Author: ModernMedia

Categories : Respiratory DiseasesTags :

Flu Season is Here, with Experts Keeping a Close Eye on New Flu Strain

On By ModernMedia
Photo by Andrea Piacquadio on Pexels

By Elri Voigt

Many regions in the Northern Hemisphere experienced a slightly earlier start to their flu season, driven in some part by a novel variant of influenza A(H3N2). As our flu season also kicks off slightly earlier than usual, Spotlight reports on the detection of this variant in South Africa and what we might expect from this year’s flu season.

As the mercury slowly starts dropping across the country, so does the risk of picking up flu. For many, this might only mean a few days of illness and discomfort, but for some, especially the elderly, it can be life-threatening.

Despite temperatures throughout most of the country remaining moderate so far, this year’s flu season has started, somewhat ahead of schedule. This is according to the National Institute for Communicable Diseases (NICD) in a press release issued on Wednesday.

What we refer to as flu, is commonly caused by one of two types of influenza viruses, influenza A and influenza B. These two are further typed into different lineages, the most common for influenza A is A(H1N1) and A(H3N2) and for influenza B, the B-Victoria and B-Yamagata.

The Yamagata lineage has not been detected since 2020 and is thought to have gone extinct, said Dr Sibongile Walaza. She is a medical epidemiologist and head of epidemiology at the Centre for Respiratory Disease and Meningitis at the NICD.

A key reason why influenza viruses continue to circulate year after year is how fast they mutate and learn to dodge our immune defenses. These mutations eventually result in different subtypes of lineages that are called clades, within which there can be further sub-clades.

It was a sub-clade of the A(H3N2) virus, known as sub-clade K, that led to the flu season starting earlier than usual in some parts of the Northern Hemisphere. The World Health Organization (WHO) reported that the variant was identified in 2025 and spread fast.

“This [sub-clade] contributed to an earlier start to the influenza season in many countries, with several reporting higher‑than‑usual levels of activity. ‘Subclade K’ accounted for the majority of influenza viruses reported across regions,” the WHO stated in a press release.

Sub-clade K was also responsible for an unusual spike in flu cases in South Africa in October and November 2025. Walaza told Spotlight there weren’t enough flu cases detected to cross the seasonal threshold for an additional flu wave, but the increase so late in the year, outside of the typical flu season, was unusual.

Early start

Usually, South Africa’s flu season starts sometime in April or May and spans the winter months, said Walaza, but it is difficult to predict exactly what will happen in any particular year.

This year’s flu season officially started in the second week of March, according to the NICD’s latest report, albeit at a low transmission level for now. 134 samples were tested between 16 and 22 March. Of those, 12 (9%) tested positive for influenza, 12 (9%) were cases of RSV and 3 (2.2%) tested positive for SARS-CoV-2.

In a rather unusual occurrence, the NICD reported that the start of this year’s RSV season coincided with that of the flu season. RSV refers to respiratory illness caused by the Respiratory syncytial virus. The RSV season usually starts before the flu season, but infections can occur all year round.

“The fact that both the flu and RSV seasons are starting at the same time means clinicians could potentially see a high burden of patients with respiratory illness in medical facilities in the coming weeks,” the NICD said in the press release.

Two potential scenarios

Professor Tulio de Oliveira, the director of the Center for Epidemic Response Innovation at Stellenbosch University, said the reality is that we do not know what to expect for this year’s flu season.

“[At]t the moment, we are working with potentially two different scenarios,” he told Spotlight.

The one scenario is that we may be in for a more extreme flu season, he explained, since last year was an unusually mild season and population immunity against the viruses that cause flu may currently be lower. The other scenario, depending on which flu virus circulates, is that South Africa may have some herd immunity because of the unusual spike in flu cases near the end of last year.

In other words, it all comes down to which flu viruses, and their subtypes end up circulating.

“I think this year we’ll have the three influenza lineages [A(H3N2), A(H1N1)pdm09 and influenza B-Victoria] circulating, but in terms of which one is going to be dominant in the season, it’s difficult to tell in advance,” Walaza said.

What we know about sub-clade K

Based on what we’ve seen so far, it does seem that sub-clade K is more transmissible, but it doesn’t appear to cause more severe disease, according to Walaza. De Oliveira added that sub-clade K has between seven and 10 mutations on the surface protein that allow it to bind to a cell’s receptor and enter the body, making it more infectious.

Whether or not it will be the driver of our flu season this year remains to be seen, but Walaza said that within the sporadic cases of flu detected and sequenced so far this year, most of the cases have been sub-clade K. In an NICD report from March, of the 24 influenza samples that were sequenced between 29 December 2025 and 22 March 2026, 11 were confirmed as being sub-clade K.

(Source: NICD Respiratory Pathogens Report Week 12 2026 report)

Experts will be keeping a close eye on circulating flu viruses with real-time genomic surveillance.

“South Africa is considered to be one of the top virus genomic surveillance places in the world,” De Oliveira said. “[A]t the moment, we don’t see a big reason for concern [about the flu season],” he said. “We do genomic surveillance every week, both with public and private laboratories – and if we see anything unusual, that’s going to be highlighted very promptly.”

Trends seen in previous flu seasons

Overall, in the last ten years, influenza A seems to be the driver of the majority of flu cases in South Africa, said De Oliveira, usually causing a big wave of flu cases at the start of the season. This is usually followed by a smaller wave of influenza B cases. In this time period, the influenza A subtype that dominates during the flu season appears to alternate between A(H1N1) one year and A(H3N2) the following year, but it also doesn’t always follow this pattern.

Zooming in more closely, Walaza said that over the last six years, 2020 and 2021 were outliers, with reduced transmission during 2020 due to the measures taken to curb the spread of the SARS-CoV-2 virus and out of season influenza transmission in 2021. Since 2022, the number of people getting flu every year has returned to roughly similar levels as before 2020.

Last year’s flu season was slightly unusual since it had started in late March, according to Walaza, but wasn’t as intense as some of the previous years as transmission remained at a low threshold level. Flu cases peaked in mid-May and then rose again slightly in October and November.

Data on influenza comes from three sentinel monitoring programmes managed by the NICD, which cover both the public and private healthcare sectors, said Walaza. A sample of healthcare facilities in the public sector and doctors in the private sector are asked to supply swabs taken from people with influenza-like illnesses or respiratory illnesses. Some general practitioners in the private sector are also enrolled in a programme called Viral Watch.

She said that the swabs are sent to the NICD laboratory and tested for the presence of different viruses, including SARS-CoV-2, influenza, RSV, parainfluenza, human metapneumovirus and rhinoviruses. If the samples test positive for flu, the sample is further tested to identify the lineage. This data is included in the weekly reports published on their website.

Members of the public can contribute to flu surveillance through an online web platform called CoughWatch. People are invited to enroll and provide weekly information on whether they have symptoms of flu or other respiratory illnesses. This is aimed at picking up trends among people who aren’t necessarily getting sick enough to go to the doctor or clinic, said Walaza and can hopefully serve as an early warning system for increases in respiratory illnesses, including flu.

CoughWatch has already opened for enrollment this year. (More information can be found here).

Flu vaccination uptake in South Africa remains low

Each year, the WHO releases recommendations on what should be in upcoming flu vaccines for the Northern Hemisphere and then later the Southern Hemisphere, usually announced around six months before the start of the respective flu seasons.

This year’s flu shot’s formulation is a trivalent one, said Walaza meaning it contains inactivated strains of all three influenza strains, including coverage for the A(H3N2) sub-clade K. Because it contains an inactivated virus, the vaccine itself cannot give someone the flu.

The level of protection offered by flu shots vary, but generally it ranges in effectiveness against preventing infection from about 30% to 60%. This means the shot will offer most people protection from severe disease and death, but it won’t necessarily prevent them from getting sick with the flu altogether.

One of the things that makes it difficult to predict effectiveness ahead of time is the possibility that a strain might circulate that is not well covered by the flu shot. De Oliveira said this “mismatch” is what we saw play out in some of the regions in the Northern Hemisphere in their last flu season.

Despite the partial mismatch between the vaccine used in the northern hemisphere and sub-clade K, several surveillance reports from the Northern hemisphere show that the vaccine nevertheless provides some protection against severe flu caused by sub-clade K.

The WHO also recently touched on this, saying that: “While current influenza vaccines help reduce the burden of disease, their effectiveness can vary by season, product, and population group. Protection is limited to one season”. The majority of flu vaccines purchased each year are by upper-middle and high-income countries, the WHO noted.

Usually, South Africa’s National Department of Health procures about 1 million flu shots for the public health sector, said Walaza and sometimes not all these doses are used.

While flu shots are made available each year, the uptake of these shots in the private sector appears to be low. Based on data collected through the NICD’s Viral Watch initiative – last year the uptake of the influenza vaccine in the private sector, among those enrolled in the programme, was only around 3.4%. This is based on data collected from 768 people enrolled, of those, 26 had gotten a flu shot. As far as Spotlight could establish, there currently isn’t any routine publicly available data on uptake in the public sector. One study of around a thousand people aged 65 and older, found that just over 32% of them had gotten the flu jab in 2018.

Spotlight asked the National Department of Health how many flu vaccines were procured for this year’s flu season. A response had not been received by the time of publication.

Low flu vaccine uptake can in part be attributed to South Africa having much milder winters and less severe flu seasons than the Northern Hemisphere, said De Oliveira.

Lack of awareness of the flu vaccine can also play a role, according to Walaza. She encourages more education and efforts by healthcare workers to inform at risk groups of the flu shot and when it will be available.

The flu shot is recommended for people who are at risk of severe disease, including older persons, pregnant women, people who are immunocompromised or with chronic medical conditions, as well as healthcare workers. But anyone aged six months and older can get the shot.

“The influenza vaccine will be available in pharmacies from the first week of April. The early start to the season means that this year, the vaccine is only becoming available as the season is getting started, so members of the public who fall into groups at high risk for severe influenza are urged to get their vaccines as soon as possible,” the NICD press release stated.

The potential of next generation flu vaccines

Earlier this year, the WHO released results from an assessment report on the value of having improved flu vaccines. “If improved, next-generation, or universal influenza vaccines are available and widely used between 2025 and 2050, they could prevent up to [an estimated]18 billion cases of influenza and save up to 6.2 million lives globally,” the report stated.

“This assessment makes clear the potential benefits that improved influenza vaccines could offer across different settings,” said Dr Philipp Lambach, WHO technical lead of the project. “It provides all those working on future influenza vaccine investments, policy development and research priorities a common set of evidence to catalyse vaccine development.”

According to the WHO, as of February 2026, there are 46 next-generation influenza vaccines in clinical development.

Republished from Spotlight under a Creative Commons licence.

Read the original article.

Categories : CancerTags :

Vaping is Likely Carcinogenic, Finds New Review

On By ModernMedia
Credit: Pixabay/CC0 Public Domain

Nicotine-based vapes (e-cigarettes) are likely to cause cancers of the lung and oral cavity, according to a new study led by UNSW Sydney and published in Carcinogenesis. The study is titled “The carcinogenicity of e-cigarettes: a qualitative risk assessment.”

The work analyses a wide body of global research and was led by UNSW cancer researcher Adjunct Professor Bernard Stewart AM, with investigators from The University of Queensland, Flinders University, The University of Sydney, as well as Royal North Shore, The Prince Charles and Sunshine Coast University hospitals.

The team brought together experts from multiple disciplines, including pharmacists, epidemiologists, thoracic surgeons, and public health researchers. Together, they examined the evidence from different scientific perspectives.

“To our knowledge, this review is the most definitive determination that those who vape are at increased risk of cancer compared to those who don’t,” Prof Stewart says.

This assessment of carcinogenicity review argues that while researchers have long focused on vaping as a gateway to smoking, less attention has been paid to whether the devices might cause cancer on their own.

It is one of the most detailed attempts yet to determine whether vaping itself may cause cancer, independent of tobacco smoking. The analysis draws together clinical studies, animal experiments, and laboratory research examining the chemicals produced by e-cigarettes.

“Considering all the findings—from clinical monitoring, animal studies and mechanistic data—e-cigarettes are likely to cause lung cancer and oral cancer,” Prof Stewart says.

He says that though the consistency of findings across those disciplines was striking, the exact number of attributable cancer cases remains unclear.

“Our assessment is qualitative and does not involve a numerical estimate of cancer risk or burden. We’ll only be able to determine the precise risk once longer-term studies are available.”

Growing public health concerns

E-cigarettes were first sold in the early 2000s. Early marketing framed them as a “safer” alternative to tobacco cigarettes, as well as a possible aid for quitting smoking.

But the colourful, flavoured devices of today have spread quickly and widely, particularly among young people.

“E-cigarettes are known to be a gateway to smoking and hence cancer,” says co-author UNSW Associate Professor Freddy Sitas. “But the extent to which they may cause cancer in their own right has not received as much attention in research. The evidence was remarkably consistent across fields. It dictated an unequivocal finding now, though human studies that estimate the risk will take decades to accumulate.”

A clear outcome

Smoking has been studied for more than a century. Though e-cigarettes are relatively new, inhaling nicotine-laced aerosols is already linked to addiction, poisoning, inhalation injuries, and burns.

While researchers wait for long-term population studies showing whether people who vape are more likely to develop cancer, they must rely on multiple other forms of evidence.

The team identified numerous carcinogenic compounds in e-cigarette aerosols, including volatile organic chemicals and metals released from heating coils.

They examined several types of evidence: biomarkers in people showing DNA damage, oxidative stress, and tissue inflammation; experiments in mice that caused lung tumours; and laboratory studies showing cellular damage and disrupted biological pathways linked to cancer.

Taking all the results together, the researchers say the evidence points strongly in one direction.

A compounding problem

There is also growing evidence that many smokers who switch to vaping don’t quit cigarettes.

“Most of those who use e-cigarettes to quit smoking end up in ‘dual-use limbo,’ unable to shake off either habit,” says A/Prof Sitas. “What we do know from recent epidemiological evidence from the U.S. is that those who both vape and smoke are at an additional four-fold increased risk of developing lung cancer.”

History repeating

A/Prof Sitas and Prof Stewart traced parallels between the early scientific evidence linking smoking to disease and emerging concerns about vaping.

It took nearly a century of scientific investigation—from the mid-1800s to the landmark US Surgeon General’s report in 1964—before smoking was officially recognised as a cause of lung cancer.

During that time, early warning signs were often dismissed or overlooked.

“Early reports linked smoking to infectious diseases such as tuberculosis, followed by cardiovascular disease, stroke and lung cancer,” A/Prof Sitas says.

He says the same pattern may now be unfolding with vaping, and that researchers should not repeat the delay that occurred with cigarettes.

“E-cigarettes were introduced about 20 years ago. We should not wait another 80 years to decide what to do.”

Source: University of South Wales

Categories : Cancer Urology

Increased Bladder Cancer Survival with New Combination Treatment

On By ModernMedia
Photo by National Cancer Institute on Unsplash

A combination of immunotherapy and targeted cancer treatment given before and after surgery may reduce the risk of recurrence and improve survival in patients with muscle‑invasive bladder cancer who cannot tolerate conventional chemotherapy. The findings come from a new study from Karolinska Institutet, published in The New England Journal of Medicine.

Muscle‑invasive bladder cancer is a serious disease with a high risk of recurrence. To lower the risk of recurrence, patients are often given cisplatin‑based chemotherapy before surgery, but around half of patients cannot receive this treatment, commonly due to impaired kidney function. In the phase 3 study, all participants underwent standard surgery, in which the bladder is removed. One of the groups also received a new combination treatment with the immunotherapy pembrolizumab and the targeted drug enfortumab vedotin before and after surgery.

Large differences between the groups

The results show that 75% of participants treated with the combination therapy were alive without recurrence two years after enrolment, compared with 39% in the control group. When the researchers looked at overall survival, a larger proportion of patients in the treatment group were also alive after two years. In addition, no tumour cells were found in the removed bladder tissue in 57% of patients in the treatment group, compared with 9% in the control group. In total, 344 participants from 27 countries took part in the study.

“These are very promising results for patients with few treatment options available before surgery. It is also reassuring that the treatment does not appear to affect the ability to proceed with surgery, which can otherwise be a concern when treatment is given beforehand,” says Anders Ullén, professor of oncology at the Department of Oncology‑Pathology at Karolinska Institutet and the study’s last author.

Side effects occurred in both groups

All patients who received the combination treatment experienced some form of side effect. Common side effects included itching and hair loss, and the most frequent serious side effect in both groups was urinary tract infection. Serious complications also occurred among those who underwent surgery alone, which the researchers note reflects the fact that many patients in this group are older and have other underlying health conditions.

“It is always important to balance the benefits of treatment against the risk of side effects. At the same time, the results indicate that the treatment may offer clinically meaningful improvements, reduce the risk of recurrence and improve survival for many patients. We hope that the findings can help inform future treatment practice,” says Anders Ullén.

Source: Karolinska Institutet

Categories : DermatologyTags :

New Research Sheds Light on Why Atopic Dermatitis So Often Begins in Childhood

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Photo by Chayene Rafaela on Unsplash

A team of researchers at the Icahn School of Medicine at Mount Sinai, Weill Cornell Medicine, and other institutions have uncovered a key biological explanation for why atopic dermatitis (eczema) so often starts in childhood. The study, in young mice, found that some types of immune cells in early-life skin are more reactive than those in adults, a difference that may help explain why children are more vulnerable to inflammation and allergic skin disease. 

The findings, reported in Nature, suggest that early childhood represents a critical window for immune-driven skin disease and may shed light on why atopic dermatitis is often the first condition in a broader pattern of allergic disease.

Atopic dermatitis (AD) affects nearly one in four children and often appears early in life. It can also precede other allergic conditions, including asthma and food allergies. Until now, scientists have not fully understood why the disease is so strongly linked to early childhood. 

“We found that allergy risk is shaped very early in life, when the skin’s immune system is biologically programmed to overreact to allergens, with important consequences for understanding how immune-mediated diseases emerge and should be treated,” says senior study author Shruti Naik, PhD, Associate Professor of Immunology and Immunotherapy, and Dermatology at the Icahn School of Medicine. “By pinpointing the cells and hormonal signals that control this window of vulnerability, we open the door to strategies that could prevent allergic disease before it spreads from the skin to the lungs, gut, and beyond.”  

The researchers discovered that a specific immune cell type, the dendritic cell, in young skin behaves differently than in adults. These cells do not overreact to everything – but when it comes to allergens, they respond faster and more strongly, setting the stage for inflammation and AD early in life. In adult skin, the same cells are far less reactive.  

To understand why allergies often start in early childhood, researchers exposed infant mice to everyday allergens such as dust mites and mould. Unlike adult mice, the infants developed strong skin inflammation, revealing a brief early-life period when the skin’s immune system is especially sensitive.  

The scientists traced this response to dendritic cells, which are unusually active shortly after birth and triggers allergic inflammation. When this pathway was blocked, the young mice did not develop skin allergies.  

The team also found that infants lack normal levels of stress hormones that later help keep immune reactions in check, allowing these allergic responses to take hold. Importantly, signs of the same immune activity were found in skin samples from children with early-onset AD, but not in adults, suggesting this early-life window may also be important in humans. 

“This work was only possible through a true clinic-to-lab collaboration – where insights from paediatric patients shaped the questions we asked in the lab,” says study co-author Emma Guttman-Yassky, MD, PhD, professor at the Icahn School of Medicine. “By studying allergic disease where it actually begins, in early life, and by modelling clinically relevant allergens and disease features, lead author Yue Xing, PhD, uncovered immune biology that simply doesn’t appear in adult models. By revealing what’s unique about the early-life immune system, this work explains why eczema so often begins in infancy.” 

Next, the investigators plan to explore ways to block this early-life immune pathway to stop allergic disease before it spreads from the skin to other organs.  

“Beyond eczema, this study reinforces a critical point for medicine,” says Dr Naik. “Children are not simply small adults when it comes to immunity. Their immune system follows a unique set of rules, and recognising that difference is essential for understanding – and ultimately preventing – allergic, immune-driven diseases that begin in childhood.” 

Source: Mount Sinai

Categories : HospitalsTags :

Burnout May Lead Family Doctors to Leave Medicine

On By ModernMedia

Of the nearly 20 000 physicians in a study led by Weill Cornell researchers,43.5% reported feeling burned out.

Photo by Usman Yousaf on Unsplash

Family physicians who report feeling burned out are nearly 1.5 times more likely to change practices or stop practising medicine entirely compared to their peers who don’t report burnout, a study by Weill Cornell Medicine researchers found. Physician burnout can include emotional exhaustion, detachment from patients and colleagues, and feeling that work is no longer meaningful.

The findings, published March 30 in JAMA Internal Medicine, also highlight the consequences for patients: people who lose their family physician may be more likely to visit the emergency room, spend more on health care and be less satisfied with their care than those who keep their doctors.

“To our knowledge, this is the first national-level study examining the association between physician burnout and turnover,” said Dr Amelia Bond, associate professor of population health sciences at Weill Cornell Medicine, who co-led the study.

To quantify burnout, Dr. Bond and her colleagues turned to the 2016-2020 American Board of Family Medicine surveys, which family physicians must complete to obtain and maintain board certification. As part of the survey, physicians are asked whether they feel burned out or callous.

The researchers then determined whether physicians changed practices or stopped practising altogether in the subsequent year, based on billing patterns in de-identified Medicare data.

Of the nearly 20 000 physicians in the study, 43.5% reported burnout. Doctors under the age of 55 were more likely to report burnout than older doctors, and women were more likely to report burnout than men.

The research suggests that workplace stress may reduce physician retention. Among physicians who reported burnout, 4.8% changed practices versus 3.4% of physicians who did not report burnout; 5.4% of physicians with burnout stopped practising entirely compared to 3.7% of physicians without burnout.

“These findings highlight the urgent need to address work conditions and professional satisfaction for both the stability of the physician workforce and the well-being of patients,” said Dr Dhruv Khullar, associate professor of population health sciences at Weill Cornell Medicine and co-lead on the study. 

Physician burnout and turnover have clinical, organisational and economic implications. “The issue definitely warrants more attention,” D. Bond said.

Further investigation could identify practices, systems and policy factors that may reduce rates of physician burnout and turnover. While this study found a correlation, additional work will be needed to establish a causal link between burnout and turnover.

Source: Weill Cornell Medicine

Categories : Neurology Pain ManagementTags :

Pain Neurons Protect Nerve Health and Offer New Therapeutic Targets

On By ModernMedia
A healthy neuron. Credit: NIH

Researchers at Karolinska Institutet, have uncovered a previously unknown mechanism that helps pain sensing nerve cells stay healthy and respond to injury. The findings, published in Nature Communications, may improve understanding of chronic pain and nerve damage and maintenance of myelin integrity.

A new study shows that a molecule called RNase4, is produced by specialised pain-sensing neurons. It plays a key role in maintaining their normal function and influences both these neurons and the structure of nearby nerve fibres, positioning pain-sensing neurons not only as sensory transducers but also as sentinels of nerve integrity.

The researchers showed that RNase4 is expressed in unmyelinated sensory neurons, including neurons that innervate the auditory organ, and in the pain-sensing neurons that innervate the face, head, dura mater, and the rest of the body. By combining multiple experimental approaches on mice, they demonstrated that loss of RNase4 alters mechanical pain responses and disrupts the myelin structure surrounding neighbouring nerve fibres. They also found that RNase4 levels increase after nerve injury, both during the pain phase and the subsequent recovery period.

“Our results point to RNase4 as part of a regulatory pathway that supports nerve integrity. This molecule has not previously been linked to pain sensing neurons, so its presence and role came as a surprise,” says corresponding author Saida Hadjab, head of the Neurobiology of pain & Therapeutics laboratory at the Department of Neuroscience.

Chronic pain is often difficult to treat, partly because the underlying biology is still not fully understood. The findings suggest that pain sensing neurons may take on a more active role in maintaining the health of surrounding nerve tissue.

“This work has enabled us to identify a novel mechanism and position RNase4 as a regulator of afferent neuron integrity and local microenvironment. The localisation of RNase4 and its function in sensory neurons made it directly relevant to hearing dysfunction, headache, and chronic pain,” says Saida Hadjab.

RNase4 shows a comparable expression pattern in human pain-sensing neurons, supporting its potential relevance in humans. While further research is required to develop therapies targeting the RNase4 pathway, these findings provide a strong foundation for advancing the study of myelin integrity and long-lasting pain in humans.

Source: Karolinska Institutet

Categories : PaediatricsTags :

Screening Tests for Autism Miss Many Children at Risk

On By ModernMedia
Photo by Helena Lopes on Unsplash

M-CHAT does not catch all children with autism in the neonatal high-risk group, shows a study from Karolinska Institutet published in JAMA Network Open. The researchers see a need to supplement the test with other assessment methods.

Children born very prematurely or with complications are screened at the age of two for early signs of autism using the M-CHAT questionnaire. In a new national study, researchers at Karolinska Institutet have investigated how well the test works in this high-risk group. The study includes 2178 children born in Sweden between 2013 and 2019 and compares M-CHAT results with later clinical diagnoses of autism.

The researchers found that the test was highly accurate in ruling out autism, but that many children with autism were still missed. The sensitivity was 62%, while the specificity – the ability to identify children without autism – was 91%. In total, 12% of the children received a positive M-CHAT result and 6% were later diagnosed with autism.

“The results show that M-CHAT works relatively well to rule out autism, but that it does not catch all children who later receive a diagnosis. In this high-risk group, more tools are therefore needed to detect children who need further investigation early,” says Ulrika Ådén, professor at the Department of Women’s and Children’s Health.

Children born extremely prematurely had both the highest proportion of positive test results and the most autism diagnoses. The researchers also saw that girls had fewer positive test results than boys, and that linguistic factors could affect the outcome – the test had higher specificity in families that spoke a Scandinavian language.

“Overall, the study shows that other developmental difficulties, such as motor or sensory problems, can affect how M-CHAT is interpreted. This needs to be taken into account when healthcare works with early screening,” says Ulrika Ådén.

Source: Karolinska Institutet

Categories : Diet and Nutrition Obstetrics & GynaecologyTags :

Study: Intermittent Fasting Positively Affects Female Hormones in PCOS 

On By ModernMedia
Photo by Sora Shimazaki on Pexels

Polycystic ovary syndrome, or PCOS, affects as many as 18% of all childbearing-age women. The condition occurs when a woman’s body produces too androgens, chiefly testosterone. Menstrual irregularity, obesity and even infertility can result.

The first line of treatment is typically hormonal birth control, said UIC professor of nutrition Krista Varady. But there can be negative side effects to mood, libido and metabolism, plus an increased stroke risk in some people, Varady said.

“We’re looking for other ways of lowering testosterone levels in these women,” she said. “One way is through weight loss. If someone loses around 5% of their body weight, they can actually help lower testosterone levels and sidestep any kind of drug intervention.”

A new study led by Varady tested how one weight-loss method — intermittent fasting — affects hormones and symptoms in patients with PCOS. Published in Nature Medicine, the research shows that restricting eating to a six-hour daily window decreased testosterone without negatively affecting female hormones. The study also showed that weight loss through calorie counting decreased testosterone. 

However, some critics of intermittent fasting have posited that the diet disrupts female hormones, Varady said.

“There’s a particular sentiment that intermittent fasting is really bad for women.” This is untrue, she said. “This study and several other studies published by our lab and others show that intermittent fasting can actually improve female hormone levels, particularly in women with PCOS.” 

Varady and her colleagues studied a type of intermittent fasting called time-restricted eating. In this method, you eat only during a set six- or eight-hour period each day. During the remaining 18 or 16 hours, you fast with calorie-free beverages and water until the next day. 

Simply put, the strategy helps people eat less, Varady said. So does counting calories, a method Varady and her colleagues tested alongside intermittent fasting in the study. But intermittent fasting had some additional benefits.

“It’s a way of reducing energy intake without having to do really complicated calorie counting,” she said about intermittent fasting. Varady and others have shown in previous work that eating only during an eight-hour window can cut around 300 to 500 calories a day.

In addition to obesity and insulin resistance, which raise risks of diabetes and heart disease, PCOS can cause ovarian cysts, acne and facial hair growth.

In a group of 76 pre-menopausal women with PCOS, the researchers tested how outcomes differed after six months between time-restricted eating between 1 and 7 p.m. daily and calorie counting. Both diet schemes ended up cutting participants’ intake by about 200 calories per day, the team found, leading to average weight loss of about 10 pounds over the six months.

Both groups also experienced a decrease in testosterone concentrations. But only time-restricted eating reduced free androgen index, the ratio between testosterone and the protein that transports it through the blood, which is a marker of how much active testosterone is reaching a body’s tissues. It also improved A1C levels, a risk marker for diabetes, Varady said.

Though intermittent fasting did not lessen other PCOS symptoms, like menstrual period irregularity, Varady suggested those symptoms might improve with longer time on the diet and greater weight loss.

About 80% of the participants in the time-restricted eating group said they were going to continue the diet, Varady said.

Story by Tess Joosse

Source: EurekAlert!

Categories : Expert Opinion Healthcare Politics and RegulationsTags :

As NHI Stalls, the Real Debate Is About Trade Offs

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ANC President Cyril Ramaphosa, with Minister of Health, Dr Joe Phaahla and his deputy Dr Sibongiseni Dhlomo, during the signing into law of the National Health Insurance Bill. (Photo: @MYANC/Twitter)

By Thoneshan Naidoo

Healthcare funding is always about trade-offs, writes Thoneshan Naidoo, CEO of the Health Funders Association. The hardest question in healthcare is not what we would like to provide, he argues, but what we can provide sustainably, fairly and at scale.

South Africa’s healthcare debate is shifting and perhaps for the first time in years, it is becoming more honest.

With the National Health Insurance (NHI) Act tied up in legal processes and no credible funding pathway emerging from the 2026 Budget, the conversation is moving away from sweeping promises about the future to a more immediate and uncomfortable question. That is how do we fund healthcare today, and what trade-offs are we willing to accept?

At the centre of that reality is a part of the system that is often misunderstood and frequently criticised – medical schemes.

They are often portrayed as profit driven and exclusionary. In reality, they are not for profit, member owned entities built on a simple but powerful principle, social solidarity. Simply put, members pool their contributions so that those who are healthy today help fund the care of those who are sick.

In practice, around 80% of members claim less than they contribute in any given year. Their contributions help fund the care of the 20% who need it most. That is not exploitation. It is the very definition of risk pooling, and it is the same principle that underpins universal health coverage.

But solidarity comes with trade-offs.

Every Rand paid out in benefits in excess of a member’s monthly contributions is funded by other members. That means decisions about what is covered, how much is paid, and when limits apply are not arbitrary. They are the result of difficult choices about what the overall pool can afford.

These trade-offs become most visible in moments of tension, when a claim is limited, a treatment is excluded, or a dispute arises. To the individual, the system can feel uncaring. But at a system level, the alternative, unlimited funding for every possible intervention, is simply not sustainable.

Even prevention, often presented as an obvious solution, is not as straightforward as it seems.

Take colorectal cancer screening. An inexpensive test such as a faecal immunochemical test can help detect disease early. But many false-positive results lead to follow up procedures like colonoscopies, even when no serious condition is ultimately found. At the same time, some cases are still missed and only diagnosed later, when treatment is more complex and more expensive.

The question is not whether prevention is valuable, it is how to fund it at scale in a way that balances early detection, over treatment and cost.

These are not abstract policy debates but are real world funding decisions that affect millions of people.

And they are taking place in a system under pressure.

Medical scheme membership is voluntary, so younger and healthier individuals often delay joining until they need care. This drives up costs for those already in the system. At the same time, schemes are required to cover a comprehensive set of 270 Prescribed Minimum Benefits, which raises the baseline cost of cover.

The result is a system that works well for those inside it but remains out of reach for many.

This is South Africa’s so-called “missing middle” – millions of working people who earn too much to qualify for public support, but too little to afford private cover. They are left exposed, paying out of pocket, and navigating a fragmented system while waiting for reforms that may still be years away.

As the NHI debate continues, this gap can no longer be treated as a future problem. It is a present reality.

The risk is that the debate remains stuck in ideology. That private healthcare is painted as inherently problematic, or that structural reform alone will resolve access challenges.

Neither is true.

Healthcare funding is always about trade-offs. There are no perfect systems, only different ways of balancing access, quality and affordability within finite resources.

If South Africa is serious about expanding access to healthcare, the debate must move beyond rhetoric and toward practical solutions.

These include using spare capacity in private facilities to treat public patients, and allowing medical schemes, through targeted regulatory reform, to offer affordable primary healthcare cover for people who are currently excluded. Done properly, this could unlock access to private healthcare for more than 10 million uninsured South Africans at a cost of as little as R400 per person per month. Combined with existing tax credits, the impact on a family’s take home pay could be close to negligible. By providing access to preventive and primary care through the private sector, they would reduce pressure on overcrowded public facilities and ease waiting times. Importantly, a strong focus on prevention and early intervention would reduce the need for costly hospitalisation over time.

Medical schemes are well placed to deliver these options, given the principles of social solidarity, community rating and cross-subsidisation that underpin their design. This approach is aligned with the Sustainable Development Goals and the core principles of universal health coverage, and could serve as a practical transitional step as South Africa moves towards the full implementation of National Health Insurance.

After all, the hardest question in healthcare is not what we would like to provide. It is what we can provide sustainably, fairly, and at scale.

*Naidoo is CEO of the Health Funders Association, an industry group that represents several medical schemes and medical scheme administrators in South Africa.

Note: Spotlight aims to deepen public understanding of important health issues by publishing a variety of views on its opinion pages. The views expressed in this article are not necessarily shared by the Spotlight editors.

Republished from Spotlight under a Creative Commons licence.

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Categories : Cardiovascular DiseaseTags :

Are Heart Failure and Atrial Fibrillation the Same Disease?

On By ModernMedia
Right side heart failure. Credit: Scientific Animations CC4.0

New research published in Nature Cardiovascular Research reveals that heart failure and atrial fibrillation share underlying genetic and molecular mechanisms, suggesting that the two cardiovascular conditions may be less distinct than previously thought.

Two serious heart conditions that often coexist

Heart failure occurs when the heart muscle is damaged and unable to pump enough nutrient-rich blood to meet the body’s needs for oxygen. Heart failure is usually evaluated in the heart’s lower chambers, called ventricles, which provide most of the pumping power.

Atrial fibrillation is an arrhythmia that originates in the heart’s upper chambers, known as the atria. During atrial fibrillation, the heart beats too fast, resulting in a lower blood flow to the body and a higher risk for clots or stroke.

Epidemiologists have observed that these two conditions aren’t independent of one another: People with heart failure are much more likely to have atrial fibrillation, and vice versa. Patients’ outcomes also tend to be worse when they have both conditions.

“This intersection between two very common, very important diseases – both of which cause a lot of morbidity and mortality and billions of dollars in annual healthcare costs – has been called an ‘epidemic in cardiology,’ yet our understanding has remained very limited,” said senior author Ivan Moskowitz, MD, PhD, a paediatric cardiologist and pathologist at the University of Chicago Medicine.

Uncovering TBX5 as a key genetic regulator

This new study was guided by previous research Moskowitz and his collaborators published in 2024, which kick-started when a former lab member created a mouse model by “turning up” a gene linked to human heart failure in the mouse heart.

“We expected to get a heart failure mouse model, but instead we got an atrial fibrillation model,” Moskowitz said. “That observation put us on the right path.”

This focused attention on a gene called TBX5. TBX5 is a transcriptional regulator: a protein in the cell nucleus that controls which genes are turned on or off at a given time. When TBX5 levels are decreased in the atrium, it disrupts the normal gene expression needed to maintain a stable heart rhythm.

Zeroing in on transcriptional responses, the researchers compared different mouse models of heart failure and atrial fibrillation, finding that an atrial fibrillation model created by removing TBX5 from the atria actually creates gene expression changes almost identical to those seen in heart failure.

“That made us think that diminished TBX5 may be important in heart failure,” Moskowitz said. “So, we looked at human gene expression data, and lo and behold, TBX5 was very downregulated in the atria of patients with heart failure, but not the ventricles.”

This finding suggested a mechanistic link: reduced TBX5 in the atrium may contribute to the development of atrial fibrillation in the context of heart failure.

Coordinated genetic response across cell types

Further analysis revealed that over 100 other transcription factors – proteins that regulate gene expression – were altered in both the heart failure and TBX5-deficient atrial fibrillation models. Almost all the key transcription factors changed in the same direction in both conditions.

“Seeing these correlations emerge effectively indicates that from the atrium’s perspective, what’s happening in the two conditions is the same,” Moskowitz said.

Using single-cell analysis, the team identified which human cell types in the atrium were involved in the disease mechanism. Cardiomyocytes and fibroblasts both showed disease-related gene changes, suggesting that the pathological response involves multiple cell types communicating with one another.

Rethinking atrial fibrillation as atrial heart failure

Strikingly, the authors argue that the results should prompt a fundamental shift in how atrial fibrillation is understood. The rhythm disorder seen in atrial fibrillation may be a symptom of underlying atrial muscle dysfunction similar to the ventricular dysfunction in heart failure.

“The coordinated change in transcription factors lead us to conclude that atrial fibrillation is not really a different disease than heart failure; it is just what we might call ‘atrial heart failure,’ a manifestation of which is atrial fibrillation,” Moskowitz said. “Instead of a rhythm disorder in the atria, we can understand it more like an atrial myopathy that is mimicking what’s happening in ventricle cells in heart failure.”

Unlocking future treatment avenues

This new perspective could have important implications for cardiovascular disease treatment. Currently, therapies for atrial fibrillation focus on controlling the heart’s electrical rhythm, often by targeting ion channels that regulate electrical signals. Moskowitz suggests a broader approach: “We may be able to go higher upstream. Rather than trying to drug the channels directly, we could think more about the response of the atrium to pressure, much like we do the ventricles in heart failure. Approaching atrial fibrillation like heart failure may be a different avenue.”

In ongoing work, the UChicago Medicine researchers are continuing to analyse these genetic and molecular pathways. They’ve already identified multiple signalling genes expressed in cardiomyocytes that are disrupted when TBX5 is “turned down,” and are working to investigate whether replenishing those signals can prevent atrial fibrillation from occurring. This combination of insight and fundamental biology is the driving force behind translational advancement.

“This intersection is a fertile ground for insight into atrial fibrillation and how it may be treated,” Moskowitz said. “We’re excited because this study provides many candidates for future investigation. We hope our work can be applied to new thinking and interventions toward a cure.”

Source: University Chicago Medicine