Categories : Obstetrics & Gynaecology Pain ManagementTags : Leave a comment

Epidurals Not Linked to Increased Harm for Newborns or Children

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Study provides strong evidence that epidural analgesia in labour is safe for newborns, say researchers

Photo by Duda Oliveira

Having an epidural during labour is not associated with clinically significant increased risks of harm to newborn babies, including brain injury, severe breathing problems, sepsis and death, or cerebral palsy later in childhood.

The researchers say these findings “support widening availability and equitable access to epidural analgesia as a safe component of intrapartum care.”

Epidural analgesia in labour provides effective pain relief and may help reduce complications in mothers after giving birth, but evidence of its effect on newborn and child health is limited.

To address this, researchers analysed data for 495 695 births in Scotland over a 13 year period (2007-2019) to examine whether epidural analgesia during labour was associated with serious neurological conditions occurring within 28 days of birth.

Only women who delivered a single baby vaginally or via unplanned caesarean section between 24 and 42 weeks of pregnancy were included in the analysis.

Further measures included other severe newborn illness, sepsis, low Apgar score (a routine test of a baby’s health) five minutes after birth, death within 28 days of birth, and cerebral palsy diagnosed at any point during childhood.

Factors such as mother’s age, ethnicity, weight, existing pre-eclampsia or diabetes, smoking history, birth location and gestational age at birth, were also taken into account.

Of nearly 500 000 women included in the study, around one in four had an epidural during labour. Overall, serious neurological conditions were rare, affecting fewer than 1 in 1000 babies. These conditions occurred at the expected rate and were no more common among babies whose mothers had an epidural compared with those who did not.

No association was found between epidural analgesia in labour and serious neurological conditions, other severe newborn illness, sepsis, low Apgar score at five minutes, death at 28 days, or cerebral palsy in childhood.

This is an observational study so no firm conclusions can be drawn about cause and effect, and the authors acknowledge that the study was limited to women delivering in Scotland, a predominantly white population, so the findings may not apply to more ethnically diverse populations or other healthcare settings.

However, this was a large study with long term follow-up of newborn and childhood outcomes, and results were consistent after additional analyses across various groups including women considered to have high risk pregnancies and preterm births, supporting the reliability of the findings.

As such, the authors conclude: “These results should reassure parents and clinicians that epidural analgesia use in labour is safe for babies and support informed, evidence based decision making about analgesic options in labour.”

Source: The BMJ Group

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Dialling Back Stiffness May Protect Muscles in Myotonic Dystrophy

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Photo by Sasun Bughdaryan on Unsplash

For decades, researchers studying myotonic dystrophy type 1 (DM1) have focused on the disease’s underlying genetic cause: a mutation that produces a toxic form of RNA, disrupting the normal processing of thousands of genetic messages inside cells. While scientists have known this widespread disruption contributes to disease, it has remained unclear which changes are most responsible for the progressive muscle weakness and wasting experienced by people living with DM1.

Now, a new study published in Nature Communications suggests that one hallmark symptom of the disease – muscle stiffness, known as myotonia—may play a much larger role in driving muscle damage than previously recognised.

“Our findings suggest that myotonia isn’t simply an uncomfortable symptom people experience,” said John Lueck, PhD, associate professor of Pharmacology and Physiology at University of Rochester Medicine and senior author of the study. “It appears to amplify the harmful effects of the disease in muscles. When we eliminated myotonia in our mouse model, we didn’t just improve muscle relaxation; we saw healthier muscles overall.”

The findings suggest that therapies aimed at reducing myotonia could help preserve muscle function while complementing emerging treatments designed to address the disease’s underlying genetic cause.

A disease caused by toxic RNA

DM1 is the most common form of adult muscular dystrophy. The inherited disorder causes progressive muscle weakness, muscle wasting, slow relaxation after muscle contraction, heart rhythm abnormalities, cataracts, excessive daytime sleepiness, and a range of other symptoms.

The disease begins with an abnormal expansion of repeated DNA segments in the DMPK gene. Rather than producing a faulty protein, this mutation creates a toxic RNA molecule that traps proteins needed to correctly process genetic instructions. As a result, hundreds to thousands of genes are improperly “spliced,” producing abnormal protein versions throughout the body. Decades of research led by URochester Medicine neurologist Charles Thornton, MD, a co-author of the study, helped establish how this toxic RNA disrupts normal RNA splicing and drives the disease.

One of the most important affected genes expresses a chloride channel that helps muscles relax after they contract. When that channel is disrupted, muscles become electrically overactive, producing the delayed relaxation known as myotonia.

Looking beyond the root cause

Most research has focused on eliminating the toxic RNA itself, with several RNA-targeted therapies now advancing toward clinical use. However, Lueck and his colleagues wanted to answer a different question: once myotonia develops, does it simply reflect the disease, or does it actively worsen muscle damage?

Previous work from the URochester Medicine team had hinted at the answer. They found that when myotonia occurred alongside another splicing defect affecting calcium channels, muscle disease became dramatically worse in mice. Treating those mice with calcium channel-blocking drugs reversed many of the effects. That finding suggested that muscle hyperexcitability might be directly contributing to muscle degeneration.

“We’ve spent years trying to understand which of the many splicing changes actually matter most,” Lueck said. “This study allowed us to isolate one of those changes and ask what happens when you permanently remove myotonia while leaving the underlying disease process in place.”

Turning down the disease’s “volume”

To answer that question, the researchers genetically corrected a single critical portion of the chloride channel gene in a mouse model of DM1. The researchers expected to reduce muscle stiffness. Instead, they saw improvements throughout the muscle.

The mice no longer developed muscle stiffness, but they also generated greater muscle force, showed healthier muscle tissue under the microscope, and experienced broad improvements in abnormal gene expression and RNA splicing. The findings suggest myotonia may act as what Lueck describes as a “volume knob” on the disease.

“The toxic RNA is still present,” he said. “But myotonia appears to turn up the damage happening in muscles. When we turned myotonia down, many aspects of muscle health improved, even though we hadn’t corrected the original genetic mutation.”

Implications for future treatments

The findings could influence how researchers think about treating DM1. Several experimental therapies currently in development are designed to eliminate the toxic RNA that causes the disease. Researchers have long used improvements in myotonia as an early sign that these therapies are working because the chloride channel is particularly sensitive to correction.

The new study suggests that reducing myotonia may itself contribute significantly to improved muscle health. In other words, treating myotonia may do more than relieve stiffness – it may actually help slow or reduce the muscle damage caused by the disease.

At the same time, existing medications that reduce myotonia – including drugs such as mexiletine and ranolazine – may deserve renewed attention. Although these medications can improve muscle stiffness, side effects often limit their long-term use, and many people with DM1 never receive them.

“If we can develop safer, better-tolerated myotonia drugs, they could become an important complement to RNA-based therapies—or provide meaningful benefit for patients who don’t have access to those advanced treatments,” said Lueck.

Source: University of Rochester Medicine

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Melatonin May Help Ease Chronic Muscle and Joint Pain, New Study Suggests

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Dipa Kamdar, Kingston University

Melatonin is best known for helping us sleep. But a new study suggests it might have another surprising use: easing muscle and joint pain.

Produced naturally by the pineal gland in the brain at night, melatonin helps regulate the body’s sleep-wake cycle. That’s why this hormone is widely used as a treatment for insomnia and jet lag.

Sleep and pain are closely linked (poor sleep can make pain feel worse, and pain can make sleep harder). But melatonin may also reduce pain directly. Researchers believe it dampens pain signals in the brain and spinal cord, reduces inflammation, calms overactive nerves and protects cells from oxidative stress – the cellular wear and tear caused when harmful molecules build up.

In the new study, researchers combined the results of 23 clinical trials involving over 2,000 participants to identify overall patterns. These trials looked at melatonin for long-term muscle and joint pain as well as pain after surgery.

Overall, melatonin reduced both pain and sleep problems in people with chronic muscle and joint pain. But the improvements were modest. On average, pain scores fell by about nine points on a 100-point scale. That’s within the range reported for some anti-inflammatory drugs in similar studies, although the two treatments haven’t been directly compared.

Melatonin’s effects may also depend on whether people already have sleep problems or other long-term health conditions. Most of the chronic pain studies included people who already had poor sleep to begin with, but none of the trials looked at results separately for people with and without sleep issues. Because of this, it’s unclear whether melatonin works better for people who struggle with sleep or whether the effects are similar for everyone.

The findings were much less convincing for pain after surgery. Melatonin did not make a noticeable difference to pain or sleep. One analysis found a tiny improvement (about 2.5 points on a 100-point pain scale), but this is far below what would matter to patients recovering from surgery.

The benefits in chronic muscle and joint pain are modest. Based on the current evidence, melatonin should be seen as a possible add-on treatment rather than a replacement for established therapies. The evidence suggests melatonin could complement treatments such as physiotherapy, exercise and anti-inflammatory medicines rather than replace them.

What we still don’t know

There is also still a lot we don’t know. The trials in this study used a wide range of doses, from 1mg to 10mg, and the researchers couldn’t determine which dose worked best.

There were hints that longer treatment helped more in chronic pain, but this was based on only a few studies. There is also very little evidence on the effectiveness of higher doses, even though they appear safe in other studies.

Melatonin is widely used and generally considered safe for short-term use, but it can cause side-effects, such as daytime sleepiness, dizziness, headaches and nausea.

People with liver or kidney conditions, or those with autoimmune conditions like rheumatoid arthritis, should speak with a doctor or pharmacist before taking it.

It is also worth noting that melatonin is regulated very differently around the world. In the US, melatonin is sold as a dietary supplement, meaning people can buy it easily in supermarkets and online without medical advice. But in the UK, melatonin is a prescription-only medicine and is only licensed for short-term sleep problems and jet lag.

For now, the findings suggest melatonin may offer modest relief for some people with chronic muscle and joint pain, particularly if poor sleep is part of the problem. It’s unlikely to replace established treatments, but it could eventually earn a place alongside them. Larger, well-designed trials will be needed before doctors can say with confidence who is most likely to benefit.

Dipa Kamdar, Senior Lecturer in Pharmacy Practice, Kingston University

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

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Opinion Piece: Why Gap Cover Has Become a Non-negotiable Conversation for Advisers

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Photo by Alex Green on Unsplash

By James White, Director: Sales and Marketing at Turnberry Management Risk Solutions

Medical aid is essential for accessing private healthcare in South Africa, but it does not always cover the full cost of treatment. Shortfalls related to specialist fees, co-payments, and sub-limits, are an ongoing reality, leaving many medical aid members exposed to significant out-of-pocket expenses. This is why gap cover is no longer an optional conversation for advisers. As these shortfalls become increasingly common, clients rely on advisers to identify where cover may fall short and to explain how these risks can be managed. Gap cover plays an important role in addressing this challenge by covering the difference between what medical schemes pay and what providers charge, making it an integral part of the advice process.

Making gap cover part of the conversation

As medical expense shortfalls become increasingly common, addressing them is becoming part of a financial adviser’s responsibility. When recommending or reviewing medical aid, it is not enough to focus only on contributions and benefits. Advisers also need to ensure that their clients are fully aware that their medical aid may not cover the full cost of treatment, particularly where specialist fees, co-payments and sub-limits apply.

Areas where clients are likely to face out-of-pocket costs need to be explained clearly, together with how gap cover can reduce them. Advisers need to position gap cover not as an optional extra, but as an essential part of ensuring that clients are not left exposed to avoidable out-of-pocket costs.

The cost of not addressing shortfalls

If financial advisers do not discuss gap cover with clients, the impact is typically not felt immediately. However, the problem becomes clear when a claim arises. If a member receives  treatment expecting their medical aid to cover the full cost, and then ends up with a large bill for the shortfall, or has to pay a large co-payment upfront, this can result in significant dissatisfaction.

The reality is that medical expense shortfalls are no longer unusual, and both the size and frequency of these costs are increasing. Specialists may charge several times the scheme rate, while co-payments and benefit limits are increasingly used by medical aids to manage costs and keep premiums affordable. Without additional cover, patients must pay these costs out of pocket, and they can run into tens or even hundreds of thousands of rands.

This is why it is important that these gaps be raised upfront. Clients rely on their advisers to explain how medical aid works and what costs may arise, so they can make informed decisions before a claim happens, rather than being caught off guard by costs that place pressure on their finances.

What advisers should be explaining

Gap cover should form part of every discussion around medical aid, rather than being treated as an optional extra. When recommending or reviewing medical aid, it is important for advisers to highlight where out-of-pocket costs may still arise, including specialist tariff gaps, co-payments, sub-limits and network restrictions.

These risks need to be explained clearly, together with how gap cover can reduce them. Discussing this upfront helps clients understand what their medical aid will and will not pay, so they are not surprised by costs when they claim. It also ensures that decisions around cover are based on a clear view of the full healthcare funding picture, not only the monthly premium.

Over time, this approach builds trust and reinforces the adviser’s role in helping clients manage healthcare costs, rather than reacting to them after the fact.

Complete advice requires a complete view of healthcare risk

Medical aid remains essential, but it does not remove the risk of medical expense shortfalls, co-payments, or sub-limits. These are now a routine part of private healthcare and need to be addressed as part of the advice process.

Advisers have a responsibility to identify and explain these risks clearly, and to make them a consistent part of every client conversation.

Helping clients understand how their medical aid works, where shortfalls may arise, and how gap cover can address those gaps ensures that their cover reflects a complete view of their healthcare costs and is genuinely aligned to their needs.

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How Did the COVID-19 Pandemic Shift Seasonal Surges of Other Respiratory Diseases?

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Study links shifts to buildup of susceptible hosts, explores similar shifts in heart-related deaths

Creative layout featuring scientifically-based 3D renderings of respiratory syncytial virus (RSV). RSV is a common contagious virus that infects the human respiratory tract. Credit: NIAID

 A German analysis explores what underlies shifts in the timing of seasonal surges of respiratory diseases, as well as shifts in surges of heart-related deaths, that occurred after the COVID-19 pandemic began. Michael Sieber and Arne Traulsen of the Max Planck Institute for Evolutionary Biology, Germany, present these findings in the open-access journal PLOS Global Public Health on July 15, 2026.

Rates of respiratory infections such as the flu and RSV typically peak during seasons when transmission rates rise. Rates of death from any cause – not just from infection – follow a similar seasonal pattern.

However, the drivers underlying the exact timing of these surges have been unclear. The COVID-19 pandemic provided a unique opportunity to explore these dynamics, since interventions like social distancing and masking disrupted typical transmission patterns of other respiratory diseases. Sieber and Traulsen analysed data on weekly respiratory infection rates and death rates in Germany, covering the last 14 years. 

The analysis showed that, pre-pandemic, respiratory infections almost always surged for a few weeks February and March. After the pandemic began, intervention efforts tamped down infections, eliminating one seasonal surge. Once infections rose again, surges shifted to December or earlier. Now, these peak weeks are gradually resuming pre-pandemic timing.

Using well-established epidemiological modelling tools, the researchers found that population-level loss of immunity after the skipped seasonal surge led to buildup of susceptible hosts, resulting in higher transmission earlier in the season. That is, seasonal transmission variations present a window of opportunity for a surge, and the size of the pool of susceptible hosts at the start of that window determines when, exactly, the surge occurs.

Similarly, typical seasonal surges in rates of death from any cause – but particularly from cardiovascular disease – also shifted earlier post-pandemic. Thus, respiratory infections may be key drivers of the timing of seasonal surges in cardiovascular deaths. More research is needed to explore this connection, but it aligns with other evidence that respiratory infections are a significant risk factor for cardiovascular disease.

On the basis of their findings, the researchers emphasize the importance of monitoring people’s infection history and improving vaccination coverage.

The authors add: “News stories of an earlier than usual onset of the flu season during the COVID-19 pandemic motivated us to look into the available epidemiological data more closely. We were surprised by the magnitude of the shift in timing of seasonal respiratory infections in Germany, and interested in trying to predict if this would turn out to be a long-term effect of the pandemic or if we should expect a quick return to the normal seasonal timing. The most recent flu seasons confirmed that the seasonal timing indeed shifts back to normal within one or two seasons, most likely due to a return to the pre-pandemic population-levels of immunity to the most common respiratory pathogens. We were even more surprised to see that the seasonal dynamics of all-cause mortality, which is dominated by cardiovascular diseases, closely followed the shift in timing of respiratory infections. This adds to the growing evidence that respiratory infections are an important risk factor for cardiovascular problems.”

Provided by PLOS
 

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Researchers Use Friendly Viruses to Tackle Inflammatory Bowel Disease

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A targeted approach using bacteriophages to disarm harmful microbes without disrupting the broader gut ecosystem

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A research team at McMaster University has developed a targeted approach to treating inflammatory bowel disease (IBD) using bacteriophages, viruses that infect specific bacteria, to disarm harmful microbes without disrupting the broader gut ecosystem.

The study, published in Science Translational Medicine and featured on the cover of the journal, brings together researchers from the Faculty of Engineering and the Faculty of Health Sciences, combining expertise in microbiome science and targeted antimicrobials to tackle a complex challenge in gut health.

Although current treatments for IBD can be effective, they can fail long-term or require escalating doses, increasing the risk of serious side effects.

IBD is shaped by a combination of genetics, immune responses and the gut microbiome. The research team focused on a group of bacteria known as adherent-invasive Escherichia coli (AIEC), which have been linked to inflammation in some people with Crohn’s disease. These bacteria can be difficult to identify and selectively target, making them an important test case for more precise microbiome-based therapies.

“One challenge is that AIEC are defined by what they do, not simply by how they appear in a microbiome analysis,” says Elena Verdu, professor in the Department of Medicine, director of the Farncombe Family Digestive Health Research Institute, and an executive member of NexusHealth.

“To identify them, we need to test their behaviour, such as their ability to adhere to and invade intestinal cells and persist in immune cells.”

Working with E. coli strains isolated from patients with Crohn’s disease, the team used controlled experimental models to isolate how AIEC contribute to inflammation and explore ways to neutralise their harmful behaviour without damaging beneficial bacteria.

To target AIEC without collateral damage, the team turned to bacteriophages, or phages, which are naturally occurring viruses that infect bacteria with remarkable precision.

“Phages work like a lock-and-key system – each phage targets only certain bacteria. That precision gives us a way to intervene without wiping out the entire microbiome,” explains Zeinab Hosseinidoust, associate professor in the Department of Chemical Engineering and the School of Biomedical Engineering and a member of the Michael G. DeGroote Institute for Infectious Disease Research (IIDR).

The team identified and characterised phages that selectively target AIEC strains isolated from patients with IBD and found that this approach significantly reduced gut inflammation.

The phages did not eliminate the bacteria entirely. Instead, they altered their behaviour by supressing a molecular “grappling hook” that helps AIEC attach to the gut lining and trigger immune responses. When that virulence mechanism was turned off, inflammation subsided.

“The bacteria were still there, but they lost the traits that drive inflammation,” says Hosseinidoust.

“We like to think of it as knocking out a few teeth. The bacteria can’t do as much damage anymore.”

The researchers also found that phage therapy enhanced the effectiveness of a commonly used steroid treatment for IBD. When combined with the phage, a lower-than-standard dose produced benefits comparable to higher doses of the drug alone.

While phages have previously been shown to increase the effectiveness of antibiotics, this is the first time a positive collaboration between phage and a non-antibiotic drug has been reported.

The findings point to a precision-medicine approach for IBD. The bacterial function targeted by the phage can be measured in stool samples and was found to be higher in a subset of patients with Crohn’s disease, suggesting a potential way to identify those who could benefit most from this therapy.

“If we can identify which patients carry the harmful bacterial function, we could, in the future, intervene with a targeted therapy designed specifically to turn down that activity,” says Verdu.

“This is what personalised medicine should look like: matching the right biological tool to the right patient,” says Hosseinidoust.

Next steps for the team include evaluating broader collections of bacterial strains from IBD patients and developing combinations of phages – work that brings the approach closer to human trials.

By Andrea Lawson

Source: McMaster University

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New Clues Raise Hopes for Better Treatment of RSV in Babies

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Future therapies for respiratory syncytial virus (RSV) must target both the virus and its immune response to ensure babies get the best possible outcomes, finds a new study by researchers at UCL and Great Ormond Street Hospital for Children (GOSH).

RSV is the biggest cause of serious illness in babies, with over three million hospital admissions worldwide because of the virus every year. It causes wheezing and breathing difficulties, and in the worst cases babies end up in intensive care. Despite this, treatment options for infants who develop severe disease remain extremely limited.

As part of the new study, published in Nature Communications and funded by Animal Free Research UK and UK Research and Innovation (UKRI), researchers built a new lab model of baby lungs to show why RSV makes infants so much sicker than adults and allow them to test new treatments before they reach patients.

The miniature model of a baby’s airways was created using real infant airway cells, blood vessel cells and neutrophils (a type of white blood cell that acts as the immune system’s primary response to infection).

To compare with an adult response to RSV, the research team also made a model of an adult’s airways.

Dr Claire Smith (UCL Great Ormond Street Institute of Child Health), who led the study, said: “This model allows us to watch early immune responses unfold and study them in a human setting that reflects the infant airway. That’s something animal models often struggle to capture, especially when it comes to age-specific effects.”

When the models were infected with RSV, the team found that baby airway cells attracted far more white blood cells than adult airway cells did. This influx can block babies’ small airways and make it harder for them to breathe.

Neutrophils normally circulate in the blood but enter lung tissue in response to infection. In the baby airway model, researchers found that the neutrophils that entered the lung tissue were more activated and triggered a stronger inflammatory reaction than in the adult model.

This effect depended on the immune cells physically moving through the infected tissue, not just responding to chemical signals released by it, making this type of model essential for studying it.

This suggests it’s the infant airway itself, not just the virus, that ramps up the immune response and causes damage to the lungs.

First author, Dr Machaela Palor (UCL Great Ormond Street Institute of Child Health), said: “These findings help explain why RSV is often much more severe in infants than in adults. The paediatric airway actively shapes how immune cells behave during the infection.”

The researchers then tested two antiviral drugs (remdesivir and RSV604). Both stopped the virus from multiplying, but only RSV604 also calmed the overactive immune response, reducing levels of a key inflammatory protein released by white blood cells – high levels of which are linked to more severe RSV disease in babies.

Remdesivir had no effect on this, suggesting that not all antivirals are equal when it comes to protecting the infant airway from immune-driven damage.

This suggests that treating severe RSV in babies may require more than just stopping the virus – it may also be important to calm an overactive immune response.

The researchers hope their findings and the new approach to research on RSV will accelerate the development of treatments better tailored to infants.

Dr Smith said: “Our model gives us a way to assess both sides of the problem at once. We can not only ask whether the drug stops the virus but also whether it helps control immune response in the infant airway.

“This work reinforces the idea that age matters in respiratory infection. Understanding how infant airways shape immune responses will be key to designing safer and more effective RSV treatments.”

Source: University College London

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Muscles Matter for Diabetes Risk, New Study Finds

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Photo by John Arano on Unsplash

A major new international study led by Curtin University, has found diabetes risk is about more than just body weight or obesity, revealing muscle health also likely plays a big role in whether people will develop the condition.

Published in one of the world’s leading diabetes journals, Diabetes Care, the study saw researchers from the Curtin School of Population Health and Dementia Centre of Excellence at the Curtin enAble Institute analyse health data from nearly 480 000 adults over 14 years – all of whom were diabetes-free at the beginning of the study.

The team found people with both excess body fat and poor muscle health – a condition known as sarcopenic obesity – were more than three-and-a-half times as likely to develop type 2 diabetes than people with healthy body composition.

It also found people with sarcopenic obesity were 19 per cent more likely to develop type 2 diabetes than people with obesity alone and 91 per cent more likely to develop type 2 diabetes than people with low muscle mass and strength (sarcopenia) alone.

Lead author and PhD candidate Zhongyang Guan said the findings challenge the common perception diabetes risk is primarily driven by body weight.

“Most people know carrying excess weight can increase the risk of type 2 diabetes, but our findings show muscle health is also an important piece of the puzzle,” Mr Guan said.

“People with both excess body fat and low muscle mass had a substantially higher risk of developing type 2 diabetes than those with obesity alone.

“This suggests we need to look beyond the number on the scales when assessing diabetes risk, as maintaining muscle strength and muscle mass may be just as important as managing body weight.”

The study found nearly 15 per cent of people with sarcopenic obesity developed type 2 diabetes within 10 years, compared with around 11 per cent of people with obesity alone and just 3 per cent of people without sarcopenia or obesity.

The link was particularly strong among women and adults under the age of 60.

Project senior lead Professor Mario Siervo said the results supported a broader approach to diabetes prevention.

“Healthcare professionals routinely monitor body weight and obesity, but our findings suggest assessing muscle health could help identify people at high risk earlier,” Professor Siervo said.

“As populations age and rates of obesity continue to rise, preserving muscle health through regular physical activity and healthy lifestyle habits could play an important role in reducing the burden of type 2 diabetes.”

Diabetes WA Clinical Services Manager Jessica Weiss said the findings highlighted the important role muscle plays in controlling blood sugar levels and reflected what health practitioners were seeing firsthand.

“We know our muscles use a lot of our glucose for fuel and working them during physical activity is a great way to help use up glucose from our blood and regulate glucose levels,” Ms Weiss said.

“Physical activity also reduces our body’s resistance to insulin, an important element to type 2 diabetes.

“The more muscle we have and the more regularly we use them, the better equipped our body is to prevent or manage type 2 diabetes.”

By Samuel Jeremic

Source: Curtin University

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Customised 3D-printed Contact Lenses in Just 20 minutes

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New platform paves the way for patient-specific lenses in a single visit to the optometrist

A breakthrough combination of new silicone materials and advanced 3D printing technology developed by University of Waterloo researchers could transform how contact lenses are manufactured.   

The award-winning innovation can produce patient-specific contact lenses in as little as 20 minutes, paving the way for specialised lenses to be designed, manufactured and dispensed during a single visit to the optometrist. The technology is described in the journal Materials and Design.

Most contact lenses are manufactured in a limited range of sizes and shapes rather than being custom-made for each person’s eye. While soft lenses are suitable for many wearers, patients with irregularly shaped corneas often require rigid lenses to achieve clear vision. Finding the right fit can require several appointments over weeks or months before patients receive lenses that fit properly and provide the function they need.  

Researchers in Waterloo’s Department of Chemistry developed the digital manufacturing platform to address these challenges.  

“We are very excited about this work because it brings us closer to contact lenses that are truly personalized,” said Dr Shirley Tang, professor in Waterloo’s Department of Chemistry. “Our technology produces lenses with patient-specific surfaces for a precise fit while delivering the optical clarity and mechanical performance expected of commercial contact lenses.”  

The platform combines custom lens design software, a newly developed silicone material, and advanced manufacturing techniques.  

Silicone is widely used in contact lenses because it is safe, biocompatible and highly oxygen permeable. However, conventional silicone materials are generally not compatible with 3D printing. To overcome this barrier, the Waterloo team developed a new hydrophilic silicone formulation specifically designed for additive manufacturing while maintaining the properties required for contact lens applications.  

“Our software designs a lens with an inner surface that precisely matches the patient’s cornea and an outer surface that provides the required vision correction,” said Dr Sayan Ganguly, Chemistry research associate at Waterloo. “The novel hydrophilic silicone material we created, combined with our manufacturing process, produces smooth, transparent lenses that are comfortable to wear.”  

Because 3D-printed objects are built layer by layer, tiny stair-step imperfections can form on curved surfaces and reduce optical clarity and wearer comfort. To address this issue, the team developed an ultra-thin, non-contact coating process that smooths the surface without altering the customised shape of the lens or compromising its optical performance.  

Laboratory testing confirmed the lenses are biocompatible and the team is preparing for in vivo studies. Researchers have filed a provisional patent for the hydrophilic silicone material and are preparing a full patent application.  

Working with the Centre for Vision and Eye Research (CEVR), a joint research institute of the University of Waterloo and the Hong Kong Polytechnic University, the researchers are advancing the technology toward commercialization.   

The project recently received a Gold Medal at the Shanghai International Exhibition of Inventions in June 2026.  

The study, “Patient-specific hard contact lenses fabricated by vat photopolymerization printing and non-contact fluidization coating,” was recently published in Materials & Design. 

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Postnatal Collapse is Rare but Can Have Deleterious Consequences

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Photo by Duda Oliveira

Sudden unexpected postnatal collapse during the first week of life is rare but can have deleterious consequences. A new study from Karolinska Institutet shows that the condition is more common than previously estimated and highlights measures that may reduce the risk.

Sudden unexpected postnatal collapse (SUPC) occurs when an apparently healthy newborn suddenly stops breathing and collapses during the first week of life. In a new study, published in the journal Acta Paediatrica, researchers investigated how common the condition is and when it occurs. 

The researchers analysed approximately 483 000 births at seven maternity units in Stockholm between 2002 and 2022 and identified 149 cases of SUPC. This corresponds to 31 cases per 100 000 live births. 

“It is important to remember that this is a very rare condition. According to our findings, it affects around 30 infants each year in Sweden, and two to four of these cases lead to death. Most cases occur during the infant’s first day of life,” says the study’s senior author, Eric Herlenius, paediatrician at Karolinska University Hospital and Professor of Paediatrics at the Department of Women’s and Children’s Health, Karolinska Institutet. 

The study found that 81 per cent of collapses occurred during the first 24 hours after birth, with half taking place within four hours of delivery. Seven per cent of affected infants died and 26 per cent sustained permanent neurological injuries. Two-thirds of the cases occurred while the infant was sharing a bed with a parent.

“Skin-to-skin contact is important for newborn infants, but parents need to ensure that the baby’s airways are always clear and visible. Adults should not fall asleep while holding their baby skin to skin, and infants should not sleep in the same bed as their parents during the first three months of life,” says Eric Herlenius

The researchers point out that SUPC still lacks a specific diagnostic code, making the condition difficult to monitor. According to the researchers, this may have contributed to an underestimation of its true incidence. 

Reviewed medical records

To identify cases, the researchers reviewed electronic medical records of infants born after at least 35 weeks of pregnancy. The records were searched for symptoms suggestive of collapse, such as episodes of apnoea, bluish skin discolouration, or sudden loss of muscle tone. Each suspected case was then assessed according to internationally established criteria for SUPC.

Since 2011, the researchers have also collected urine samples from affected infants and compared them with samples from healthy infants of the same age. They found higher levels of a prostaglandin E2 metabolite in infants who experienced SUPC during the first days of life, the same period during which most collapses occurred

“We believe that clearer guidelines for safe skin-to-skin care and safe sleep environments are needed and could help reduce the number of cases further,” says Eric Herlenius. 

At the same time, the researchers aim to improve understanding of the biological mechanisms underlying the condition, including the elevated levels of prostaglandin E2 metabolite observed in some affected infants. By studying the relationship between these levels and the brainstem’s control of breathing, the researchers hope to gain a better understanding of why some newborns develop SUPC and, in some cases, sudden unexpected death. 

Source: Karolinska Institutet