Categories : Dentistry PaediatricsTags : Leave a comment

Brush-on Treatment Could Halt Cavities and Prevent Fillings

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Photo by Hush Naidoo Jade Photography on Unsplash

Every year, untreated tooth decay sends thousands of young children to emergency departments for dental problems doctors can’t treat. Many eventually undergo surgery under general anaesthesia, while others endure pain and infection.

A simple, inexpensive liquid called silver diamine fluoride, or SDF, could spare many of those children. Applied to a cavity with a tiny sponge-tipped applicator in about a few second’s time per tooth, SDF arrests decay without drilling, shots or sedation.

Dentists have used SDF successfully for decades in many countries, and off label in the United States since 2014, when it was approved as a medical device to treat tooth sensitivity. However, it has lacked the large US population clinical trials for efficacy and safety that are needed for FDA approval as a drug to treat cavities.

Now, a University of Michigan-led clinical trial has produced that evidence.

Published in JAMA Pediatrics, the Phase III trial enrolled 830 children under age 6 who were recruited through dental offices, pediatric medical practices, Head Start and Early Head Start programs in Michigan, New York and Iowa.

Researchers found that 38% SDF arrested tooth decay in more than half of children’s affected baby teeth when treated at 6-month intervals. Unlike conventional treatment, which removes part of the tooth before placing a filling, SDF is simply painted onto the cavity.

“This is a very effective and safe treatment – even in children as young as 1,” said Margherita Fontana, professor of dentistry at the University of Michigan School of Dentistry and the study’s lead investigator.

Tooth decay is the most common chronic disease of childhood, affecting more than 40% of US children. Left untreated, cavities can cause severe pain, infection, difficulty eating and sleeping, missed school and repeated medical visits.

SDF may be especially valuable for very young children, older adults, people with developmental or physical disabilities, patients with severe dental anxiety, and others who cannot easily tolerate or access conventional dental treatment, Fontana said.

Its primary drawback is cosmetic, she said. The silver permanently darkens the decayed portion of the tooth.

“If we want more children and families to benefit from this treatment, we need rigorous evidence showing both that it works and that it’s safe. From a public health perspective, if we want broader implementation across the United States, including in medical settings, we need carefully collected data in U.S. populations, and we now have that,” Fontana said.

The study began in 2018 and progressed even with the challenges of the COVID-19 pandemic.

“In medicine, clinicians want high-quality evidence before changing practice,” Fontana said. “It is important to have data they can refer to because young children often see paediatricians years before they ever visit a dentist, broader acceptance could allow many more cavities to be treated while a referral to a dental home is successful, and before they become painful, infected or require surgery.”

The product used in this trial, Advantage Arrest 38% SDF, was provided by Elevate Oral Care.

Amr Moursi, professor of paediatric dentistry at New York University College of Dentistry, said the study provides important data for broadening use of SDF.

“Our results support FDA approval of SDF for managing arrest of tooth decay in young children. Removing SDF from off-label status would be an important innovation which could lead to increased utilisation by providers, enhanced payments by insurers and more consistent product quality,” said Moursi, a co-principal investigator on the study.

For some children, reapplying SDF every few months may be all that’s needed until the baby tooth naturally falls out. For adults, it may serve as a long-term treatment or as a bridge until restorative procedure is affordable or practical.

“For almost anyone, this can arrest the decay and stop the infection and the pain it causes,” Fontana said. “This could benefit many people.”

Source: University of Michigan

Categories : RheumatologyTags : Leave a comment

Drug Reduces the Risk of Developing Rheumatoid Arthritis, Clinical Trial Finds

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Rheumatoid arthritis. Credit: Scientific Animations CC4.0

A clinical trial led by researchers from Hospital Clínic de Barcelona, the August Pi i Sunyer Biomedical Research Institute (IDIBAPS) and The Institute for Advanced Chemistry of Catalonia (IQAC-CSIC) has compared the effectiveness of abatacept and hydroxychloroquine in preventing the development of rheumatoid arthritis in patients with palindromic rheumatism, an autoimmune disease that progresses to arthritis in approximately half of all patients. The trial was conducted over two years across 14 hospitals throughout Spain and involved 70 patients with palindromic rheumatism. The findings, published in Nature Medicine, indicate that abatacept is significantly more effective than hydroxychloroquine in preventing the onset of arthritis.

Palindromic rheumatism is characterised by intermittent episodes of joint inflammation, with acute flare-ups lasting a few days and resolving spontaneously. However, around half of patients eventually develop rheumatoid arthritis, a chronic disease that causes irreversible joint damage. This risk is particularly high in individuals with biomarkers such as rheumatoid factor and anti-citrullinated peptide antibodies. The presence of these two autoantibodies – proteins of the immune system that mistakenly attack the body’s own organs and tissues – is used in the diagnosis of the disease.

Until now, in the absence of clinical trial evidence, the standard approach has been to treat patients with palindromic rheumatism using hydroxychloroquine, a drug with anti-inflammatory and immunosuppressive properties aimed at improving disease symptoms. In this context, the team led by Raimon Sanmartí, head of the Inflammatory Arthropathies Research Group at IDIBAPS, conducted a two-year clinical trial involving 70 patients with palindromic rheumatism. The objective was to compare the effectiveness of hydroxychloroquine with abatacept, a lymphocyte inhibitor – a type of white blood cell that attacks the joints after mistakenly identifying them as a threat – in reducing progression from palindromic rheumatism to rheumatoid arthritis

The results show that treatment with abatacept significantly reduces progression to rheumatoid arthritis. Only 20% of patients receiving abatacept developed arthritis, compared with 50% of those treated with hydroxychloroquine. Furthermore, patients treated with abatacept not only avoided progression to rheumatoid arthritis in most cases, but also experienced a significant improvement in palindromic rheumatism symptoms. “The study shows that patients treated with abatacept are more likely to achieve complete remission of attacks associated with acute pain and joint swelling, and that their inflammatory episodes are less severe,” explains Isabel Haro, Head of the Peptide Synthesis and Biomedical Applications Unit at IQAC-CSIC. The research team also highlights that both drugs proved safe and well tolerated throughout the trial.

Early intervention

“The results of this study indicate that we can intervene at an early stage to modify the natural course of the disease and reduce the risk of patients developing more severe and irreversible conditions,” says Sanmartí. “This opens the door to a paradigm shift in the treatment of these patients.”

The study, which involved several national research centres, also analysed the evolution of a number of biomarkers (autoantibodies) developed by the CSIC research group during patient follow-up. “Although no significant differences were observed between abatacept and hydroxychloroquine in terms of autoantibody responses, this work demonstrates the value of immunomodulatory approaches in the early stages of disease, when it is still possible to prevent progression to more severe and chronic forms,” notes Haro.

Rheumatoid arthritis is a disease that significantly affects patients’ quality of life and places a considerable burden on healthcare systems. Preventing its development in a substantial proportion of cases represents an important advance in the management of rheumatic diseases.

Source: Institute for Advanced Chemistry of Catalonia

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Long-term Relationships with Family Physicians Linked to Fewer Urgent Hospitalisations

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Photo by Cottonbro on Pexels

A new study published in the American Academy of Family Physicians finds that keeping patients connected to the same practice and physician over time may help reduce avoidable hospital use.

This retrospective cohort study using longitudinal data from 100 450 patients across 48 general practices in and around Amsterdam found that patients registered with their practice for longer than 5 years had 9% to 21% lower odds of urgent hospital admission and 17%-28% lower hospital costs compared to those registered for 0 to 5 years.

Consistently seeing the same general practitioner was associated with 6% to 7% lower hospital costs, but not with fewer urgent admissions. Researchers measured continuity associations with urgent hospital admissions and hospital costs in two ways: duration of the general practitioner-patient relationship and how concentrated a patient’s visits were with one physician. 

The researchers concluded, “Our study suggests an association between continuity in general practice and hospital use and costs. Although there is an overwhelming amount of evidence regarding the benefits of continuity of care for both patients and GPs, this study shows that continuity is also associated with fewer urgent admissions and lower hospital costs.”

Source: EurekAlert!

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Opinion Piece: How Medical Aid Regulation Changes Are Shaping the Future Demand for Gap Cover

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By Brian Harris, CEO at Turnberry Management Risk Solutions

28 July 2026 – Medical aid remains essential for accessing private healthcare in South Africa, but it does not always cover the full cost of treatment. While regulations such as Prescribed Minimum Benefits (PMBs) ensure that members have access to a defined level of care for certain conditions, medical schemes still apply tariff limits, treatment protocols, co-payments and other funding rules that can leave members exposed to out-of-pocket costs. At the same time, healthcare costs continue to rise, placing additional pressure on how schemes fund treatment. As a result, medical expense shortfalls are becoming increasingly common, making gap cover an essential part of helping clients manage their healthcare costs and protecting them against unexpected expenses.

Protection within limits

PMBs are a clear example of how scheme rules and funding limits influence what medical schemes ultimately pay for. They are designed to ensure that all medical scheme members have access to treatment for a defined list of emergencies, chronic, and life-threatening conditions. However, they do not provide unlimited funding for every treatment option, and there is often a misunderstanding about this.

When it comes to PMBs, cover is still subject to scheme rules, treatment protocols, formularies, and designated service provider requirements. In many cases, cover is also aligned to the level of care that would ordinarily be available in the public healthcare system. This becomes particularly important in areas such as oncology, where newer or more specialised treatments may fall outside what a scheme is required to fund in full.

As a result, members may still face co-payments, sub-limits, or shortfalls that need to be paid for out of pocket, even when the condition itself qualifies as a PMB.

How scheme rules create shortfalls

PMBs are only part of the picture when it comes to medical expense shortfalls. Even where treatment is covered, medical schemes reimburse according to their own tariffs and funding rules, while healthcare providers may charge significantly more. The difference between what the scheme pays and what the provider charges is the member’s medical expense shortfall.

At the same time, medical schemes use co-payments, benefit limits, Designated Service Providers (DSPs) and authorisation requirements to manage rising healthcare costs and keep contributions affordable. If these rules are not followed, or if treatment falls outside the approved funding structure, members may still need to pay part of the cost themselves.

This means that having medical aid does not always guarantee that treatment will be covered in full. Even where treatment is approved, members can still face significant out-of-pocket expenses.

Advice is essential

As funding rules become increasingly complex, advisers need to take on a more proactive role in helping clients understand and navigate the healthcare landscape. Many clients do not fully understand how PMBs, DSPs, funding rules and scheme tariffs affect what their medical aid will ultimately pay. The reality often only becomes clear at the claims stage, when members discover that they are responsible for part of the cost themselves.

Explaining these rules clearly, together with where medical expense shortfalls may arise, is therefore becoming an increasingly important part of the healthcare funding discussion. Regular reviews and clear guidance also help ensure that changes to scheme rules, benefits, and healthcare costs do not leave clients exposed to unnecessary or unexpected out-of-pocket expenses.

Future-proofing healthcare advice

Medical aid and gap cover should not be treated as once-off decisions. Scheme rules, pricing structures and healthcare costs continue to change, which means healthcare advice needs to be reviewed regularly to ensure that cover remains appropriate.

Helping clients understand how their medical aid works, where medical expense shortfalls may arise, and how gap cover can be structured forms an important part of responsible advice. Regular reviews also help ensure that changes to benefits, family circumstances or healthcare needs do not leave clients exposed to unnecessary costs.

As regulation continues to shape how healthcare is funded in South Africa, gap cover is becoming an increasingly important part of managing healthcare costs. Brokers and financial advisers play an essential role in ensuring their clients have medical aid and gap cover that together provide the right level of protection.

Turnberry Management Risk Solutions (Pty) Ltd is an authorised Financial Services Provider (FSP no. 36571). Underwritten by Lombard Insurance Company, an Authorised Financial Services Provider (FSP 1596) and Insurer conducting non-life insurance business.

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Researchers Demystify the Molecular Mechanisms of General Anaesthesia

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Left: Surface model of the bacterial sodium channel NavMs with one of the four subunits coloured light blue and the others grey. The anaesthetic sevoflurane (coloured spheres) sits in a pocket at the interface of two adjacent subunits. Right: Close-up of the binding pocket. The semi-transparent surface exposes the underlying ribbon and a tyrosine amino acid (light blue), which is key to binding sevoflurane (coloured sticks). Credit: Dr Karl Herold

Researchers at Weill Cornell Medicine and Birkbeck, University of London, have identified a site where a commonly used anaesthetic binds to sodium ion channels, revealing a molecular mechanism that may explain how these drugs dampen communication between neurons. Ion channels are proteins that regulate the flow of charged particles across cell membranes, enabling neurons to generate electrical signals. By reducing this signalling, inhaled anaesthetics help suppress brain activity, producing unconsciousness and immobility during surgery.

The findings, published June 19 in Nature Communications, shed light on a longstanding mystery: For 175 years, doctors have safely used inhaled anaesthetics to render patients unconscious, but didn’t fully understand how these drugs work.

“Sodium channels are critical for communication between neurons in the brain, and anaesthesia breaks down that communication,” said Dr Hugh Hemmings, senior associate dean for research and chair of the Department of Anesthesiology at Weill Cornell, who co-led the research. “So, there’s good reason to believe that the unconsciousness produced by volatile anaesthetics is related to their effects on sodium channels.” 

The study provides the first atomic-level view of how the anaesthetic sevoflurane binds to sodium channels and stabilises them in an inactive state. “The insights we gain from this study may enable us to design safer, more selective anaesthetics, with fewer side effects,” said Dr Karl Herold, co-first author and senior research associate at Weill Cornell.

Anaesthetising a bacterial counterpart

As far back as the 1970s, scientists suspected that inhaled, volatile anaesthetics could interact with ion channels – in particular, the voltage-gated sodium channels that play a crucial role in cell-to-cell communication throughout the nervous system. But determining how this interaction inhibits neuronal activity has been challenging because mammalian sodium channels were too large and complex for detailed structural analysis.

The researchers turned to a marine bacterium, Magnetococcus marinus, that uses voltage-gated sodium channels to swim toward nutrients and oxygen. Although structurally simpler than their mammalian counterparts, the bacterial channels operate similarly and share the same sensitivity to anaesthetics. “Volatile anaesthetics bind through weak, low-affinity interactions that are very hard to capture structurally,” Dr Herold said. “A bacterial channel that behaves like ours but is small enough to crystallise lets us finally see where sevoflurane sits and how it holds the channel inactive.”

Discovering a binding pocket

The Weill Cornell team joined forces with Birkbeck researchers, co-senior author Dr Bonnie Ann Wallace and co-first author David Hollingworth. The UK-based researchers have extensive expertise in structural analysis of these bacterial channels bound to a variety of drugs, including those that affect neuronal activity.

Using high-resolution X-ray crystallography, the researchers captured detailed snapshots of sevoflurane bound to the channel. They discovered that the anaesthetic tucks into a small pocket at the edge of the channel’s pore-forming region, but away from the pathway through which sodium ions flow. Binding in this pocket stabilises the channel in an inactive state, making it less likely to open and allow sodium ions through, thereby reducing a neuron’s ability to transmit electrical signals.

This interaction is key to the drug’s molecular effects. When the researchers altered a single amino acid in the binding pocket, sevoflurane could no longer bind effectively and lost its ability to keep the channel in its inactivated state.

The researchers are now working on translating their findings to the mammalian system. “The bacterial channel is just a testing ground,” Dr Hemmings explained. “If naturally occurring mutations affecting anaesthetic binding exist in humans, studying them could help explain why some people respond differently to anaesthesia and may provide new insights into the biology of consciousness.”

“As anaesthesiologists, it’s our responsibility to understand how these drugs work, so we can resolve issues when people don’t react well to anaesthesia,” said Dr Hemmings, who is also anaesthesiologist-in-chief at NewYork-Presbyterian/Weill Cornell Medical Center.

Source: Weill Cornell Medical Center

Categories : DermatologyTags : Leave a comment

Researchers Find Dormant Melanocytes in Vitiligo, Suggesting a New Treatment Strategy

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How changes in melanocyte attachment to the extracellular layer drive vitiligo
Under normal conditions (left), melanocytes adhere to laminin-211 in the basement membrane through dystroglycan, maintaining their mature pigment-producing state. In vitiligo (right), remodelling of the basement membrane increases laminin-332 and promotes integrin α3β1-mediated adhesion, activating signalling pathways, including c-Jun, that drive melanocyte dedifferentiation and loss of pigment production. Credit: Osaka Metropolitan University


Vitiligo is an autoimmune disease in which the body’s immune system attacks and destroys melanocytes, the cells that produce the skin pigment melanin. Once the melanocytes are gone, the skin turns white, leading to the characteristic skin patches of the disease.

However, the standard model of vitiligo doesn’t explain some of its unusual features. Some vitiligo lesions re-pigment and treatments sometimes restore pigmentation even in areas that lack melanocytes, suggesting that the melanocytes may not be fully destroyed.

A team from Osaka Metropolitan University team led by Specially Appointed Professor Ichiro Katayama and Specially Appointed Associate Professor Lingli Yang has found evidence that melanocytes do not completely disappear from vitiligo skin and instead enter a “dedifferentiated-like state” in which the mature cells revert to a more primitive form, losing many of their specialised functions including the production of pigment.

“This study uncovers a new mechanism underlying the development of vitiligo, which could change how we treat the disease,” Dr Yang explained.

Their research adds to a body of research that shows that cells do not just respond to chemical signals, but also to what they are physically attached to. As melanocytes are located on the basement membrane, the thin layer that separates the epidermis from the dermis, the membrane provides instructions that help them remain functional pigment-producing cells. 

However, the extracellular matrix surrounding melanocytes is remodelled in vitiligo patients. Usually, melanocytes bond with laminin-211; however, in vitiligo patients, the basement membrane becomes enriched in laminin-332. Because their preferred binding partner is no longer available, melanocytes change how they attach. Instead of using their preferred attachment agent, dystroglycan, they attach through integrin α3β1 instead.

These changes activate pathways that are commonly activated when cells are remodelling. In this process, the actin cytoskeleton of the cell is reorganised, gene expression is altered, including that of genes associated with an immature melanocyte state. The findings suggest a self-reinforcing cycle in which changes to the basement membrane drive melanocyte dedifferentiation, while the dedifferentiated melanocytes become less able to maintain a healthy basement membrane, further promoting the disease process.

“This was an exciting discovery for us, as most current treatments largely focus on suppressing autoimmune attacks and reducing inflammation, but if dormant melanocytes are still present in lesions, that might change the way we treat the disease,” Professor Katayama said. “New treatment avenues such as reactivating existing cells or restoring their normal attachment to the basement membrane may be possible.” 

When the researchers used pharmacological inhibitors targeting the signalling pathways activated by this adhesion switch, they were able to restore expression of mature melanocyte markers, recover pigmentation-related gene expression, and reverse many features of the dedifferentiated-like phenotype.

“This was an exciting aspect of our research, as it suggests that changing gene expression isn’t permanent and this process may be reversible,” Dr Yang explained. “We found that drugs were able to restore melanocyte function and pigmentation-related characteristics. The next step will be to perform clinical studies to see if this approach is a viable way to manage the disease.”

The findings were published in Nature Communications.

Source: Osaka Metropolitan University

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New WHO Guidelines: Up to 45% of Dementia Risk Could Be Prevented or Delayed

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Photo by Jusfilm on Unsplash

The World Health Organization (WHO) has released updated guidelines on reducing the risk of cognitive decline and dementia, providing countries with evidence-based recommendations to help prevent or delay the onset of dementia across the life course.

Dementia is a condition caused by brain diseases and affects memory, thinking and the ability to function. More than 57 million people live with dementia worldwide and nearly 10 million people get newly diagnosed every year. Alzheimer disease is the most common form of dementia and is estimated to account for 60–70% of cases.

While there is no cure for dementia, up to 45% of the risks can be attributed to modifiable risk factors such as tobacco, alcohol use, social isolation, physical inactivity, air pollution and noncommunicable diseases (NCDs), including high blood pressure and diabetes. Beyond health, dementia affects a person’s independence, dignity and safety.

“We know more today than ever before about what drives dementia risk, and these guidelines translate that knowledge into action,” said Dr Tedros Adhanom Ghebreyesus, WHO Director-General. “Countries now have clear, evidence-based recommendations they can put into practice immediately to protect people’s cognitive health.”

WHO’s new guidelines reflect the latest evidence and innovations in dementia risk reduction providing proven interventions that can effectively lower dementia risk through early awareness and timely action. They represent an important opportunity to reduce the burden of dementia in the coming decades through stronger integration of services for noncommunicable diseases, mental health and brain health.

Reducing risk, preventing illness

The updated guidelines reflect significant growth in the evidence base since WHO first issued recommendations on dementia risk reduction in 2019. They provide consolidated recommendations on addressing unhealthy behaviours, managing medical conditions, and reducing exposure to environmental factors that may contribute to cognitive decline and dementia.

The guidelines recommend several healthy behaviours and lifestyle interventions to reduce dementia risk, including cognitive training and cognitive stimulation and engagement in social activities for adults who have normal cognition or are experiencing mild cognitive impairment.

The updated advice also includes interventions that reduce risk of NCDs, including increasing physical activity, stopping tobacco use, reducing alcohol consumption, adopting a healthy diet, and a new recommendation to reduce exposure to air pollution.

Management of cardiometabolic conditions such as hypertension, diabetes, and high cholesterol can also help reduce dementia risk. Further, hearing aids may be offered as part of risk-reduction strategies.

As an intervention to reduce the risk of cognitive decline and/or dementia, the guidelines do not recommend supplementation with vitamins B and E, omega-3 polyunsaturated fatty acids (PUFA) and multivitamins/minerals in the absence of a diagnosed deficiency, due to the lack of evidence of any potential benefits to outweigh unexpected harmful effects. 

Human and economic cost

Dementia affects an individual’s ability to live independently, work and function, while placing substantial burdens on families and carers. It carries a major economic loss, costing the global economy an estimated US$ 1.3 trillion annually. About half of this cost is driven by unpaid care provided by families and friends. Understanding risk factors and taking action to prevent dementia can improve health and quality of life, helping people live longer, healthier and more independent lives.

Source: World Health Organization

Categories : PaediatricsTags : Leave a comment

Kids Do Feel the Cold. So Why Won’t They Wear a Jumper?

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Zachary Kadolf/Unsplash

Joshua Pate, University of Technology Sydney

It happens just when you need to leave. Bags are packed. Shoes are on. Then your child decides a jumper is impossible.

You say, “put your jumper on”.

They say, “I’m not cold”.

Do kids really not feel the cold like adults do? Or are they just expressing their independence? And when should you insist?

A clue from pain research

I study how children experience pain, and pain research offers one clue about this jumper battle.

A child may scrape their knee during a game and barely notice until the game stops. The scrape was there throughout, but chasing a friend or reaching the next base kept winning their attention.

Cold can slip into the background in a similar way. A child’s fingers may be cooling while the playground remains far more compelling. Then the game ends.

Their attention returns to their hands at around the same time their moving muscles stop producing so much heat. Suddenly, the jumper may seem like a better idea.

So “I’m not cold” can mean, “I can feel it and I’m comfortable”.

It can also mean, “the jumper feels worse” or “I want to keep playing”. Sometimes it means, “I am four years old and this has become a matter of principle”.

Similarly, when parents ask, “but aren’t you cold?” we’re often asking several questions at once.

Will you still be warm when you stop running? What if the wind picks up? How about later, when we’re standing still on the sideline at the soccer field?

Children report the present moment, and parents factor in the forecast.

What cold actually feels like

Your skin contains sensory nerve endings that respond as its temperature changes.

One cool-sensitive channel, called TRPM8, helps convert cooling at the skin into electrical activity in sensory nerves.

This is the same channel that menthol activates, which is why mint can make your mouth feel cool even when there’s no real temperature change.

And as you know with mint, a strong cooling sensation can sometimes become uncomfortable or even painful. Other factors such as wind, wetness, contact with cold surfaces, movement, and how much time we’re outside can all influence how we experience temperature.

For example, a parent who is standing still in a playground, clutching a coffee, may be acutely aware of the gap in their coat where the icy wind is sneaking in.

But children tend to run, climb and jump in bursts – and moving muscles produce heat.

Children also differ from adults in body size, body composition, metabolism and how their circulation responds to cold.

One 2024 laboratory study, done indoors, looked at children aged six to nine. It found their sedentary metabolic rates (how much energy you’re burning when you’re resting) were around 39% higher compared to adults in the study.

Their skin was also warmer over parts of their torso, and the skin on their hands recovered temperature and bloodflow faster than adults after being exposed to the cold.

So it’s not that kids don’t feel cold at all, but they may have a quite different experience from an adult standing in the same air.

Bodies prepare for what comes next

We often learn about thermoregulation – how the body maintains its core temperature – as though the body were simply a thermostat. The body detects a temperature change, then bloodflow changes, and sweating or shivering bring it back towards the middle.

But our movement and behaviour also play an important role in maintaining this balance. When we’re cold we may walk into sunshine, curl up, or add a layer; when we’re hot we take one off. A child who keeps running may already be generating the warmth they need.

Bodies also prepare for expected demands. Researchers use the term allostasis to describe this wider process of how the body maintains stability through change.

Some adjustments happen automatically. For example, before we exercise, our heart rate and breathing begin adjusting for the work ahead. Others involve choices, such as moving into the sun, seeking shelter or reaching for warmer clothing.

But young children outsource some of this forecasting to adults.

Kids supply the live report from inside their body. We add the weather forecast and the schedule. We pack snacks for hunger that has yet to arrive, spare clothes for puddles yet to be found, and jumpers too.

What the jumper itself feels like

A jumper creates its own sensations. It may feel scratchy, bulky or restrictive. It can make climbing harder, then become hot and sweaty as soon as the child starts running.

Tags, seams and some fabrics can feel intensely unpleasant, especially for children with tactile sensitivities. Clothing tags and light touch, for example, can cause marked discomfort for some autistic children.

A child may genuinely prefer mildly cold skin over an irritating texture.

So it’s worth asking whether “aren’t you cold?” is the right question. Others may work better:

are you comfortable?

will you be running or sitting still?

would you rather wear the jumper or carry it?

These questions help children connect what they feel now with what they may need later.

When should parents insist?

Parents should be firmer when a child is very young, wet, unwell, exposed to strong wind or likely to remain outside for a long time.

Persistent shivering or numbness means it is time to get warm. Increasing clumsiness, unusual drowsiness, confusion or reduced responsiveness can indicate hypothermia, where the body’s core temperature has fallen dangerously low. Hypothermia is a medical emergency.

But for ordinary winter outings, flexible layers allow the plan to change. A jumper can be carried, added when activity slows, and removed when the child warms up again.

Your child reports the weather inside their body. You keep an eye on the weather outside it. A jumper in the bag lets your child feel heard, lets you keep the forecast in view, and lets everyone finally get out the door.

Joshua Pate, Associate Professor of Physiotherapy, University of Technology Sydney

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

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Newer Obesity Drugs Linked to Fewer Alcohol-related Hospitalisations

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Use of newer GLP-1 receptor agonists for obesity or diabetes was associated with a reduction in hospital admissions suggesting a potential role for the treatment of alcohol-use disorder

Photo from Pixabay CC0

Use of newer GLP-1 receptor agonists (semaglutide or tirzepatide) for obesity or diabetes by people with alcohol-use disorder was associated with a reduction in alcohol-related admissions to hospital, finds a study published online in the open access journal BMJ Open.

The findings suggest a potential role for the drugs semaglutide and tirzepatide in the treatment of alcohol-use disorder.

While GLP-1 receptor agonists are used primarily for the treatment of type 2 diabetes and obesity, there have been reports of reduced alcohol consumption among patients taking the drugs, prompting the authors to investigate the potential impact on alcohol-related hospitalisations among adults with alcohol-use disorder.

The study compared alcohol-related hospitalisations in 40 703 adults with alcohol-use disorder and type 2 diabetes or obesity who started a newer GLP-1 receptor agonist (semaglutide or tirzepatide) or a comparator drug between 1 January 2018 and 31 December 2024. Participants were split across four trials involving clinically distinct populations – the anti-diabetic medication (ADM) trial, anti-obesity medication (AOM) trial, medications for alcohol use disorder with type 2 diabetes (MAUD- T2D) trial, and medications for alcohol-use disorder with obesity (MAUD-obesity) trial.

Compared to participants taking an active comparator drug, those taking GLP-1 receptor agonists had a lower risk of alcohol-related admission to hospital during all four trials.

Use of GLP-1 receptor agonists was associated with a 26% lower risk of alcohol-related hospital admission than other diabetes medicines during the diabetic medication (ADM) trial, and a 32% lower risk of alcohol-related hospital admission than other obesity medicines during the anti-obesity medication (AOM) trial.

In the MAUD trials, the active comparators were drugs for alcohol-use disorder including acamprosate, disulfiram and naltrexone. Compared with taking drugs for alcohol-use disorder, use of GLP-1 receptor agonists by adults with type 2 diabetes was associated with a 63% lower risk of alcohol-related admission to hospital during the trial, and for adults with obesity use of GLP-1 receptor agonists was associated a 65% lower risk of alcohol-related hospitalisations.

The authors acknowledge several limitations to their study. Most importantly, alcohol-use disorder is under-captured due in part to stigmatisation, and when documented, it may also be recorded variably with lower reporting in areas of high social deprivation. Alcohol-related outcomes may have been under captured as they were defined using diagnosis codes and laboratory testing for alcohol exposure, and the study captured hospitalisations from treatment initiation to discontinuation in a trial environment, so treatment effects in an average clinical setting may differ.

Finally, there may have been some confounding in relation to socioeconomic status, underlying clinical stability or alcohol-use disorder severity, and healthcare engagement, as newer GLP-1 receptor agonists are higher-cost therapies and patients with access to these medications may differ from comparator groups.

The risk of residual confounding was greatest in the MAUD trials, as reflected by the reduced risk of non-alcohol-related hospitalisations with use of GLP-1 receptor agonists. The authors say the results of the MAUD trials should be interpreted with greater caution as there were also high rates of treatment discontinuation increasing the potential for bias.

Nevertheless, the authors conclude, “Initiation of newer GLP-1 receptor agonists among patients with alcohol-use disorder was associated with a lower observed risk of alcohol-related hospitalisation, with similar associations across populations with type 2 diabetes and obesity.

“These findings may suggest a potential role for GLP-1 receptor agonists in the context of alcohol-use disorder.”

Source: The BMJ Group

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Can a Faecal Microbe Transplant Improve Chronic Insomnia?

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Photo by Andrea Piacquadio: https://www.pexels.com/photo/young-man-in-sleepwear-suffering-from-headache-in-morning-3771115/

In a randomised clinical trial published in the Journal of Internal Medicine, ingesting capsules containing faecal microbes from healthy donors helped treat symptoms of insomnia.

One month after treatment, participants receiving faecal microbiota capsules showed significantly higher sleep efficiency and reduced wake after sleep onset, as measured by overnight polysomnography. Patient questionnaires also showed that sleep quality scores improved from 2 to 6 months in the intervention group compared with the placebo group.

“Our findings provide clinical evidence that targeting the gut microbiota may offer a promising new therapeutic strategy for chronic insomnia disorder,” said co–corresponding author Yanping Bao, PhD, of Peking University, in Beijing. “This work also strengthens our understanding of the gut–brain axis as an important regulator of human sleep.”

Source: Wiley