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Ultrasound Brings Faster Diagnosis Closer to Home for Mpumalanga Patients

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Almost 3000 scans performed in five months as Bophelo First Trust and Dis-Chem Better Tomorrow Starts Here strengthen diagnostic capacity across six public hospitals

Patients at five Mpumalanga hospitals are benefiting from faster diagnosis following the launch of a point-of-care ultrasound programme by Bophelo First Trust (BFT), a South African Public Benefit Organisation (PBO), in partnership with Dis-Chem. The initiative has so far trained 14 clinicians and deployed 10 portable ultrasound machines, enabling surgical, emergency and trauma teams to scan patients at the bedside and reduce the need for referrals to other facilities.

BFT’s model strengthens existing public health systems through structure, continuity and measurable impact. It enables targeted operational support programmes that help unlock underutilised healthcare infrastructure and increase patient access to care.  Through collaborative partnerships, it develops and implements scalable healthcare support initiatives focused on reducing surgical backlogs, increasing procedural throughput, expanding access to diagnostic capability, strengthening operational healthcare capacity and supporting long-term public-sector sustainability.

Uptake has been strong since the programme launched in May, says BFT CEO Dr Mark Wadley. “Targeted operational interventions have the potential to unlock additional healthcare capacity within existing public-sector infrastructure. With point-of-care ultrasound, a trained clinician can perform a focused scan beside the patient and interpret the findings in real time. This means patients can be assessed sooner and, where appropriate, avoid the need to travel elsewhere for imaging.”

The programme addresses a significant diagnostic gap in a province serving close to five million people. Since May, clinicians had performed 2,865 scans covering abdominal, vascular, trauma and musculoskeletal applications.

“Better Tomorrow Starts Here addresses pressing societal health challenges across South Africa and looks to find practical ways to improve access to quality care,” says Joshila Shiba, Dis-Chem’s Head of Health Equity and Sustainability. “This programme shows how targeted, practical interventions can unlock additional healthcare capacity within existing public-sector infrastructure and aligns with Dis-Chem’s purpose of increasing access to quality healthcare access. We want to help build, support and strengthen healthcare ecosystems across South Africa.”

“Our Better Tomorrow Starts Here initiative reflects our commitment to societal health challenges by aligning our business goals with sustainable development in South Africa and connecting our overarching “Better Health Starts Here” purpose with a broader commitment to contributing positively to the country’s future.”

Dr David Marubini, one of the 14 clinicians trained through the programme, says access to ultrasound is particularly valuable in surgical care, where delays in diagnosis can affect treatment decisions.

“Before we had ultrasound in our department, a patient arriving with severe abdominal pain or injuries from a road accident often had to wait before we could see what was happening internally. Sometimes they had to be transferred to another hospital first,” says Dr Marubini.

“Now I can scan at the bedside within minutes and answer urgent questions straight away. Is there internal bleeding? Does this patient need to go to theatre now, or can we safely manage them here? It doesn’t replace a full radiology service, but it allows us to make decisions sooner and with greater confidence.”

Dr Wadley says the initiative could provide a scalable model for strengthening diagnostic capacity in public hospitals across South Africa.

“Clinician participation is expanding and more hospitals are showing interest. The next phase will focus on improving how the clinicians’ ultrasound images and video clips are stored and uploaded to the cloud. This will support AI-assisted quality assurance and training, helping to maintain scanning standards as more clinicians are trained. In turn this will further strengthen diagnostic capacity in the province” concludes Dr Wadley.

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Why MRI is Changing Prostate Cancer Diagnoses

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Preparing a patient for a prostate MRI

As we approach Movember with a focus on men’s health, we talk to Dr Hein Els, a radiologist specialising in abdominal imaging at SCP Radiology and Dr Louw-Waldi Vlok, a urologist at Mediclinic Panorama, about why MRI has become such an important tool in detecting prostate cancer and guiding diagnosis.

It’s often not the man who notices something first. His partner may mention noticing he has been up three or four times a night. He’ll put it down to getting older or having a cup of tea too late in the evening. What happens next is usually a visit to your GP…

How common is prostate cancer in the first place?

“Prostate cancer is the top invasive cancer reported in men in South Africa and also one of the most treatable, when it’s caught early,” says Dr Vlok. “Knowing what to look out for and understanding how far diagnosis and treatment have come, can reduce the fear and uncertainty around the disease. Today’s imaging technology means men get answers faster, treatment only when necessary and fewer invasive procedures than they would have a decade ago.”

What are the symptoms of prostate cancer?

“It is very important to realise that in the early stages of prostate cancer the patient will often have no symptoms at all”, says Dr Vlok. “Some men may have symptoms of an enlarging prostate which can include:  Needing to urinate more often, particularly at night, a weak or interrupted urine flow and even an inability to urinate and difficulty starting or stopping urination.

As the disease progress and grows beyond the prostate the symptoms will increase:

  • Blood in urine or semen
  • Pain in the pelvis or lower back

Are there any unusual or less obvious signs?

“Yes,” says Dr Vlok, “and these are the ones men are least likely to connect to the prostate.” In more advanced cases, prostate cancer can cause:

•           Unexplained pain in the lower back, hips or pelvis

•           New or worsening erectile difficulties

•           Unexplained weight loss or persistent fatigue

•           Swelling in the legs or feet

‘These signs can point to the cancer having spread beyond the prostate, most often to the bones. They can also have entirely unrelated causes, so the sensible response is to get checked rather than to worry. Catching a change early is exactly what makes modern diagnosis so effective.

These symptoms don’t automatically mean cancer. An enlarged prostate or inflammation of the prostate is common with age and usually benign, but any of these changes are worth mentioning to your doctor.

How was prostate cancer diagnosed before MRI?

For decades, the standard path was a physical examination and a PSA blood test. In many cases this is still the standard workup. The test measures the amount of prostate-specific antigen (PSA) in your blood. PSA is a protein produced by both cancerous and noncancerous tissue in the prostate, a small gland that sits below the bladder in males. If either raised concern, a biopsy followed.

This approach had/has a real drawback: Without imaging to guide it, a biopsy could miss cancer that was there or flag concern in men who didn’t actually need treatment. The biopsy itself was usually systematic. A urologist took a set number of tissue samples from across the prostate using ultrasound guidance, without being able to see whether any specific area actually looked suspicious. It worked but was something of a blind search. Some cancers were missed simply because the needle didn’t pass through them, while other men went through an invasive procedure and a period of anxious waiting, for a result that turned out to be low risk or clear. If the result was clear and symptoms carried on, only then would an MRI be ordered.

How does MRI fit into prostate cancer diagnosis now?

“This reactive approach was certainly not ideal,” says Dr Els. The international standard has fundamentally changed and the sequence is different. After a raised PSA result, the patient is usually sent to radiology for a multiparametric MRI of the prostate, before any biopsy is considered”, says Dr Els.

“This is a detailed scan that maps the prostate and identifies areas that look suspicious,’ Dr Els explains. ‘It’s non-invasive: No incisions, just a detailed set of images generated using magnetic fields rather than radiation. We review the scan and score any area of concern, so the urologist has a clear picture of where and how likely, anything significant might be. If there’s a concerning lesion, a targeted, MRI-US fusion guided biopsy is performed.”

The major advantage is that many men with a clear or low-risk MRI avoid a biopsy altogether. When an area does need sampling, the biopsy can be targeted precisely, which means fewer samples, a more accurate result and a much shorter path to an answer.

This shift is supported by the PRECISION and MRI-FIRST trials and endorsed by the European Association of Urology and the American Urological Association.

What does the MRI tell the specialist?

‘Once the prostate is imaged, we don’t just report whether something looks suspicious but we give it a score, says Dr Els. ‘This is called PI-RADS, short for Prostate Imaging Reporting and Data System and it runs from 1 to 5. The number tells your doctor how likely it is that what’s showing on the scan is aggressive cancer and whether a biopsy is worth doing at all.’

  • Scores 1 and 2: Usually mean no dangerous cancer is seen. Your doctor may simply monitor you over time
  • Score 3: The scan cannot give a clear answer either way. Doctors will look at other information, such as your PSA blood test, before deciding on a biopsy
  • Scores 4 and 5: Mean a high chance of cancer and a biopsy is usually recommended

This shift, from a blind search to a targeted, image-led approach, is one of the most significant improvements in prostate cancer care in the last 15 years and it’s an area in which SCP Radiology has invested heavily to get right.

Prostate cancer, when found early, has excellent outcomes. The combination of a simple blood test and non-invasive, expert-led imaging means most men now get a clear, accurate picture of their prostate health with far less uncertainty than in the past.

‘Our radiologists work closely with urologists across the circle of care, to make sure every scan is read with the depth of experience this diagnosis deserves,’ explains Dr Els.

And, if you’re reading this because you’ve noticed a change in someone else, not yourself: Raising it is worth the slightly awkward conversation. It’s often exactly what starts the process early.

FAQs

Is a prostate MRI painful or invasive?

No. It uses magnetic fields and involves no incisions.

If my PI-RADS score is low, do I still need a biopsy?

Usually not. A low score, 1 or 2, generally means your doctor will monitor you over time, rather than proceed to biopsy.

How long does the process take, from a raised PSA result to an answer?

This varies because the MRI is done before any biopsy. Many men reach a clear answer or avoid a biopsy altogether, in far fewer steps than under the older approach.

Is prostate cancer treatable if caught early?

Yes. It’s one of the most treatable cancers in men when detected early, which is why regular check-ups matter, even in the absence of symptoms.

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When Coping is No Longer Enough: Rethinking Workplace Stress and Mental Health

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Photo by Samson Balogun on Unsplash

Most workplaces run on an unspoken rule that being professional means keeping it together. You get to work, hit your deadlines, sit through meetings and deliver, regardless of what may be happening in your personal life or the challenges you might be dealing with emotionally and mentally. 

For a while, many people manage. But the 2025 Profmed Stress Index suggests that for a lot of South African professionals, that is no longer working. Nearly a third of respondents said stress was affecting their sleep and their ability to exercise, while just under 30% reported changes to their eating habits. Another 44.05% still felt overwhelmed despite using coping strategies such as exercise, mindfulness and therapy, and almost half were concerned about the long-term impact of stress on their mental health.

As Mental Health Awareness Month gets under way, those numbers raise an uncomfortable point. Many professionals are already doing what they have been told to do about stress, and yet, it’s still not enough.

How stress has changed

According to Justine Lacy, Clinical Executive at Profmed, the nature of professional stress has shifted over the past decade. Before COVID-19, it mostly came from the ordinary challenges of life. During the pandemic, it was driven by fear: lost income, health worries and the rising cost of living. Since then, the main source has been work itself, through heavy workloads, toxic workplaces and poor work-life balance.

Justine Lacy, Clinical Executive at Profmed

These pressures no longer arrive one at a time. They overlap and feed each other, which makes stress more persistent and harder to manage. It also builds slowly. Constant tiredness that rest doesn’t fix, a shorter temper than usual, trouble concentrating or small mistakes that aren’t like you are easy to put down to a busy month. Pressure becomes a mental health concern when it stops being temporary, when rest doesn’t help, and when it starts to affect someone’s health, relationships or ability to function.

The person who still looks fine

Many people assume that someone who is struggling will eventually show it in their work. Justine says that often isn’t the case. Plenty of professionals keep meeting deadlines while dealing with serious distress, and sometimes their output stays strong because they are working harder to make up for it, at considerable personal cost.

“We often look for a drop in performance as the warning sign, but by then we may have missed months of struggle,” she says. The earlier signs are usually changes in energy, behaviour, engagement and wellbeing.

The expectation to stay composed makes this harder. People known as dependable may worry about looking incapable or letting colleagues down, so they put off asking for help. Over time, that delay can lead to burnout, poorer decisions and a growing sense of isolation.

Why self-care has limits

Exercise, mindfulness and therapy all help. But they work on the person, and the problem often sits in the job. “You can’t self-care your way out of a situation that’s continually creating stress,” Justine says. Exercise won’t shorten someone’s working week, and mindfulness won’t fix unrealistic expectations or a toxic team.

The World Health Organization lists excessive workloads, lack of control, job insecurity, poor organisational culture and lack of support as workplace mental health risks. None of those can be solved by an individual. As Justine puts it: “Individuals need healthy coping mechanisms, but organisations also need to create environments where people can thrive, not just survive.”

What employers can do

A wellness day or an employee assistance programme has value, but Justine says real support starts with the causes of stress. She points to three things:

Supportive leadership. Managers check in regularly, encourage open conversations and model healthy behaviour themselves.

Healthy work design. Workloads are reasonable, deadlines are realistic and boundaries outside working hours are respected.

Psychological safety. Employees can ask for help or admit they are struggling without fearing the consequences.

Check-ins also need to happen more often than the annual survey. “Burnout rarely happens overnight,” Justine notes, and employers who watch for absenteeism, withdrawal, irritability or persistent fatigue can step in early. The question to ask, she says, is “How do we create a workplace where fewer people reach that point in the first place?”

The cost of waiting

Justine calls cost one of the biggest barriers to getting help early. Many people hold off on seeing a psychologist or psychiatrist until they are in significant distress, and by then the problem is usually harder to treat.

She believes medical schemes and healthcare providers are well placed to move mental healthcare from a crisis response to early intervention, so people can get support when stress first becomes a concern and not only once it becomes a diagnosis.

Success shouldn’t cost your health

Justine’s message to professionals is simple. Mental health matters as much as physical health, and seeking support early is a sign of strength, not weakness. You don’t need to wait until you are burnt out or in crisis. Pay attention to the early signs and check in with yourself and the people around you.

“Being resilient doesn’t mean carrying every burden alone,” she concludes.

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‘Microexons’ Linked to Autism Cases Without a Genetic Basis

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Source: Pixabay CC0

New research from scientists at King’s College London, the University of Toronto, the Sloan Kettering Institute and the Francis Crick Institute advances understanding of the genetics of autism spectrum disorder (ASD).

In a study published in Nature, researchers identified hundreds of new microexons – short gene segments that appear to play a key role in ASD and other neurological conditions – and developed a machine-learning approach to predict the impact of ASD-associated genetic variants on the regulation of these segments.

Autism is characterised by multifactorial genetics. Hundreds of genomic variants have been associated with autism, and these deliver a genetic diagnosis in 15 per cent of people with autism diagnoses.

Dr Benjamin Blencowe, King’s College London and University of Toronto

That means that for 85 per cent of people with an ASD diagnosis, a genetic link is unknown. Dr Benjamin Blencowe, the study’s co-senior author, believes that many contributing genetic factors may have remained undetected because they occur in regions of the genome that do not have a known function.

The genomic regions surrounding microexons are one such example. Through alternative splicing, these very short snippets of DNA – which range from three to 27 DNA “letters” long – can be included or excluded from the messenger RNA instructions used to make proteins. The resulting proteins vary slightly in composition yet contribute to a greater diversity of critical protein functions.

In the newly published study, Dr Guillermo Parada, the study’s co-lead author and a postdoctoral fellow at King’s College London and the Francis Crick Institute, used a computational tool he developed called MicroExonator to analyse over 100 terabytes – enough storage for 25 million smartphone photos – of publicly available RNA sequencing data. He identified more than 1500 new microexons, of which nearly 300 appeared to be specifically spliced in the brain.

The researchers also observed that many of the newly discovered microexons are concentrated in genes associated with critical brain-specific processes, further supporting the idea that these tiny DNA fragments contribute to neurological function.

The researchers then asked whether DNA variants found in the genome of people with autism might preferentially impact the expanded repertoire of microexons.

To answer that question, Dr Parada and study co-lead author and postdoctoral fellow Dr Hannes Bretschneider teamed up with Dr Quaid Morris, a faculty member at Memorial Sloan Kettering Cancer Center and Vector Institute and co-senior author on the study, to build and apply a machine-learning model that identifies the key regulatory features governing whether a microexon is spliced in or out of messenger RNAs. This so-called regulatory code encompasses specific sequences of DNA letters flanking microexons.

What surprised me was that the sequences the model identified as important closely matched those conserved throughout vertebrate evolution.

Dr Guillermo Parada, King’s College London and the Francis Crick Institute

DNA sequences that are highly conserved, or the same, between species generally have critical functions.

Through a collaboration with Dr Stephen Scherer and Brett Trost, both scientists at The Hospital for Sick Children and professors of molecular genetics at Temerty Medicine, the researchers applied their model to whole-genome sequence data from thousands of people with autism and neurotypical sibling pairs, and analysed the predicted impact of ASD-associated genetic variants on the microexon regulatory code.

Using our model, we were able to show that rare genetic variants generally have the largest predicted effects on the splicing of neuronal microexons.

Dr Benjamin Blencowe

The model further pinpointed a subset of rare variants predicted to alter microexon splicing that are associated with autism. The research team also found that the variants predicted to affect microexons are predominantly detected among the 85 per cent of people with an autism diagnosis previously lacking a genetic link to autism.

These new findings build on over a decade of research from the Blencowe lab to uncover the role of microexons in ASD, including earlier work showing that microexons are frequently misregulated in the brains of people with autism and that mice lacking microexon splicing display multiple ASD-like behaviours.

“In terms of future work, it will be important to understand how disrupted microexons affect interactions between proteins that are important for nervous system development and function,” says Dr Blencowe. One of the research programmes in his lab is also exploring new therapeutic approaches to target microexon dysregulation.

Dr Blencowe says that beyond helping to define some of the missing genetics of ASD, their study provides a valuable resource to advance research in the field.

The researchers believe that the machine-learning model they developed can be used to characterise newly discovered genetic variants and their effects in other neurological conditions, like schizophrenia and epilepsy, where microexons are believed to play a role.

This story has been adapted from a version that appears on the University of Toronto website.

Source: King’s College London

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Diabetes Masks Alzheimer’s Biological Changes in the Brain

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Neurons in the brain of an Alzheimer’s patient, with plaques caused by tau proteins. Credit: NIH

Research led by King’s College London suggests diabetes may mask biological changes linked to Alzheimer’s disease, raising the possibility that the underlying biology of Alzheimer’s differs between people with and without diabetes.

Diabetes is a major risk factor for Alzheimer’s disease, and the two conditions share several biological processes, including mitochondrial dysfunction, inflammation, oxidative stress and impaired insulin signalling. This suggests that diabetes may contribute to the progression of changes in the brain associated with Alzheimer’s disease.

The paper, published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, examined mitochondrial DNA copy number (mtDNA-CN) in post-mortem samples from three regions of the human brain: the hippocampus, amygdala and cerebellum.

The team found that Alzheimer’s disease and diabetes were associated with opposing changes in mitochondrial DNA. Alzheimer’s was associated with lower mtDNA-CN, while diabetes was associated with higher levels across all three brain regions.

When people with diabetes were removed from the analysis, mtDNA-CN was 19 to 30 per cent lower in people with Alzheimer’s compared with cognitive controls. In contrast, among people with Alzheimer’s, those with diabetes had significantly higher mtDNA-CN than those without diabetes. Levels were 41 per cent higher in the hippocampus, 52 per cent higher in the amygdala and 64 per cent higher in the cerebellum. Surprisingly, all diabetes cases, including those with and without dementia, had higher mtDNA in these three regions than non-diabetic controls.

These opposing effects suggest that including people with diabetes in Alzheimer’s studies could reduce or mask differences associated with Alzheimer’s itself.

The findings suggest that diabetes may change the way Alzheimer’s disease is associated with mitochondrial changes, rather than simply being a background health condition. This could mean that the relationship between Alzheimer’s and mitochondrial DNA may be different in people with diabetes compared with those without diabetes.

“The key finding of our study in relation to Alzheimer’s disease is that grouping both diabetic and non-diabetic data for mtDNA-CN together can result in loss of real changes which may be important in disease mechanisms. Our research supports the growing view that Alzheimer’s disease can affect people in different ways at a biological level, and that conditions such as diabetes may contribute to these differences.”

Senior author Dr Afshan Malik

“We were surprised to find that mtDNA-CN was higher in the brains of people with diabetes. We don’t yet know whether this represents a response to cellular stress, a compensatory mechanism, or something else and what this means for the brain function. Our next step is to use multi-omics approaches to understand the biological consequences of this change and how it may affect brain function.”

First author Dr Aakruti Kaikini

The study provides a possible explanation for why previous studies of mitochondrial dysfunction in Alzheimer’s disease have produced conflicting results, potentially making it more difficult to diagnose patients.

In the future the researchers hope the results could be important for developing better ways to identify and understand Alzheimer’s disease, tailoring treatments to individual patients and designing future dementia clinical trials.

Source: King’s College London

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ADHD Drugs May Ease Subjective Brain Fog in Perimenopause

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Photo by Karolina Grabowska on Pexels

An estimated 44–60% of perimenopausal women report cognitive changes such as forgetfulness and difficulty concentrating (brain fog). No FDA-approved pharmacological intervention exists. A scoping review suggests ADHD medications may help. Results will be presented at the 2026 Annual Meeting of The Menopause Society in San Diego, 20–24 October 2026.

The menopause transition involves a significant decline and fluctuation in oestrogen that mediates catecholaminergic signalling in the prefrontal cortex. This produces quantifiable deficits in working memory, attentional control and processing speed that overlap with ADHD symptom domains.

Researchers reviewed original studies of lisdexamfetamine (LDX) and atomoxetine (ATX) in biological women aged 45–60 with last menstrual period <10 years ago (exclusions included transgender women, disordered sleep, surgical menopause, primary ovarian insufficiency, premature/early menopause and prior/current cancer). Both stimulant (LDX) and non-stimulant (ATX) agents significantly improved self-reported executive function, shown by marked reductions in total Brown Attention Deficit Disorder Scale (BADDS) scores versus placebo. Neuroimaging in a subset taking LDX supported these findings.

Improvements were confined to subjective brain fog; objective measures (working memory, sustained attention) showed little or no significant change. Cross-sectional data linked higher baseline ADHD symptom severity to greater perimenopausal symptom burden, though the impact of a formal ADHD diagnosis on somatic and psychological complaints was inconsistent.

The authors conclude that these agents may improve subjective executive function (but not objective cognition) by modulating catecholaminergic pathways disrupted in the menopause transition. Findings open a potential non-hormonal option for perimenopausal executive dysfunction, but larger studies are required before clinical recommendation.

“Many women at perimenopause notice changes in focus, memory and organisation that look a lot like ADHD, and the two can be hard to tell apart. Our review found early signs that ADHD medications may help women feel more on top of their daily lives. While it’s too early to recommend these medications, a quick screen for ADHD symptoms is a simple step that could help women get the right care,” said Jennifer Tat (University of Tennessee Health Science Center).

“For most women, brain fog at menopause is a temporary condition that does not lead to permanent cognitive changes or dementia. However, it can last long enough to disrupt work and daily routines and cause significant stress and anxiety. That’s why studies like this are important in helping to identify additional options for symptoms,” said Dr Stephanie Faubion (medical director, The Menopause Society).

Details: “Brain Fog or ADHD? Executive Dysfunction in Perimenopause: A Scoping Review of the Role of ADHD Medications.” More information: www.menopause.org.

Source: The Menopause Society via EurekAlert!

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SA’s Health Insurance Market Surges as Medical Scheme Costs Rise

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With high annual increases, medical schemes are becoming less affordable, but SA’s health insurance market is bringing in previously uninsured South Africans into private healthcare for the first time.

Photo by Cottonbro on Pexels

19 OCTOBER 2026, Johannesburg: South Africa’s biggest medical schemes are increasing rates by 7% to 9% for 2027, more than double the Council for Medical Schemes (CMS) guideline, pushing medical scheme cover further out of reach for working South Africans. Meanwhile, a different part of the private health insurance market is growing, reaching South Africans who have never had private cover before.

According to the CMS, medical scheme membership has held steady at nine million lives for more than a decade, slipping from about 17% of South Africans a decade ago to under 15% today. Over the same period, health insurance has grown to approximately 1.5 to two million lives, according to industry estimates.

Depending on the options selected, health insurance may provide access to defined primary healthcare, medication and specified accident or emergency benefits. These insurance offerings are deliberately different from medical schemes, which must cover prescribed minimum benefits (PMBs), and offer additional benefits depending on their rules and benefit options.

Kaelo, which provides health insurance, gap cover, and other employee benefits primarily through employers, says demand has risen sharply. Its membership has grown by more than 30% per year over the past two years, and over the same period it has quoted on cover for nearly 1.5 million lives.

“Health insurance and medical schemes are largely two distinct markets,” says Jordan Bortz, actuary at Kaelo. “The typical health insurance member has never been on a medical scheme. Several of our largest clients are employers whose staff earn around R10,000 a month or less. Many cannot afford the monthly cost of medical scheme cover.”

“Some of the employees may never buy private cover on their own, but when the employer provides it, or subsidises a portion of the cost, a significant number of people gain access to private healthcare for the first time,” says Bortz.

For lower-income earners, the affordability gap keeps widening. Health insurance products can cost as little as R300 per month, while entry-level medical scheme cover starts at approximately R1,500. Because health insurance premiums have risen more slowly than medical scheme contributions, that gap grows each year. “Every year, medical scheme cover moves a little further away from what many working South Africans can afford,” says Bortz. “After the latest increases, the gap is wider than it’s ever been. Health insurance gives those employees a way into private healthcare that they otherwise wouldn’t have.”  

Group-based cover can cost up to half the price of the same benefits bought by individuals. Employers can also subsidise all or part of the cost of health insurance.

For employers, the business case goes beyond price. Workers without cover often go untreated for everyday illnesses and chronic conditions, and lose working hours queuing for care. So, employers face reduced productivity and increased absenteeism.

Access to primary healthcare and chronic medication supports improved attendance, wellbeing and workplace productivity. “Based on Kaelo’s internal modelling, the value to employers may be many multiples higher than programme spend, depending on factors such as the industry and utilisation. Even if the employer subsidises only a portion of the premium, they get almost the full benefit,” says Bortz.

Kaelo’s health insurance plans range from accident and emergency cover to a comprehensive offering covering 27 chronic conditions, GP consultations, dentistry and optometry through the Prime Cure network. Kaelo Gap and Western Gap cover address the other side of rising increases: as schemes contain price rises by narrowing hospital networks and tariff limits, gap cover may pay qualifying medical expense shortfalls and co-payments, subject to the policy terms. Direct-to-consumer demand for both health and gap cover is growing at a similar double-digit pace.

The focus on mental health also differentiates Kaelo, as it has been built into Kaelo’s gap, health and life products for close to two decades. “We consider the whole person,” says Bortz. “Mental health has a knock-on effect on mortality and morbidity, and on how people perform at work.”

Health insurance does not replace medical scheme cover, but it does offer a first step into private healthcare for those who have never had it. “For most of the people we cover, the choice was never medical scheme or health insurance,” says Bortz. “It was health insurance or nothing.”

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Experimental Brain Implants are on the Rise. What Happens After the Trials are Over?

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AI image created with Grok

Nathan Higgins, Monash University

In 2024, Elon Musk’s Neuralink put its first brain implant into a human amid doubt from scientists and allegations of animal cruelty.

Two and a half years later, that first patient is one of more than 20 “neuralnauts” who use their implants to participate in the online world.

Brain implants are becoming smaller, more compatible with human bodies, and dramatically more capable. People with paralysis can use brain-computer interfaces to produce speech almost instantaneously. Earlier this year, researchers in the United Kingdom showed volunteers wearing a headset could control robotic limbs and their natural ones at the same time.

As the industry takes off, we will see more and more clinical trials of devices that are implanted in the brain. In a recent study, my colleagues and I tried to address an increasingly important question: when a clinical trial of an experimental neural device ends, what does that mean for the human participants?

Tough questions

There is no simple answer. Some participants may be able to continue using an implanted device “off-label” as part of a special access scheme, or if the trial sponsor enrols participants into a follow-up study.

But if the trial sponsor is funded by a research grant or venture capital, they may not be able to cover the costs of potentially lifelong device support.

Participants may need to have their device removed at the end of the trial, even if they have benefited from it.

These scenarios are not hypothetical.

This is becoming a significant issue in Australia, where a new generation of neurotech companies is taking off.

Last year, Melbourne-based company EpiMinder received FDA authorisation to market their continuous seizure monitoring system for epilepsy.

Synchron has raised well over A$300 million for its “minimally invasive” endovascular brain-computer interface and has recently commenced its latest Australian clinical trial.

No rules, yet

Yet Australia currently has no rules about how trial organisers should be required to support participants for the long term.

Nor are there rules about how participants should be supported when trials are suspended or devices discontinued.

Current guidance offers little direction on what ethical arrangements should involve.

The Australian clinical trial handbook requires researchers to “clearly explain” whether participants will have continued access. However, this is difficult in practice.

Trials of implantable systems often last several years. This makes it difficult for participants to anticipate what their future needs and preferences will be once the trial comes to a conclusion.

Asking the experts

We brought together an expert panel of 24 clinicians, bioengineers, consultants, bioethicists and research governance professionals to develop recommendations on post-trial responsibilities in Australia.

If the sponsor is able to give participants the option of post-trial use, we recommend giving participants and their loved ones a realistic picture of what continued use will look like.

Which clinical and technical supports will remain available, and who will provide them? Will surgery and maintenance be covered by public healthcare or private health insurance? What costs might participants face themselves?

Years may pass before a device receives regulatory approval or becomes eligible for reimbursement. Participants should be provided with updates on changes to funding, regulatory status or manufacturers’ commercial plans that could affect their ongoing care.

This does not always happen in neurotechnology research. Transparency helps participants assess their participation and plan for life after the trial.

Geographic barriers

Geographic and socioeconomic factors also bear on continuing access to device support. Trials are often run from metropolitan teaching hospitals. Some participants may need to make repeated visits to the trial site for outpatient care or inpatient stays.

Flights and accommodation may need to be arranged for participants who must travel interstate, particularly as laws around psychosurgery vary between states. This can complicate access to local care.

We recommend anticipating barriers to continuing device use that may disproportionately affect some participants. During recruitment and study design, research teams should engage participants’ primary treating physicians to discuss what aspects of post-trial support can be safely (and lawfully) taken on locally.

Some procedures will still require specialist expertise, but sharing post-trial support could reduce travel costs and dependence on the original research team. Better treatment for pioneersThe end of a clinical trial should not mean losing access to a device when better planning and coordination between trial organisers could have made continued use possible.

Ultimately, these trial participants are pioneers who put their brains in researchers’ hands to help develop promising new treatments.

Nathan Higgins, Postdoctoral Research Fellow, Monash Bioethics Centre, Monash University

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

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Indigo Light Might Prevent and Treat Myopia

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Graphical abstract, Cell Reports Medicine (2026).

As technology use increases and children spend less time outdoors, researchers have noticed an epidemic increase in myopia over the past six decades also known as the ‘myopia boom’. Myopia, or nearsightedness, has become a major health problem across the world, largely impacting children and adolescents.

“It is projected that nearly half of the world’s population could be myopic by 2050,” said Rafael Grytz, PhD, professor in the University of Alabama at Birmingham Department of Ophthalmology and Visual Sciences. “Myopia results in higher risk to develop glaucoma, retinal detachments and other blinding disease later in life.”

However, a new study published in Cell Reports Medicine suggests that controlled exposure to the indigo light, wavelengths that are abundant in sunlight but mostly absent indoors, could be an effective treatment for myopia. Partnering with researchers from Cincinnati Children’s Hospital Medical Center, this study poses a new treatment and prevention strategy that could impact current ophthalmologic practices and environment lighting standards.

The right wavelengths for developing clear vision

Myopia develops in children and can be defined as the condition when the eye is deemed too long. This extended length causes the light that enters the eye to focus in front of the retina. This results in distant objects’ appearing blurry and out of focus. While standard glasses and contact lenses may improve sight and mitigate myopia symptoms, they do not slow the development of the condition.

Grytz, lead author of the paper, says indigo light can likely be used to slow the progression of myopia in children because it has proved to be composed of just the right wavelengths to completely suppress myopia development in juvenile animal models.

“If we can implement indigo light into our indoor environment or provide it directly to the eye, we may slow the progression of myopia and even work to prevent it from developing at all,” Grytz said.

While the sun is abundant in indigo wavelengths, the modern age of increased indoor time and exposure to white LED light via technology use and modern lighting design present a clear correlation to the myopia boom.

The indigo wavelengths were found by optimizing opsin 5 activation while accounting for light that is filtered out by the ocular lens. OPN5 is a protein that exists in the retina that serves as a light sensing receptor.

Earlier work in animal models that rely on night vision suggested that violet light could suppress myopia by activating OPN5. But violet wavelengths did not work in different animal models that rely on daytime vision with an eye very similar to that of humans, because the ocular lens blocks most violet light below about 400 nanometers.

Corresponding author Richard Lang, Ph.D., director of research in the Division of Ophthalmology at Cincinnati Children’s, says that “human lenses don’t transmit a lot of light in the ultra-violet spectrum.”

Based on this finding, Grytz predicted the optimal wavelength that could stimulate OPN5 in the animal model eye. This prediction led the team to explore slightly longer wavelengths, including indigo wavelengths. Ultimately, the team established a new metric, called the μ-opic, that can quantify how effectively different light wavelengths may protect against myopia.

“We found that indigo light from 419 to 446 nanometers were the most effective wavelengths,” Lang said. “So, if indigo light can suppress myopia in these tests, then it should also be quite effective in humans.”

The future of myopia treatment

Grytz founded Electric Indigo, a UAB startup that focuses on developing ways to practically manage myopia. This startup was founded with the support of UAB’s Bill L. Harbert Institute for Innovation and Entrepreneurship. HIIE offers the infrastructure necessary to help UAB faculty, staff, and students bring new ideas and technologies to market across the region and beyond.

“At Electric Indigo, we have developed eyewear with LEDs in the frame that emit indigo light at controlled conditions to the eye to effectively treat and slow myopia progression in children,” Grytz said.

Grytz says this approach offers a simpler and new strategy that could surpass current treatment options, which may have difficult side effects and limited efficacy levels.

Compared to the increasingly popular red-light therapy, Indigo Eyewear presents an easier approach to treatment by offering a practical method of exposure.

“If our hypothesis is confirmed that absence of indigo light indoors caused the myopia boom, our eyewear will be the first treatment that attacks the root cause of this epidemic,” Grytz said.

Source: University of Alabama at Birmingham

Categories : Neurodegenerative DiseasesTags : Leave a comment

Synaptic Vesicles Shed Light on Parkinson’s Disease

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Neurotransmitters at a synapse. Credit: Scientific Animations CC4.0

Brain cells that release dopamine package it into tiny membrane-bound sacs called synaptic vesicles. And these vesicles differ from vesicles used by brain cells that release other neurotransmitters, a study led by Cedars-Sinai Health Sciences University investigators shows.

The study, published in Science Advances, could lead to better understanding of Parkinson’s disease, a movement disorder that causes dopamine-releasing brain cells to progressively die. The death of these cells leads to the movement problems that characterise the disease.

“Our research sheds light on the different ways brain cells release chemical messengers, which the cells use to communicate with each other,” said Katlin Silm, PhD, assistant professor of Biomedical Sciences and Neurology and senior author of the study. “We identified key differences between brain cells that release dopamine and those that release other brain chemicals.”

Synaptic vesicles help brain cells to communicate by fusing with the cell membrane and releasing their contents into the space between cells. In the brains of laboratory mice, investigators found that dopamine-containing synaptic vesicles carry a distinct set of proteins compared to those containing other messenger chemicals.

“Our findings show that a vesicle’s composition is critical to determining how brain messenger chemicals are released,” said Silm, also a research scientist in the Board of Governors Regenerative Medicine Institute. “The differences we identified help explain the unique properties of dopamine release and lay the groundwork to explore how this affects the long-term stability of dopamine-producing brain cells.”

Source: Cedars Sinai