find out what happens to the heart over time when people are exposed to too much light at nighttime.”
The research included 11 071 people who are part of the UK Biobank study. All participants wore a light sensor on their wrists for seven days to measure light levels over night. Three years later, participants were given a cardiac MRI scan to carefully examine the structures and functions of the heart.
Researchers compared people who were exposed to light levels of more than three lux with people exposed to almost no light at night.
This showed that people with high exposure to nighttime light had thickening of the wall of the left ventricle (one of the chambers of the heart), reducing the space inside of the chamber. There were signs that the heart muscle’s ability to flex during a heartbeat was reduced. This is an early indicator of heart dysfunction. Researchers also found changes in the right ventricles and left atria (two other chambers of the heart).
Professor Qi said: “This is the first study of its kind, and it shows that exposure to higher levels of light at nighttime is linked to cardiac remodelling. This is where the structure and function of the heart changes and we typically see it in response to chronic stress or injury to the heart. It’s our body’s way of adapting to that stress, but ultimately it weakens the heart and can lead to heart failure.
“Light pollution has emerged as a new risk factor for cardiovascular disease. Our findings, together with evidence from other studies, suggest that reduction of nighttime light exposure should be considered as one of the potential strategies for preventing heart disease by clinicians and policy makers.”
In an accompanying editorial Professor Thomas Münzel from University Medical Center Mainz, Germany and colleagues said: “It is time for clinicians, particularly those managing patients with heart failure or atrial fibrillation, to start asking about the sleep environment: how dark the bedroom is, whether the patient works night shifts, and how much screen use occurs after sunset. The advice is simple and inexpensive: blackout curtains, warm-coloured bedside lighting, and covering the small standby LEDs on household electronics. From a public health perspective, the implications are larger still. Light pollution is one of the few environmental hazards that cities can control directly and affordably. Shielded fixtures, warm-spectrum bulbs, and dimming or motion-activated streetlights are already available, energy-efficient, and climate-friendly.
“Ultimately, this study is more than an interesting observation. It provides a crucial link between what satellites already show us, i.e. a planet glowing ever brighter at night, and the clinical reality unfolding inside our chests: hearts that are becoming stiffer, weaker, and less efficient. The relationship is biologically coherent, the effect sizes are clinically meaningful, and the dose–response is unambiguous: more light, worse outcomes. The takeaway is clear, darkness deserves recognition as a vital sign, as essential to cardiovascular health as blood pressure control and clean air.”
When psychiatrists assess the same patient, they agree on the diagnosis in only about half of cases, according to a new study from the University of Copenhagen. The findings raise concerns about potential misdiagnosis, inappropriate treatment, and errors in psychiatric research.
In the 1970s, psychiatric diagnoses were marked by considerable uncertainty and disagreement. Since then, organisations such as the American Psychiatric Association and the World Health Organization (WHO) have worked to develop standardised diagnostic criteria that psychiatrists around the world can use.
These efforts have shaped modern psychiatry by establishing common, criteria-based systems for diagnosing mental disorders across institutions and national borders.
However, a new study, led by researchers at the University of Copenhagen, suggests that major challenges remain. In the study, 1038 psychiatrists and physicians working in psychiatry from 19 countries were presented with nine written patient case descriptions. Each participant was assigned two cases and asked to determine the most appropriate diagnosis.
The results surprised the researchers.
“Our study shows that when two psychiatrists diagnose the same patient, they will agree only 55% of the time. We consider that worryingly low. In fact, it is similar to the levels reported in some of the studies conducted in the 1970s, which prompted the development of standardised diagnostic criteria in the first place,” says Professor and Consultant Psychiatrist Julie Nordgaard.
“This is not about psychiatrists doing a poor job. Rather, it reflects the fact that, despite the existence of diagnostic systems, clinicians continue to differ in how they interpret symptoms and which features they consider most important. We need a greater degree of consensus, otherwise patients risk receiving changing diagnoses and treatments,” she adds.
Same symptoms, different diagnoses
The study found substantial variation in diagnostic agreement across different mental disorders. Diagnoses within the schizophrenia spectrum proved particularly challenging.
“Cases that could be diagnosed either as schizophrenia or schizotypal disorder generated especially high levels of disagreement. In many of these cases, agreement among participants was well below 50%,” says PhD candidate Mateo Boberg, the study’s first author.
According to Boberg, one reason is that symptoms frequently overlap across psychiatric disorders. For example, obsessive thoughts may occur in both obsessive-compulsive disorder (OCD) and schizophrenia.
“These are not random errors. There is a clear pattern to the disagreements. This likely reflects the fact that diagnostic categories are not as clearly defined as we have assumed, when experienced psychiatrists can interpret the same symptom presentations so differently.”
Diagnostic uncertainty undermines research
Disagreement about diagnoses is an obvious concern for patients. But the researchers argue that diagnostic uncertainty also threatens the reliability of some kinds of psychiatric research¸ explains Professor Mads Gram Henriksen:
“In research, it is essential that we know exactly what we are studying. If a considerable part of participants enrolled in a study on treatment of personality disorders actually suffer from schizophrenia, the study’s results become difficult to interpret. Which condition is the treatment having – or not having – an effect on? Personality disorders or schizophrenia?”
The researchers argue that progress in psychiatric research risks remaining limited until there is a clearer and more widely shared understanding of what mental disorders are and how they can be distinguished from one another. Greater diagnostic agreement, they say, is a prerequisite for the breakthroughs needed to improve patient care.
“WHO’s ICD-10 diagnostic system, which participants in the study used to assess the cases, contains more than 200 diagnoses, a complexity that may contribute to uncertainty. At the same time, many psychiatric conditions are inherently multifaceted,” says Julie Nordgaard and concludes:
“In our view, it is necessary to take a step back and develop more precise descriptions of psychiatric disorders so that clinicians can distinguish them more clearly. It may also be necessary to reduce the number of diagnostic categories.”
Modern medicine prides itself on being a universal science, built on evidence from clinical trials.
But there’s a bias in medical research. While Africa accounts for roughly 25% of the global disease burden and 19% of the global population, the continent’s people are largely invisible in some clinical trials.
The scale of the erasure is revealed in a landmark study of 2,472 randomised controlled trials globally published between 2019 and 2024.
I led this team of researchers, who scrutinised the world’s most influential medical publications to quantify African representation. They included the New England Journal of Medicine, The Lancet, the Journal of the American Medical Association, Nature Medicine, and the British Medical Journal. There were also three leading cardiovascular journals in the study: Circulation, the European Heart Journal and the Journal of the American College of Cardiology.
I am a physician-scientist working at the intersection of cardiometabolic epidemiology and biomedical data science. I also focus on large-scale population studies in Africa and data-driven cardiovascular prevention.
Randomised controlled trials are a cornerstone of evidence-based medicine. Introduced in the mid-20th century, they rigorously evaluate the safety and effectiveness of treatments by randomly assigning participants to different groups. This is done to minimise bias. Trials like these have been central to major medical breakthroughs, from cardiovascular therapies to vaccines. They continue to guide clinical decisions and the development of new treatments worldwide.
What we discovered
Our findings show a profound imbalance in the global clinical research landscape. Across the five most prestigious general medical journals, only 3.9% of trials were conducted exclusively in Africa. In cardiovascular health, the numbers drop to a statistical whisper. Of the major trials published in leading cardiology journals, just two studies (0.6%) were conducted solely on African soil.
This is a crisis of scientific accuracy. When clinical trials exclude African populations, they produce evidence that lacks “external validity”. This refers to how well the results of a study can be generalised beyond the participants. It asks whether findings from a clinical trial will still hold true when applied to different populations, settings, or real-world conditions.
Without that validity, doctors are essentially conducting unmonitored experiments on millions of patients every day.
Modern medicine cannot claim to be universal if entire populations remain invisible in the evidence base. Biology, health systems and disease patterns are not identical across the world.
The gap and why it matters
Many treatments used across the continent are based on evidence generated in non-African populations, raising concerns about their applicability.
Moreover, most Africa-based trials still focus on infectious diseases, despite the rising burden of non-communicable diseases such as cardiovascular disease.
Emerging evidence shows that genetics, environment and diet can radically alter how a body responds to a drug. It therefore makes no medical sense that an entire continent is left out of the trial net.
There’s also evidence showing that certain treatments have different safety profiles in Black patients. Diabetes and gout are just two examples. So are certain common blood pressure medications, such as angiotensin-converting enzyme (ACE) inhibitors. Research shows that they carry a three- to four-fold higher risk of severe, life-threatening side effects in people of African descent compared to other populations.
When clinical trials exclude populations, doctors are forced to extrapolate findings from one population and apply them to another.
The study also highlights a dangerous lag between global research funding and the evolving reality of African health. The new data show that nearly 76% of trials conducted exclusively in Africa focused on infectious diseases. But the continent is undergoing a massive epidemiological shift. Non-communicable diseases – heart disease, stroke, and diabetes – now account for about 38% of all deaths in many African nations.
The middle class in Africa has tripled to 300 million people from roughly 100 million people in the early 2000s. More people are now living long enough with lifestyles that increase the risk of chronic conditions such as heart disease, diabetes, and hypertension. Consequently, there is a growing need and market for long-term treatments that manage these diseases, rather than short-term therapies for infections. Yet cardiovascular trials continue to be discouraged.
Even within the continent, the data show deep “black holes” of information. South Africa accounted for over 62% of all trials conducted on the continent. Central Africa, a region that’s home to more than 180 million people, was virtually non-existent in the global research record. It contributed less than 3% of the continent’s limited trial output. Possible reasons include South Africa’s decades of cumulative investment, seen in stronger academic hubs, research governance, experienced trial units, and more established sponsor relationships. Other regions face barriers like fewer resourced research institutions, less access to trial platforms, and sometimes language and publication issues that can reduce visibility in top-tier journals.
The inequity extends into the hierarchy of science itself. Even when African sites are included in large, multicontinental trials, they are often relegated to the role of “recruitment hubs” rather than scientific partners. Our study found that African scientists led only 3.6% of multicontinental trials that included an African site.
Towards a new era of African science
Africa should not simply be a location where studies are conducted.
It must be a place where research is conceived, led and interpreted. The current model creates a cycle of external dependence where international institutions manage the funding and the data. This leaves local research systems fragile and unable to translate evidence into national policy.
There is need for “ring-fenced” funding for African-led research, the development of regional trial networks, and a mandate for medical journals to report on the diversity of trial populations.
There are signs of a rising momentum. Organisations like Alliance for Medical Research in Africa are working to equip a new generation of African investigators. Africa must create a research ecosystem that is too important for the global community to ignore.
Every day in South Africa, an estimated 23 people die by suicide, while another 460 attempt suicide.
The impact is particularly concerning among younger people. Globally, suicide is the third-leading cause of death among people aged 15 to 29, according to the World Health Organization’s (WHO) latest estimates.[1] The South African Depression and Anxiety Group (SADAG) is also seeing the extent of the need first-hand as its helplines currently receive between 2 500 and 3 000 calls a day, with around one in four serious suicide-related calls.[2]
“People are crying out for help, and the calls we receive every day show us just how many people are struggling,” says SADAG’s Operations Director Cassey Chambers. “For us to make a meaningful difference and prevent suicides, we can’t just intervene at the point of crisis. People need help recognising the warning signs to make it easier to talk openly about suicide and know where they can turn for help. We need families, friends, schools, workplaces and communities to understand that talking about suicide is crucial and that asking someone directly if they are struggling can open the door to getting them the support they need.”
Every conversation counts
This World Suicide Prevention Day (10 September), Cipla is partnering with SADAG to encourage more of these conversations before someone reaches crisis point. The initiative supports SADAG’s 2026 World Suicide Prevention Day campaign, Every Conversation Counts, which provides South Africans with practical resources to help them understand what to say, how to respond and where to find support.[3]
As part of the campaign, Cipla is introducing the Postcard Wall of Hope, an interactive activation where members of the public can write and share messages of encouragement and support for people they may never meet.
“Sometimes, a few words can mean more than we realise. The Postcard Wall* of Hope is about sharing those words while they can still reach someone, reminding them that their life matters and that it is okay to speak about how they are feeling,” says Paul Miller, CEO of Cipla Africa.
Members of the public can read a postcard, take one that speaks to them or write a message for somebody else to find.
“You don’t have to know who will eventually read your postcard or what they may be going through,” says Miller. “It could simply remind someone that they matter or encourage them to keep going and reach out. The Wall is a way of showing that our words don’t only have to come when it is too late. We can use them now to start conversations and remind people that support is available.”
When to start the conversation
SADAG advises people to take changes in a loved one’s behaviour seriously. Warning signs can include talking about death or suicide, withdrawing from loved ones, risky or self-harming behaviour, giving away personal belongings or a sudden change in mood after a period of depression.[4]
“Importantly, asking somebody directly about suicide does not increase their likelihood of attempting it. SADAG encourages people to ask directly if they are thinking about suicide, listen without judgement and encourage them to seek professional help,” adds Cassey Chambers.
Starting a conversation doesn’t mean you need to know exactly what to say or have all the answers. It can begin with noticing that somebody isn’t themselves and asking how they are really doing. “What matters is that we don’t allow our fear of saying the wrong thing to stop us from saying anything at all,” concludes Miller.
Help is available
Anyone experiencing emotional distress, or concerned about someone they know, can contact SADAG for free telephonic counselling and support:
Cipla Mental Health WhatsApp: 076 882 2775 – daily, 08:00–17:00
For more mental health and suicide-prevention resources, visit the SADAG website: https://www.sadag.org
*The Postcard wall will be launched during Mental Health month in October as malls in Cape Town, Johannesburg and Durban.
References
[1] World Health Organization (2025), *Suicide worldwide in 2021: Global health estimates*. WHO reports suicide as the third-leading cause of death globally among people aged 15–29.
[2]South African Depression and Anxiety Group (SADAG), World Suicide Prevention Day 2026 media information.
[3] South African Depression and Anxiety Group (SADAG), *Every Conversation Counts: World Suicide Prevention Day 2026*.
[4] South African Depression and Anxiety Group (SADAG), *Understanding Suicide*, suicide warning signs and guidance on supporting somebody who may be suicidal.
Ischaemic and haemorrhagic stroke. Credit: Scientific Animations CC4.0
A clot forms. Blood flow to the brain is blocked. Starved of oxygen, neurons begin to die.
This scenario, known as an ischaemic stroke, plays out in roughly 21 000 people worldwide each day, threatening long-term disability or even death. In recent years, clot-busting drugs and mechanical tools for removing them have revolutionised care.
Yet, even with the clot gone and the vessel clear, up to 50% of patients never recover neurologically. New research from CU Boulder and the University of Antwerp helps explain why.
The study, published in the journal PNAS, reveals in unprecedented detail how the brain’s own defence mechanisms against stroke can backfire, triggering additional micro-clots in minor vessels which can damage tissue long after the primary culprit is gone.
“We now have a way to explain why so many of these patients are not seeing neurological improvements,” said co-author Debanjan Mukherjee, an assistant professor of mechanical engineering at CU Boulder. “Our findings also point to a new potential target for therapeutics that could be extremely impactful for stroke patients.”
The mystery behind ‘no reflow’
Doctors have long known that removing a stroke-causing clot cannot always restore full blood flow to the brain. But why this phenomenon, known as “no reflow,” occurs has remained a mystery.
To unravel it, Mukherjee, who studies the physics of blood flow, teamed up with senior author Frederik Denorme, an assistant professor of biology at the University of Antwerp who studies, as he puts it, “life after the clot.”
“The dogma used to be that you just need to get rid of that blood clot and then all problems should be solved,” said Denorme. “We now know that is not the case.”
In fact, only about 1 in 10 surviving stroke patients recover completely after a stroke; 25% have minor impairments; and half have moderate to severe impairments.
To examine what, precisely, goes on in the brain after a clot is removed, the research team first turned to mice.
Using a technique called intravital microscopy, they observed in real time how blood flowed in the brain, and cells behaved, in the hour after mice suffering from stroke underwent endovascular thrombectomy. The procedure involves threading a tool through a blood vessel to pluck out an obstructive clot.
While blood quickly started flowing again post-procedure, the researchers were stunned to see that in many mice, it flowed haphazardly, in fits and starts, even reversing course at certain points.
“We saw it with our own eyes. Blood that was flowing left all of a sudden flowed right and vice versa,” said Denorme. “It was remarkable.”
A Jekyll and Hyde protein
An even closer look revealed that, as the brain tried to divert blood around the original obstruction, tiny clots formed where the haphazard channels converged.
To drill down on why those clots formed, Mukherjee’s FLOWLab recreated this scenario using computer simulations. In other research, his lab has recreated similar scenarios using a 3D artificial brain filled with fake blood.
These experiments implicated von Willebrand factor—a protein best known for stopping bleeding when we get a cut.
In its resting state, Mukherjee explained, von Willebrand factor is coiled up like a ball of string inside blood vessels, waiting for distress signals from the body that make it stretch out and start forming clots to stop bleeding.
In a brain experiencing a stroke, something else unfolds the ball.
“If there is some kind of fluid motion induced after the clot is removed, it can stretch out that ball into an extended thread that attracts platelets, forms new clots and blocks flow even after the original culprit clot is gone,” Mukherjee said.
Meanwhile, the study showed, the brain’s inflammatory response to stress interferes with safeguards that normally keep the protein’s clotting efforts in check, creating what the authors call “a perfect storm” of collateral damage.
Other experiments, looking at blood from stroke patients at the University of Washington in St. Louis, suggest a similar phenomenon happens in humans too.
“We are the first to really show in this hyperacute phase of stroke what is happening with these cells inside blood vessels,” said Denorme.
More research is necessary to determine why no reflow happens in some stroke patients but not others. But the study did find that stroke patients with higher blood levels of a pro-inflammatory compound called Interleukin 6 had more overactive von Willebrand factor and fared worse long-term.
The researchers envision a day when therapeutics targeting von Willebrand factor, or the inflammatory compounds that exacerbate its clotting capabilities, could be given to stroke patients alongside clot-busting drugs and surgery.
Notably, several such drugs already exist and are approved for use for other disorders.
“It’s early days. But now that we have a lead on what drives these micro-clots, we have a promising new avenue to explore for improving recovery,” said Denorme.
For years, hospitals have relied on the unpaid, unprotected labour of trainee-specialists to fill their rosters, but these doctors are reaching a breaking point.
Across South Africa’s public sector hospitals, a growing number of aspiring specialists are choosing to work for free — sometimes for years at a time — in pursuit of the coveted title.
Nearly every step of the 12 to 15 years of training required to specialise or sub-specialise can only happen in the public sector, but provincial health departments, bruised by more than a decade of austerity and graft, have few paid posts to offer.
As a result, hundreds of local doctors and hopeful specialists are stuck in a nightmarish competition to be the most impressive candidate. There are waiting lists for both paid and unpaid positions.
Once the paid positions are filled, doctors from poorer backgrounds who did not get placed are at a dead end, perpetuating historical injustices and undercutting transformation targets. “A new apartheid,” several doctors call it.
The volunteer specialists Spotlight interviewed knew they were lucky to have the option to specialise, but their stories suggest it’s a dubious privilege.
They endure the financial and emotional stress of specialising without pay for a number of reasons, passion, to take over the family practise, or, most commonly, to secure a ticket out of the public healthcare sector.
But to reach the predictable hours and high income of specialist private practise, they must first navigate a clinical wasteland left behind by years of budget cuts and mismanagement by provincial health departments.
The gruelling unpaid route to specialisation they describe crosses a financial abyss with toll gates guarded by sometimes powerful bullies and dotted with legal and professional traps that could cast a long shadow over the futures they’re working to build.
How to spot a clinical spectre
South Africa’s phantom doctors have many names; they’re called fellows, volunteers or supernumeraries, depending on the facility.
The role was originally created as part of a regional programme that allows foreign doctors to train in South African hospitals. These trainees’ salaries are covered by their home governments and they’re not guaranteed a work visa through the Department of Home Affairs or accreditation from the Health Professions Council of South Africa (HPCSA) once they are qualified. Only 3% of the 5 772 doctors added to the government’s payroll between January and May were not South African citizens.
In recent years, so many South African doctors have accepted such unpaid positions that some provincial health departments advertise such “opportunities” and plan their budgets accordingly.
Spotlight was unable to quantify South Africa’s unpaid trainee specialist workforce. Only two of the eight medical schools surveyed between April and July provided trainee data and requests for the HPCSA’s list of active training codes for specialists and sub-specialists went unanswered. A training code is a non-negotiable prerequisite for sitting specialist exit exams regardless of funding source or employment status of the trainee. When cross-referenced with provincial payroll data, such a list could help estimate the extent to which the health system relies on unpaid expertise.
Anecdotal evidence suggests however that the trend started around 2020 in the Western Cape, where many interviewees say they wouldn’t mind working for the state. These days, Gauteng and KwaZulu-Natal’s cohorts of unpaid citizen specialists appear to be increasing too.
Interviews with numerous local supernumeraries suggest they often endure toxic hierarchies, bullying and administrative neglect, but they prefer to suffer in silence, terrified that seniors will fail them in expensive tests.
Specialist exams are officially set by the Colleges of Medicine (CMSA), but there are usually only a few qualified specialist examiners for each academic circuit. So, in reality, trainees are often being examined by their own department heads or a close colleague.
Pride, debt and resentment
The cutthroat race to build a standout CV starts as soon as medical students graduate. It’s no longer enough to gain experience as a medical officer and then to apply for a job as a registrar a couple of years later, there simply aren’t enough paid positions for either.
Any job posting can draw hundreds of applications from equally qualified candidates.
The resulting competition is harsh, and requirements ever shifting and often unstated.
Naeema Govender*, an aspiring anaesthesiologist in Gauteng, says it took her a couple of failed interviews to figure out how to decode a government job ad.
Experience in intensive care and internal medicine, she says, are now de facto requirements for anyone applying for a job as an anaesthesia registrar (or trainee-specialist) whether the advert says so or not, and “anaesthesia experience” really means a minimum of two years’ experience.
In highly competitive fields such as urology, registrar candidates are now expected to have completed two out of three major specialist exams (usually written during training) before they even apply.
Pulling shifts for free ends up being a good way to get an edge over others.
After a string of unsuccessful interviews for paid jobs, Meera Patel*, another anaesthesiologist-in-training, says she accepted a supernumerary post at Steve Biko Academic Hospital in Tshwane out of sheer desperation.
“I used to tell anyone who would listen that I would never subject myself to it,” she says. The extra experience did help Patel to get a paid registrar job in the Western Cape, but it left her feeling deep resentment for having to compromise her principles and work without pay to crack the system.
In Johannesburg, Govender says she also reluctantly took an unpaid position to beef up her CV. She’s still conflicted about the exploitation she felt forced into.
“I don’t know if I should be proud or ashamed,” she tells Spotlight.
Paranormal planning
The unpaid trainee specialist workforce does little to eventually increase the number of qualified specialists available to the public at government hospitals, so private healthcare appears to be the overall winner.
Once doctors are qualified specialists, they often flee to the private sector or emigrate. This is perhaps illustrated by the fact that 30% of the 22 405 doctors employed by the state are under the age of 35.
The trend has ultimately turned the public sector clinical platform into a subsidised training ground for private healthcare, argues Bernhard Gaede, an associate professor and head of the Department of Family Medicine at the University of KwaZulu-Natal.
There also seems to be an element of privatisation-by stealth unfolding.
Trainees are increasingly being supported by foundations or private hospital groups to fill a growing niche for sub-specialists, says Marthinus Dicks, a member of the South African Medical Association’s (SAMA) subcommittee for registrars.
At the Groote Schuur Hospital unit where Dicks is training to be a clinical haematologist, he says he’s one of only two who are paid a government salary. He also logged unpaid hours before he was offered a paid post.
He worries that the private money is taking pressure off the government to fulfil its training role. At the same time, he knows his already high workload would be much heavier without his three fellowship-supported colleagues. “It’s just not a life I want to imagine,” he says.
Between the free labour, private funding and foreign trainees, there’s little incentive for cash-strapped health provincial health departments to create permanent posts, according to a SAMA submission to the ministerial advisory committee on health staff.
The unpaid trainee specialist workforce isn’t mentioned in the health department’s health staffing reform plan, which lapses in 2030. The document does outline a five-year plan to improve clinical supervision, boost specialist retention and to develop a broader network of clinical support for trainees by 2025.
A progress report was submitted to Health Minister Dr Aaron Motsoaledi in March but critics say the plan is unlikely to have made a difference because the government lacks the high-quality data on public and private sector personnel that would be needed for implementation.
South Africa needs a Workforce Intelligence Authority that collates and cleans workforce data to be used for planning, suggests governance expert Professor Alex van den Heever. In July, he presented a draft policy brief to SAMA which also proposes ring-fencing training funds to protect salaries from provincial mismanagement and extending training subsidies and accreditation to private health facilities.
Without structural changes to address waste and mismanagement, Van Den Heever argues, simply giving provinces more money to counteract austerity will make no difference.
In the meantime, the government now deliberately budgets for clinical gaps to be filled by volunteers, says Sharon Twum-Boafo, head of SAMA’s registrar subcommittee.
“It’s ludicrous,” she says, “without the volunteers, many hospitals would simply not have enough doctors to cover 24-hour rosters.”
A legal void
Unpaid trainee specialists carry a heavy workload with few administrative and legal protections.
Since they lack a payroll number, they’re locked out of the blanket indemnity for healthcare workers employed by the state. Instead, government compels them to buy expensive private malpractice cover just to log hours for free in public hospitals.
Once they’re in the facility, Spotlight is told that it is possible they might be pressured to perform unsupervised, high-risk procedures far beyond their insured scope.
Speaking to Spotlight, several of these phantom physicians described their fear of being held personally liable for costs in potential lawsuits. Some are privately insured for millions of rands, which means that they would make for more lucrative targets than the government, where mediation often leads to lower payouts.
Ruan Vlok, head of SAMA’s employment law unit, agrees that unpaid specialists might become litigation lightning rods.
“It could become an easy making money machine for attorneys,” he says.
There are long term risks too.
Private insurance premiums are tied to clinical outcomes, so a pattern of bad events could drive up a doctor’s insurance premiums, or even render them uninsurable, the ultimate career-ending risk for a specialist.
Unfinished business
Some unpaid trainees face another tough reality.
They are often summoned to fill critical service gaps left by paid, full-time consultants who have vanished to moonlight in the private sector.
Dual practise is allowed within certain parameters, but enforcement of the rules is patchy across provinces and facilities. Money is one of the factors driving moonlighting among the state’s contracted specialists, whose salaries have not kept pace with inflation. A SAMA report estimates that in 2022, doctors were earning about as much as they were in 2013.
In order to save money, provincial health departments have limited the number of paid overtime hours that consultants can log. In this case, says Vlok, doctors are fully within their rights to refuse to work for free.
Ironically, this is when those who choose to work for free become extra useful in hospitals.
Yet should the phantom doctors themselves attempt to pull a paid shift to survive, they could be threatened with disciplinary action, heavy fines, or the immediate deactivation of their training numbers.
Under HPCSA and university rules, trainee registrars are legally barred from doing private paid work. Worse still, when a crisis occurs, these supernumeraries find themselves locked in dual contracts with universities and hospitals, with little protection from either.
An uneasy peace
The rights of the health system’s unpaid workforce have never been challenged in court, Vlok says, in part because doctors fear that any litigation would lead to them being targeted or failed in their exit exams.
Because supernumeraries aren’t officially employees, they’re also excluded from recourse through the country’s labour dispute resolution body, the Commission for Conciliation, Mediation and Arbitration and the Bargaining Council, leaving them with no mechanism for redress.
Local supernumeraries technically sign away they rights by agreeing to work without pay, but Vlok argues the state is taking advantage of a vulnerable group because the public sector is the only route to specialisation.
The regulations that allow foreign trainees to work in South Africa do not cater to or even make provision for South African citizens, Vlok says. In his view, the Labour Relations Act and the Basic Conditions of Employment Act should take legal precedence, under which he believes unpaid trainees clearly meet the criteria of an employee.
“I don’t use this word lightly,” he says, “this is abuse.”
It’s unclear how much longer the strained peace will hold.
One exhausted trainee specialist told Spotlight: “We have to fix the medical system, it’s broken. Who is going to look after us when we’re old?”
*Spotlight granted the doctors quoted in this article anonymity because of the risk of reprisals from provincial health departments and the hospitals where they are working.
Norepinephrine-induced RHOB is a key regulator of circadian intraocular pressure rhythm
Photo by Cottonbro on Pexels
Glaucoma is an eye disease that causes progressive damage to the optic nerve, leading to loss of sight. One major risk factor is an increase in intraocular pressure (IOP), or the pressure inside the eye. This pressure fluctuates throughout the day and is known to rise at night. However, the detailed molecular mechanisms on why this happens have not been fully understood.
Using human cells and mouse models, researchers at Kyushu University have found a new molecular pathway that explains why IOP increases at night. The neurotransmitter norepinephrine (also known as noradrenaline) increases the levels of a molecule called RHOB in the eye’s drainage system called the trabecular meshwork. This weakens the eye’s ‘cleaning function’, resulting in increased IOP. The team expects these findings will lead to the development of new approaches for the early detection of glaucoma, as well as new treatments for controlling IOP by targeting RHOB. Their results were published in the journal Communications Biology.
IOP is maintained by balancing fluid production and fluid drainage within the eye. As with many bodily functions, it is regulated by the circadian clock. In the case of the eye, IOP increases at night. Elevated IOP is a key factor in identifying the onset of glaucoma, but because pressure tends to be lower during the day, regular checkups can potentially miss these warning signs.
Because the circadian clock regulates IOP, disruptions to a person’s internal clock can lead to increased risk of glaucoma. This is why there is a higher risk of glaucoma in the elderly whose body clocks are desynchronising.
Fig.1. Graphical abstract of the research results Using mice, researchers found that norepinephrine released from the sympathetic nervous system increases RHOB levels and suppresses the eye’s drainage system, thereby contributing to the rise in intraocular pressure at night.
“Previous studies have found that signals from the sympathetic nervous system contribute to the nighttime rise in eye pressure, but that underlying process was not well understood,” explains first author of the study, Associate Professor Keisuke Ikegami from Kyushu University’s Faculty of Agriculture. “Most of the fluid in the eye is drained through a tissue called the trabecular meshwork. These cells also help keep the drainage pathway clear by taking up and removing small particles and waste. We also know that norepinephrine is a chemical that is released by the sympathetic nervous system. We decided to investigate how norepinephrine can change the function of fluid drainage in the eye and whether it can explain why eye pressure increases at night.”
The team began by exposing human and mouse trabecular meshwork cells to norepinephrine and compared changes in their genetic activity. They identified 18 genes that increased in both systems and focused on one called RHOB. RHOB is a molecule that is involved in controlling cell shape, movement, and intracellular transport.
Norepinephrine increased RHOB in the trabecular meshwork cells, and when RHOB was removed from human cells, their ability to take up and clear particles increased. In contrast, increasing RHOB reduced the cleaning activity and fluid movement in the eye. Testing in mice, the team used eye drops that inhibit a chemical pathway that controls RHOB activity, the RHO-ROCK pathway. The results showed that the eye drops reduced the nighttime rise in eye pressure.
While these results are not intended for immediate clinical application, they have identified the RHOB pathway as a new potential target for suppressing nocturnal increase in IOP. While ROCK inhibitors are used in glaucoma treatments today, further verification is needed to determine the most effective time of day for administration and how they alter IOP rhythm.
“Loss of vision from glaucoma occurs slowly, so early detection is crucial. We hope our work will lead to new treatment regimens and strategies for administering medicines to achieve the greatest effect,” concludes Ikegami.
A human neutrophil interacting with Klebsiella pneumoniae (pink), a multidrug–resistant bacterium that causes severe hospital infections. Credit: National Institute of Allergy and Infectious Diseases, National Institutes of Health
What if part of the answer to antibiotic resistance has been growing in plants, fungi and microorganisms all along? Scientists say hundreds of thousands of natural compounds remain largely unexplored as researchers race to protect some of the world’s most important antibiotics.
An international team of scientists led by the University of Pretoria (UP) is calling for a renewed search of the natural world for molecules that could disarm antibiotic-resistant bacteria and potentially make existing medicines effective again.
Researchers from UP, the University of Oxford in the UK, the National University of Lesotho, Kwame Nkrumah University of Science and Technology in Ghana, and the University of North Texas Health Science Center in the US collaborated on a major review of beta-lactam (β-lactam) antibiotics and the bacterial enzymes that destroy them.
Published in Natural Product Reports, the paper highlights a largely untapped opportunity. More than 400 000 naturally occurring compounds have been catalogued, yet only a small fraction has been investigated for their ability to inhibit β-lactamases, enzymes that can render important antibiotics ineffective.
“Antibiotic resistance is often presented as a search for the next completely new antibiotic, but there is another important possibility: protecting the medicines we already have,” said Professor Vinesh Maharaj, Director of UP’s Biodiscovery Centre, Acting Dean of the Faculty of Natural and Agricultural Sciences, and co-author of the paper. “Nature has already provided some of the compounds that have transformed infectious-disease treatment. We should not underestimate what remains to be discovered in the enormous chemical diversity of plants and microorganisms.”
The stakes are high. β-lactam antibiotics, including penicillins, cephalosporins and carbapenems, account for an estimated 60% to 65% of the antibiotic market. But bacteria have evolved increasingly sophisticated defences against them.
Among the most important are β-lactamases. These enzymes effectively break open the part of the antibiotic that allows it to work. More than 2 000 unique β-lactamases have been identified, including enzymes capable of undermining some of medicine’s last-line antibiotics.
The review cites estimates that bacterial antimicrobial resistance (AMR) directly caused approximately 1.14 million deaths in 2021. South Asia and sub-Saharan Africa together accounted for around 47% of global fatalities associated with bacterial AMR, while AMR is projected to cause about 8.2 million deaths annually by 2050 if current trends continue.
For co-author Dr Phanankosi Moyo, a biochemist and natural-product drug discovery scientist in UP’s Department of Plant and Soil Sciences, this makes the search particularly important for Africa.
“Sub-Saharan Africa carries a disproportionate burden of antimicrobial resistance, so this is not an abstract future problem for our region,” Dr Moyo said. “We need new antibiotics, but we also need smarter ways of extending the life of the antibiotics we have. Natural products give us an extraordinary starting library of chemical structures, and modern science now gives us far better tools to find the useful ones.”
Making existing antibiotics work again
There is already a powerful precedent.
Clavulanic acid, one of medicine’s best-known resistance blockers, is itself a natural product. Originally isolated from the bacterium Streptomyces clavuligerus, it has little antibacterial activity of its own. Instead, it blocks certain β-lactamases and protects an antibiotic from destruction.
Combined with amoxicillin, it became the widely used antibiotic treatment amoxicillin-clavulanic acid, a combination commonly marketed under the brand name Augmentin®. Its success demonstrated an important principle: scientists do not always have to replace an antibiotic. Sometimes they can disable the bacteria’s defence and allow the existing drug to work again.
The international team reviewed how scientists are trying to apply that principle to newer and more difficult forms of resistance.
Among the toughest targets are metallo-β-lactamases such as NDM, VIM and IMP. These enzymes use zinc to break down antibiotics and are resistant to the inhibitors used against many other β-lactamases.
Yet the natural world is producing intriguing leads. In one study examined in the review, a natural-product-derived compound called CS-23 inhibited NDM-1 and reduced the amount of the antibiotic meropenem needed to stop an NDM-1-producing strain of E. coli by 32-fold, restoring its effectiveness in the experimental system.
The review also highlights carnosic acid as the first reported natural product to inhibit NDM-1 through an allosteric mechanism. Instead of targeting the enzyme where it usually performs its chemical reaction, the compound acts elsewhere on it, offering researchers another possible route for disabling bacterial resistance.
Searching nature with new tools
The researchers argue that scientists now need to widen the search beyond familiar sources. Potential hunting grounds include Streptomyces and other microorganisms, fungi, plants, marine organisms and even lichens.
They can also search far more efficiently than previous generations. Modern approaches including metabolomics, structural biology, medicinal chemistry, computational screening, biocatalysis and synthetic biology can help identify promising molecules, understand how they work and modify them into better drug candidates.
“The next important β-lactamase inhibitor may not arrive as a ready-made medicine,” Prof Maharaj said. “Nature may give us the starting structure, and then chemistry, microbiology, structural biology and computational science can help us turn that starting point into something clinically useful.”
The international collaboration brings together expertise in natural-product chemistry, microbiology, phytomedicine, biochemistry and antibiotic-resistance research across Africa, the UK and the US.
There are still significant hurdles. A compound that works in a laboratory may struggle to enter bacterial cells, be unstable, lack sufficient selectivity or prove difficult to manufacture at scale. The researchers say promising natural compounds therefore need to be developed alongside medicinal chemistry and other modern drug-discovery approaches.
Finding broad-spectrum inhibitors capable of blocking several classes of β-lactamases at once is a particularly ambitious long-term goal.
“We have been in this race with bacteria since the first antibiotics were introduced,” Dr Moyo said. “The difference today is that we understand resistance at a molecular level and have technologies earlier generations could not have imagined.”
Much of the chemical diversity of plants and microorganisms has yet to be explored. This research shows that nature not only offers a simple cure for antibiotic resistance, but that it may still contain valuable starting points for protecting some of the medicines on which modern healthcare depends.
Harnessing artificial intelligence and metabolomics for discovery
Researchers at UP’s Biodiscovery Centre are working with collaborators to combine artificial intelligence, metabolomics and experimental screening to systematically sift through the centre’s in-house repository of approximately 11 000 plant samples in search of novel β-lactamase inhibitors.
By integrating computational prioritisation with chemical profiling and biological testing, the team aims to narrow this vast natural-product resource to the most promising candidates and accelerate the discovery of compounds that can overcome bacterial resistance mechanisms and help restore the effectiveness of existing β-lactam antibiotics.
Can nature help outsmart antibiotic resistance?
400 000 naturally occurring compounds have been catalogued
60% to 65% of the antibiotic market
2 000 unique β-lactamases
1.14 million deaths in 2021 due to AMR
47% of global fatalities associated with bacterial AMR occur in South Asia and sub-Saharan Africa
8.2 million deaths annually by 2050 if current trends continue
“South Africa’s diabetes epidemic will not be solved by the next pharmaceutical breakthrough. It will be solved by fundamentally reshaping how healthcare is organised and paid for”
– Lungile Kasapato, CEO of PPO Serve.
Diabetes is now South Africa’s leading killer, accounting for more deaths than HIV and TB combined. Global headlines celebrate GLP-1 receptor agonists (RAs) as a breakthrough for metabolic disease and obesity. But this narrative ignores a fundamental reality: for most South Africans, these drugs are inaccessible. Priced between R3 000 and R6 000 per month, they remain unaffordable. Even as cheaper generics become widely available, they won’t solve the problem alone. Without the clinical infrastructure to support treatment, and the social support to access healthy food, access means little.
“We’re pushing an incomplete solution,” says Lungile Kasapato, CEO of PPO Serve, a healthcare management company implementing value-based care in South Africa for over a decade. “GLP-1 RAs offer real benefits – sustained weight loss, reduced inflammation, lower cardiac risk, protection against comorbidities. For someone facing diabetes, these outcomes matter. But we’re acting as if a drug alone can solve a system failure. It can’t. A medication prescribed into a broken healthcare system is just a product. It’s not a national health strategy.”
The scale of the crisis is staggering. Forty percent of low-income South Africans’ diet consists of ultra-processed foods. Across the broader population, nearly 30% have undiagnosed hypertension. Most discover their condition only after complications like strokes or heart attacks emerge. By the time they reach treatment, the system can only manage disease with medications, never addressing what caused it in the first place. When a GLP-1 RA is prescribed in this fractured environment, initial sustained progress stalls because the infrastructure to maintain results was never built.
“This fragmentation isn’t accidental,” says Kasapato. “It’s structural. Fee-for-service rewards volume, not health. A provider, working alone, gets paid for each visit, test, or procedure – regardless of whether the patient’s health improves. With no teamwork or incentive to coordinate, follow-ups become inconsistent and inadequate. Every encounter is transactional, continuity is impossible, and no one is accountable for the patient actually getting better. As long as we pay for activity instead of results, we won’t fix the system or build the infrastructure these medications need.”
PPO Serve’s The Value Care Team, implemented in partnership with the Government Employees Medical Scheme (GEMS), demonstrates what a different payment structure creates. GPs, nurses, dietitians, and care coordinators work together, sharing accountability for patient outcomes rather than billable procedures. Coordination becomes the norm, and prevention becomes profitable, meaning early intervention can stop complications before they escalate. Medication works better because the system supports it, including addressing the social issues that drive obesity in the first place. This is what reshaping incentives creates.
“The real choice isn’t just about drug access,” says Kasapato. “It’s about payment models, and the system it creates. Cheaper GLP-1 RAs could be available tomorrow – generics are already arriving. But availability achieves little without the organisation to deploy them. The conversation must progress from funding medications to funding the teams and systems that make them work. South Africa’s diabetes epidemic will not be solved by the next pharmaceutical breakthrough. It will be solved by fundamentally reshaping how healthcare is organised and paid for.”
