Author: ModernMedia

The HIV Dormancy Mystery Could Unlock the Path to a Cure

Colourised scanning electron micrograph of HIV (yellow) infecting a human T9 cell (blue). Credit: NIH

For over three decades, HIV has played an elaborate game of hide-and-seek with researchers, making treating – and possibly even curing – the disease a seemingly insurmountable obstacle to achieve.

But scientists at Case Western Reserve University have made a breakthrough discovery that could fundamentally change strategies for treating HIV.

The team identified for the first time how HIV enters a dormant state in infected cells that allows the virus to “hide” from the immune system and current treatments. 

The researchers believe the finding, just published in Nature Microbiology, challenges decades of scientific assumptions and opens a new approach to possibly eliminating the deadly virus. 

“This discovery rewrites what we thought we knew about how HIV goes into this stealth mode in the human body,” said study lead Saba Valadkhan, an associate professor in the Department of Molecular Biology and Microbiology at the Case Western Reserve School of Medicine. “We’ve shown that HIV actually orchestrates its own survival by reprogramming host cells to create the perfect hiding place.”

The team discovered that HIV uses a clever survival trick that explains why it’s been impossible to cure. After HIV invades a cell, it sneaks its genetic code into the cell’s DNA, then tricks the cell into going to sleep, which also puts the virus to sleep, making both completely invisible. This tactic makes the infected cell invisible to the immune system and unreachable by even today’s most advanced HIV drugs. The virus stays hidden in these dormant cells until the right moment to “wake up” and spread again, creating an undetectable reservoir that ensures HIV never goes away completely.

“What we’ve uncovered is that HIV doesn’t just randomly go dormant – it actively manipulates the host cell to create conditions for its own survival,” said study collaborator Jonathan Karn, Distinguished University Professor and chair of the Department of Molecular Biology and Microbiology. “This gives us specific targets to attack.”

The findings may extend far beyond HIV treatment. The researchers believe similar dormancy actions could be triggered by other viruses – including herpes, hepatitis and other retroviruses – potentially leading to new therapies for many viral diseases. 

“We may have uncovered new tactic viruses use to trick the host cells to do their bidding,” Valadkhan said.

This discovery is also important for protecting public health worldwide because viruses like HIV – which can permanently insert themselves into a person’s DNA – could potentially be used as future viral threats and pandemic preparedness.

Source: Case Western Reserve University

Poor Sleep May Accelerate Brain Ageing

Poor sleep may accelerate brain ageing, a new study shows. Photo by Andrea Piacquadio

People who sleep poorly are more likely than others to have brains that appear older than they actually are. This is according to a comprehensive brain imaging study from Karolinska Institutet, published in the journal eBioMedicine. Increased inflammation in the body may partly explain the association.

Poor sleep has been linked to dementia, but it is unclear whether unhealthy sleep habits contribute to the development of dementia or whether they are rather early symptoms of the disease. In a new study, researchers at Karolinska Institutet have investigated the link between sleep characteristics and how old the brain appears in relation to its chronological age. 

The study includes 27 500 middle-aged and older people from the UK Biobank who underwent magnetic resonance imaging (MRI) of the brain. Using machine learning, the researchers estimated the biological age of the brain based on over a thousand brain MRI phenotypes. 

Low-grade inflammation 

The participants’ sleep quality was scored based on five self-reported factors: chronotype (being a morning/evening person), sleep duration, insomnia, snoring, and daytime sleepiness. They were then divided into three groups: healthy (≥ 4 points), intermediate (2-3 points), or poor (≤ 1 point) sleep. 

“The gap between brain age and chronological age widened by about six months for every 1-point decrease in healthy sleep score,” explains Abigail Dove, researcher at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, who led the study. “People with poor sleep had brains that appeared on average one year older than their actual age.” 

To understand how poor sleep can affect the brain, the researchers also examined levels of low-grade inflammation in the body. They found that inflammation could explain just over ten per cent of the link between poor sleep and older brain age. 

“Our findings provide evidence that poor sleep may contribute to accelerated brain ageing and point to inflammation as one of the underlying mechanisms,” says Abigail Dove. “Since sleep is modifiable, it may be possible to prevent accelerated brain ageing and perhaps even cognitive decline through healthier sleep.” 

Several possible explanations 

Other possible mechanisms that could explain the association are negative effects on the brain’s waste clearance system, which is active mainly during sleep, or that poor sleep affects cardiovascular health, which in turn can have a negative impact on the brain. 

Participants in the UK Biobank are healthier than the general UK population, which could limit the generalisability of the findings. Another limitation of the study is that the results are based on self-reported sleep. 

The study was conducted in collaboration with researchers from the Swedish School of Sport and Health Sciences, and Tianjin Medical University and Sichuan University in China, among others. It was funded by the Alzheimer’s Foundation, the Dementia Foundation, the Swedish Research Council, the Loo and Hans Osterman Foundation for Medical Research, and the Knowledge Foundation. The researchers report no conflicts of interest. 

Source: Karolinska Institutet

Pancreatic Alpha Cells also Secretly Produce Significant Amounts of GLP-1

New study uncovers natural hormone shift that could transform type 2 diabetes treatment

A 3D map of the islet density routes throughout the healthy human pancreas. Source: Wikimedia CC0

A new study from Duke University School of Medicine is challenging long-standing views on blood sugar regulation — and pointing to a surprising new ally in the fight against type 2 diabetes. 

Published in Science Advances, the research reveals that pancreatic alpha cells, once thought to only produce glucagon – a hormone that raises blood sugar to maintain energy when fasting or exercising – also generate GLP-1, a powerful hormone that boosts insulin release from beta cells and helps regulate glucose. GLP-1 is the same hormone mimicked by blockbuster drugs like semaglutide. 

Using mass spectrometry, Duke researchers found that human alpha cells may naturally produce far more bioactive GLP-1 than previously believed. 

Led by Duke scientist Jonathan Campbell, PhD, the team of obesity and diabetes researchers analysed pancreatic tissue from mice and from humans across a range of ages, body weights, and diabetes statuses. They found that human pancreatic tissue produces much higher levels of bioactive GLP-1 and that this production is directly linked to insulin secretion. 

“Alpha cells are more flexible than we imagined,” said Campbell, an associate professor in the Division of Endocrinology in the Department of Medicine and a member of the Duke Molecular Physiology Institute. “They can adjust their hormone output to support beta cells and maintain blood sugar balance.” 

This flexibility could change the approach to treating type 2 diabetes, where beta cells in the pancreas can’t make enough insulin to keep blood sugar at a healthy level. By boosting the body’s own GLP-1 production, it may offer a more natural way to support insulin and manage blood sugar.  

Switching gears 

In mouse studies, when scientists blocked glucagon production, they expected insulin levels to drop. Instead, alpha cells switched gears – ramping up GLP-1 production, improving glucose control, and triggering stronger insulin release.  

“We thought that removing glucagon would impair insulin secretion by disrupting alpha-to-beta cell signaling,” Campbell said. “Instead, it improved it. GLP-1 took over, and it turns out, it’s an even better stimulator of insulin than glucagon.” 

To test this further, researchers manipulated two enzymes: PC2, which drives glucagon production, and PC1, which produces GLP-1. Blocking PC2 boosted PC1 activity and improved glucose control. But when both enzymes were removed, insulin secretion dropped and blood sugar spiked – confirming the critical role of GLP-1. 

Implications for diabetes treatment 

While GLP-1 is typically made in the gut, the study confirms that alpha cells in the pancreas can also release GLP-1 into the bloodstream after eating. This helps to lower blood sugar by increasing insulin and reducing glucagon levels. 

Common metabolic stressors, like a high-fat diet, can increase GLP-1 production in alpha cells – but only modestly. That opens the door to future research: If scientists can find ways to safely boost GLP-1 output from alpha cells they may be able to naturally enhance insulin secretion in people with diabetes.  

But measuring GLP-1 accurately hasn’t been easy. The team developed a high-specificity mass spectrometry assay that detects only the bioactive form of GLP-1 – the version that actually stimulates insulin — not the inactive fragments that often muddy results. 

“This discovery shows that the body has a built-in backup plan,” Campbell said. “GLP-1 is simply a much more powerful signal for beta cells than glucagon. The ability to switch from glucagon to GLP-1 in times of metabolic stress may be a critical way the body maintains blood sugar control.” 

Source: Duke University

Innovative UK Project to Test Drones for Cardiac Arrest Response

Credit: University of Surrey

A project to test how drones can be integrated into the UK’s 999 emergency response system to rapidly deliver defibrillators to patients experiencing out-of-hospital cardiac arrest (OHCA) has been launched by the University of Surrey, Air Ambulance Charity Kent Surrey Sussex, South East Coast Ambulance Service NHS Foundation Trust. 

With survival rates for OHCA in the UK currently below 10%, a key challenge is the delay in delivering life-saving defibrillation. While public Automated External Defibrillators (AEDs) are widely available, getting them to a patient in time is often difficult. This 16-month project will explore using drones to rapidly deliver AEDs to the scene of an emergency. 

This research is the first step towards integrating drone technology into our emergency response systems. Our ultimate goal is to develop and test the procedures needed to seamlessly introduce drone delivery of AEDs into the 999-emergency system 

Dr Scott Munro, Lecturer in Paramedic Practice at the University of Surrey and co-lead on the project

The initiative, which has been funded by the National Institute for Health and Care Research (NIHR), will be divided into two sections: in the first, researchers will develop and refine the drone delivery process through a series of simulations, coordinating 999 call taking, Air Traffic Control, ambulance dispatch and drone operators.  

In the second part, interviews will be conducted with a diverse group of people -including OHCA survivors, family members, responders and members of the public – to understand the public’s perception of drone technology, including any barriers or concerns, and to ensure ease of use for responders. 

This project is a great example of how NIHR’s RfPB programme supports life-saving innovation. Using drones to deliver defibrillators could help emergency teams reach patients faster, improve survival after cardiac arrest, and bring cutting-edge technology directly to the NHS frontline, while working with the public to ensure it’s used safely and effectively. 

Professor Kevin Munro, Director of the NIHR Research for Patient Benefit (RfPB) Programme

Rapid intervention is vital in managing out-of-hospital cardiac arrests. As demand continues to grow, the opportunity to integrate this technology into future healthcare systems represents real progress in ensuring ambulance services can work with the communities they serve to strengthen the chain of survival and give patients the best chance of a positive outcome Being a partner in this research, we are eager to explore how this new initiative could strengthen our cardiac arrest care pathway. 

Dr Craig Mortimer, Research Manager at South East Coast Ambulance Service NHS Foundation Trust (SECAmb)

Source: University of Surrey

Webber Wentzel Secures Landmark Constitutional Court Ruling Reforming South Africa’s Parental Leave Laws

Photograph by Drew Hays on Unsplash

Webber Wentzel’s Pro Bono team represented Mr and Mrs van Wyk in a landmark case that has resulted in the Constitutional Court confirming that South Africa’s statutory four months of parental leave may be shared between both parents. The ruling marks a significant step toward gender equality in the workplace and family law.

The case challenged the unequal parental leave provisions under section 25 of the Basic Conditions of Employment Act (BCEA), which granted birthing mothers up to four months of maternity leave while limiting fathers to only 10 days.

Webber Wentzel argued that section 25 of the BCEA unfairly discriminated against fathers and placed an undue burden on birthing mothers by not allowing families to decide who should be the primary caregiver. The court agreed and criticised the 10-day leave for fathers by rejecting the cultural norms that reinforce gendered parenting roles as inconsistent with constitutional values.

The application was supported by the Commission for Gender Equality (CGE) and Sonke Gender Justice (Sonke). CGE advocated for equal parental leave for adoptive and surrogacy-commissioning parents, which the court partially granted. Sonke’s request for an equal 16-week leave for both parents was not granted.

The Constitutional Court, in a unanimous judgment delivered by the Honourable Justice Tshiqi, confirmed that sections 25, 25A, 25B and 25C of the BCEA, along with corresponding provisions of the Unemployment Insurance Fund Act (UIF Act), are unconstitutional. The Court held that these provisions violate the rights to equality and human dignity under sections 9 and 10 of the Constitution.

The Minister of Employment and Labour accepted that differentiation exists between birthing mothers and other categories of parents is automatically unfair as it is based on grounds specified in section 9(3) of the Constitution. Further, the Minister acknowledges that there is a need for reform in the current legislation pertaining to the parental leave regime contained in the BCEA.

As a result of the ruling in the Constitutional Court, the 4 months of maternal and the 10 days of parental leave will be combined into a total of 4 months and 10 days, which parents may now share as they choose. If no agreement is reached, the leave will be split equally. Where only one parent is employed, that parent will be entitled to the 4 consecutive months of parental leave.

The Constitutional Court also confirmed that the same parental leave provisions apply to adoptive parents and commissioning parents in a surrogacy arrangement.

The Constitutional Court has suspended the declaration of invalidity of the relevant BCEA and UIF Act provisions for a period of 36 months, to allow the legislature to remedy the necessary constitutional defects.  In the interim, the following principles will apply:

  • A single parent or a parent who is the only employed parent is entitled to four months’ consecutive parental leave.
  • Parents who are both employed may share the allocated parental leave of four months and 10 days between them, concurrently or consecutively.
  • An adoptive parent of a child younger than two years is entitled to four months’ consecutive parental leave.
  • If an adoption order is granted in respect of two parents, they may share the allocated parental leave of four months and 10 days between them, concurrently or consecutively.
  • A commissioning parent is entitled to four months’ consecutive parental leave.
  • Where there are two commissioning parents, they may share the allocated parental leave of four months and 10 days between them, concurrently or consecutively.

Employers are encouraged to review and, where necessary, update their leave policies and employment contracts to reflect the new parental leave framework.

“This judgment is a powerful affirmation of the constitutional rights to equality and dignity,” said Nkosinathi Thema, senior associate, Webber Wentzel. “It recognises that caregiving is not the exclusive responsibility of mothers and that both parents should have the freedom to decide how best to care for their child.”

The Webber Wentzel team comprised Ayanda Khumalo, Nkosinathi Thema and Lize-Mari Doubell. Counsel Nasreen Rajab-Budlender SC, Liam Minné and Sanan Mirzoyev appeared on a pro bono basis.

The judgment can be read here.

Ends…

Founded in 1868, Webber Wentzel is a leading full-service law firm providing clients with innovative solutions to their most complex legal and tax issues across Sub-Saharan Africa. With over 450 lawyers, their multi-disciplinary expertise is consistently ranked top tier in leading directories and awards, both in South Africa and on the African continent. Their collaborative alliance with Linklaters and their deep relationships with outstanding law firms across Africa provide clients with market-leading support wherever they do business.

Improvements in Mental Health Best Predict Life Satisfaction

A new model for evaluating changes to life satisfaction can be used to inform public health measures to improve people’s sense of wellbeing.

Photo by Ketut Subiyanto on Unsplash

 On October 2 in the open-access journal PLOS Global Public Health, Steve Haake from Sheffield Hallam University and colleagues published a model for evaluating life satisfaction. They demonstrate their model using participants in a weekly running event as a case study, finding that increases in health, especially mental health, most strongly predict improvements in life satisfaction.  

 In the UK, where the study was conducted, the average life satisfaction on a scale of 0 to 10 is 7.5, as last measured in 2024. Personality is the most significant factor for a person’s life satisfaction, but many other factors that are more variable over time—such as relationship status or economic conditions—also influence how people feel about their lives. Health is another major contributor to a person’s general feelings of wellbeing, and thus the researchers aimed to evaluate how regularly participating in communal physical activity increases ratings of life satisfaction. 

The study focused on participants of a free, weekly 5k event called Parkrun, over 78,000 of whom responded to a survey about their life satisfaction. The survey included questions about other factors that can influence someone’s sense of fulfillment, including general health status and activity levels both before and throughout their participation in Parkrun events. The researchers matched these survey responses to almost a million participants who had done at least one parkrun in the previous 12 months. 

 A sense of improved health was most closely tied to increases in life satisfaction. The majority of Parkrun participants were already highly active and rated their health as “good” or “very good.” However, when the researchers looked at individuals who rated their health as “very bad” at the start of their participation in Parkrun, they found that these people had much greater capacity to improve their increases in life satisfaction compared to people who initially viewed their health as “good.” 

While physical health also had significant effects, the biggest changes in life satisfaction were related to mental health. The survey asked participants about their happiness, general mental wellbeing, and feelings of personal achievement and fun. Higher ratings of these responses were most closely related to growing life satisfaction. 

 The researchers were also able to measure differences for variables not affected by participation in the activity, such as age and gender. Age has a non-linear relationship with life satisfaction, being the lowest in early middle age, and older people were more likely to report a sense of improvement in life satisfaction. This was also true of women compared to men. 

In addition to the health and life satisfaction benefits, the estimated economic benefits of parkrun to the UK economy were estimated to be £668m. This included £75m for the number of runs or walks completed (£1.92 per run or walk per person), £132m for the increase in activity after participation, and £463m for an estimated improvement to health status of 3% (found in a previous study).

 Not only can these data inform public health measures, such as organized physical activity, but this study presents a model for evaluating changes to life satisfaction that can be more broadly applied.

The authors add: “Our previous paper showed that life satisfaction increased for those participating in parkrun – what we didn’t know was how parkrun ‘worked’.  This new paper has given us an answer to this question: health status, increases in activity level and the pleasure from cumulative parkruns.  Rather than the physical aspects of parkrun, it is the improvements to mental health that are most important, things like happiness, a sense of personal achievement and having fun.  Importantly, we now have a model that we can use for any public health initiative, even if it’s not related to health.  In a world of limited resources, the model is a useful way of working out which initiatives are most effective.”

Provided by PLOS

e-Cigarettes Could Unravel Decades of Tobacco Control

New research finds that UK teens who vape are 33% more likely to smoke cigarettes

Photo by Nery Zarate on Unsplash

Teens who regularly use e-cigarettes are equally as likely as their peers from the 1970s to take up cigarette smoking, despite a substantial reduction in the prevalence of teenage cigarette use over the last 50 years, according to a study co-led by the University of Michigan.

U-M researchers, in collaboration with Penn State University and Purdue University, concluded that teenagers who had never used e-cigarettes had an approximately less than 1 in 50 chance of weekly cigarette use, whereas those who had previously used e-cigarettes had more than a 1 in 10 chance. More importantly, teenagers who reported consistent e-cigarette use had nearly a 1 in 3 chance of also reporting current conventional cigarette use.

The study illustrates shifts in the likelihood of youth cigarette use over time and the impacts of e-cigarettes on this trend. The results were derived from three longitudinal studies collected by the Centre for Longitudinal Studies at the University College of London, following teens from three different U.K. birth cohorts.

The research was published in the journal Tobacco Control and was supported by the National Cancer Institute, part of the National Institutes of Health, and a seed grant from the Criminal Justice Research Center at Penn State University, while data collection by the Centre for Longitudinal Studies was supported by funding from the Economic and Social Research Council.

“The use of e-cigarettes and the proliferation of e-cigarettes have really disrupted those awesome trends and improvements. For kids who have never used e-cigarettes, we do see those historic declines in risk,” said Jessica Mongilio, a research fellow at the U-M School of Nursing and one of the lead researchers on the study. “But for kids who do use e-cigarettes, it’s almost as if all of those policies and all of those perceptions have done nothing, and they’ve got a really high risk of smoking cigarettes.”

Over the past few decades, cigarette smoking has evolved from a once glamorous status symbol to an unhealthy and socially discouraged practice, according to the researchers. This evolution was, in large part, driven by aggressive campaigning that labeled cigarette smoking as a public health risk.

By the late 1990s and into the early 2000s, cigarette smoking was structurally and socially stigmatized, embedded in national federal regulations and health policy. In recent years, cigarette smoking in youths dropped to an all-time low, according to research from the Centers for Disease Control.

E-cigarettes, colloquially known as vapes, often sold in bright colorways and in fruity flavors, have quickly emerged as a perceived “safer” alternative to the conventional cigarette. They stand to threaten decades of advocacy, health policy and cultural aversion toward smoking in both the U.K. and United States, the researchers say.

The Millennium Cohort Study, or MCS, tracked teens born in England, Scotland, Wales and Northern Ireland in 2000 and 2001 and who were children when e-cigarettes were first commercialised. The British Cohort Study tracked individuals born in 1970, who were teenagers during the 1980s when cigarette use was fairly common and in their 40s when e-cigarettes were commercially available. Finally, the National Child Development Study tracked individuals born in 1958, who were young children when cigarette use was at its cultural peak.

“We took data from different cohorts, essentially different generations of people who live in the U.K., and looked at their probability of smoking cigarettes at least once a week, based on some well-known risk and protective factors,” Mongilio said. “For the most recent cohort, we also examined how use of e-cigarettes changed those probabilities.”

According to Mongilio and her collaborators, it’s not entirely clear whether e-cigarette use directly caused cigarette use, but it’s clear their incidences are strongly related. Still, the MCS cohort will be continuously surveyed over time to further understand how the use of e-cigarettes during the critical developmental teen years will affect their health in the long term.

Ultimately, with the findings of this study, the researchers hope to demonstrate the profound impact of e-cigarettes on today’s youth in an attempt to exact meaningful legislative, social and economic change.

“The more you can build evidence – the bigger the pile of support – the harder you can make it to ignore. This will lead toward policy changes and toward increased regulations for e-cigarettes and for producers of e-cigarettes,” Mongilio said. “I think we’re in a place where change is possible and to have increased regulations and enforcement of those regulations for companies that are producing e-cigarettes.”

Source: University of Michigan

No ‘Beneficial’ Level of Alcohol Consumption for Dementia Risk

Photo by Apolo Photographer on Unsplash

Any amount of alcohol consumption may increase risk of dementia, according to the most comprehensive study of alcohol consumption and dementia risk to date.

Led by the University of Oxford, Yale University, and the University of Cambridge, the research challenges previous suggestions that light-to-moderate drinking may have a protective effect against dementia. The study is published in BMJ Evidence-Based Medicine.

Alcohol consumption is widespread and is linked with an increased risk of many diseases. Heavy drinking has previously been linked to higher risk of dementia. The connection between moderate levels of drinking and higher risk of dementia was uncertain with some studies suggesting that moderate drinking may even reduce dementia risk. However, recent studies involving brain scans have shown that drinking alcohol even at low levels may increase the risk of dementia.

This study combined observational data from more than half a million participants in two large and diverse population studies: the US Million Veteran Program and UK Biobank to assess whether self-reported alcohol use was linked with risk of developing a broad range of types of dementia.

The researchers also investigated links between genetically-predicted likelihood of drinking alcohol and alcohol use disorder for more than 2.4 million participants in 45 individual studies. This approach helped the researchers overcome some of the difficulties in distinguishing correlation from causation.

Key findings:

  • Observational analyses seemed to support previous findings that current low and moderate drinking is associated with lower risk of dementia when compared with non-drinking and heavy drinking; however, some current non-drinkers were previously heavy drinkers, which could account for their increased dementia risk compared to consistently low drinkers;
  • Genetic analyses, however, revealed a continuously increasing trend of higher dementia risk with greater alcohol intakes, suggesting that any level of alcohol consumption increases the risk of dementia, with no evidence that drinking alcohol may have a protective effect;
  • A doubled increase in a person’s genetically-predicted risk of alcohol use disorder was associated with a 16% higher risk of dementia, while a three times higher increase in number of alcoholic drinks per week increased the risk of dementia risk by 15%;
  • The study also showed that people who later developed dementia reduced their alcohol intake before diagnosis, another explanation for prior findings of protective effects of alcohol, rather than true benefit.

Dr Anya Topiwala, Senior Clinical Researcher at Oxford Population Health, Consultant Psychiatrist, and lead author of the study, said ‘Our findings challenge the common belief that low levels of alcohol are beneficial for brain health. Genetic evidence offers no support for a protective effect – in fact, it suggests the opposite. Even light or moderate drinking may increase the risk of dementia, indicating that reducing alcohol consumption across the population could play a significant role in dementia prevention.’

Dr Stephen Burgess, Statistician at the University of Cambridge, said ‘The random nature of genetic inheritance allows us to compare groups with higher and lower levels of alcohol drinking in a way that allows us to make conclusions that untangle the confusion between correlation and causation. Our findings do not only hold for those who have a particular genetic predisposition, but for anyone who chooses to drink, our study suggests that greater alcohol consumption leads to higher risk of dementia.’

Dr Joel Gelernter, Professor at Yale University and senior author of the study, said ‘These results, which add to our understanding of the relationship between alcohol and dementia, have clinical implications – there was a time when medical knowledge seemed to support that light drinking would be beneficial to brain health, and this work adds to the evidence that this is not correct’.

This study adds to growing evidence that alcohol use, even at moderate levels, may have no safe threshold when it comes to brain health, reinforcing the case for preventive strategies that reduce alcohol consumption in the general population.

The study, ‘Alcohol use and risk of dementia in diverse populations: evidence from cohort, case–control and Mendelian randomisation approaches‘, is published in BMJ Evidence-Based Medicine.

Source: Oxford University

Prediabetes Remission Possible Without Dropping Pounds, Our New Study Finds

Photo by Kenny Eliason on Unsplash

Andreas L. Birkenfeld, University of Tübingen and Reiner Jumpertz-von Schwartzenberg, University of Tübingen

There’s a long-held belief in diabetes prevention that weight loss is the main way to lower disease risk. Our new study challenges this.

For decades, people diagnosed with prediabetes – a condition affecting up to one in three adults depending on age – have been told the same thing by their doctors: eat healthily and lose weight to avoid developing diabetes.

This approach hasn’t been working for all. Despite unchanged medical recommendations for more than 20 years, diabetes prevalence continues rising globally. Most people with prediabetes find weight-loss goals hard to reach, leaving them discouraged and still at high risk of diabetes.

Our latest research, published in Nature Medicine, reveals a different approach entirely. We found that prediabetes can go into remission – with blood sugar returning to normal – even without weight loss.

About one in four people in lifestyle intervention programmes bring their blood sugar back to normal without losing any weight. Remarkably, this weight-stable remission protects against future diabetes just as effectively as remission achieved through weight loss.

This represents a significant shift in how doctors might treat overweight or obese patients at high risk for diabetes. But how is it possible to reduce blood glucose levels without losing weight, or even while gaining weight?

The answer lies in how fat is distributed throughout the body. Not all body fat behaves the same way.

The visceral fat deep in our abdomen, surrounding our internal organs, acts as a metabolic troublemaker. This belly fat drives chronic inflammation that interferes with insulin – the hormone responsible for controlling blood sugar levels. When insulin can’t function properly, blood glucose rises.

In contrast, subcutaneous fat – the fat directly under our skin – can be beneficial. This type of fat tissue produces hormones that help insulin work more effectively. Our study shows that people who reverse prediabetes without weight loss shift fat from deep within their abdomen to beneath their skin, even if their total weight stays the same.

Subcutaneous fat can be beneficial. Photo by Andres Ayrton on Pexels

We’ve also uncovered another piece of the puzzle. Natural hormones that are mimicked by new weight-loss medications like Wegovy and Mounjaro appear to play a crucial role in this process. These hormones, particularly GLP-1, help pancreatic beta cells secrete insulin when blood sugar levels rise.

People who reverse their prediabetes without losing weight seem to naturally enhance this hormone system, while simultaneously suppressing other hormones that typically drive glucose levels higher.

Targeting fat redistribution, not just weight loss

The practical implications are encouraging. Instead of focusing only on the scales, people with prediabetes can aim to shift body fat with diet and exercise.

Research shows that polyunsaturated fatty acids, abundant in Mediterranean diets rich in fish oil, olives and nuts, may help reduce visceral belly fat. Similarly, endurance training can decrease abdominal fat even without overall weight loss.

This doesn’t mean weight loss should be abandoned as a goal – it remains beneficial for overall health and diabetes prevention. However, our findings suggest that achieving normal blood glucose levels, regardless of weight changes, should become a primary target for prediabetes treatment.

This approach could help millions of people who have struggled with traditional weight-loss programmes but might still achieve meaningful health improvements through metabolic changes.

For healthcare providers, this research suggests a need to broaden treatment approaches beyond weight-focused interventions. Monitoring blood glucose improvements and encouraging fat redistribution through targeted nutrition and exercise could provide alternative pathways to diabetes prevention for patients who find weight loss particularly difficult.

The implications extend globally, where diabetes represents one of the fastest-growing health problems. By recognising that prediabetes can improve without weight loss, we open new possibilities for preventing a disease that affects hundreds of millions worldwide and continues rapidly expanding.

This research fundamentally reframes diabetes prevention, suggesting that metabolic health improvements – not just weight reduction – should be central to clinical practice. For the many people living with prediabetes who have felt discouraged by unsuccessful weight-loss attempts, this offers renewed hope and practical alternative strategies for reducing their diabetes risk.

Andreas L. Birkenfeld, Professor, Diabetology, Endocrinology and Nephrology, University of Tübingen and Reiner Jumpertz-von Schwartzenberg, Professorship for Clinical Metabolism and Obesity Research, University Hospital and Medical Faculty, University of Tübingen

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

Vitamin D2 Supplements May Actually Lower Vitamin D3 Levels

Photo by Michele Blackwell on Unsplash

Taking vitamin D2 might lower the body’s levels of the more efficient form of vitamin D, vitamin D3, according to new research from the University of Surrey, John Innes Centre and Quadram Institute Bioscience. 

Many people take vitamin D supplements to support their bone and immune health and meet the UK government recommendation of 10 micrograms (µg) each day, especially during the winter months. 

There are two forms of vitamin D supplements available: vitamin D2 and vitamin D3. Researchers have found that taking vitamin D2 supplements can lead to a drop in the body’s concentration of vitamin D3, which is the form our bodies naturally produce from sunlight and use most effectively to raise overall vitamin D levels.  

The study, published in Nutrition Reviews, analysed data from randomised controlled trials and found that vitamin D2 supplementation resulted in a reduction in vitamin D3 levels compared to those not taking a vitamin D2 supplement. In many of the studies, the vitamin D3 levels went lower than in the control group. 

Vitamin D supplements are important, especially between October and March, when our bodies cannot make vitamin D from sunlight in the UK. However, we discovered that vitamin D2 supplements can actually decrease levels of vitamin D3 in the body, which is a previously unknown effect of taking these supplements. This study suggests that subject to personal considerations, vitamin D3 supplements may be more beneficial for most individuals over vitamin D2. 

Emily Brown, PhD Research Fellow and Lead Researcher of the study from the University of Surrey’s Nutrition, Exercise, Chronobiology & Sleep Discipline

This research supports a previous study published in Frontiers in Immunology, led by Professor Colin Smith from the University of Surrey, which suggests that vitamin D2 and D3 do not have identical roles in supporting immune function. Vitamin D3 has a modifying effect on the immune system that could fortify the body against viral and bacterial diseases

We have shown that vitamin D3, but not vitamin D2, appears to stimulate the type I interferon signalling system in the body – a key part of the immune system that provides a first line of defence against bacteria and viruses. Thus, a healthy vitamin D3 status may help prevent viruses and bacteria from gaining a foothold in the body.

Professor Colin Smith, University of Surrey

Further research into the different functionalities of vitamin D2 and D3 should be a priority in deciding whether vitamin D3 should be the first-line choice of vitamin D supplement, subject to individual requirements. 

Source: University of Surrey