Category: Metabolic Disorders

Categories : Metabolic DisordersTags :

Scientists Discover Why Diabetes is Less Common at High Altitudes

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The low oxygen levels at high altitude have long been known to be associated with lower diabetes rates. Photo by Mike Markov on Unsplash

Scientists have long known that people living at high altitudes, where oxygen levels are low, have lower rates of diabetes than people living closer to sea level. But the mechanism of this protection has remained a mystery.

Now, researchers at Gladstone Institutes have explained the roots of the phenomenon, discovering that red blood cells act as glucose sponges in low-oxygen conditions like those found on the world’s highest mountaintops.

In a new study in the journal Cell Metabolism, the team showed how red blood cells can shift their metabolism to soak up sugar from the bloodstream. At high altitude, this adaptation fuels the cells’ ability to more efficiently deliver oxygen to tissues throughout the body, but it also has the beneficial side effect of lowering blood sugar levels.

The findings solve a longstanding puzzle in physiology, says Gladstone Investigator Isha Jain, PhD, the senior author of the study.

“Red blood cells represent a hidden compartment of glucose metabolism that has not been appreciated until now,” says Jain, who is also a core investigator at Arc Institute and a professor of biochemistry at UC San Francisco. “This discovery could open up entirely new ways to think about controlling blood sugar.”

The Hidden Glucose Sink

Jain has spent years probing how low blood-oxygen levels, called hypoxia, affect health and metabolism. During a previous study, her team noticed that mice breathing low-oxygen air had dramatically lower blood glucose levels than normal. That meant the animals were quickly using up glucose after they ate—a hallmark of lower diabetes risk. But when the researchers used imaging to track where the glucose was going, major organs couldn’t account for it.

“When we gave sugar to the mice in hypoxia, it disappeared from their bloodstream almost instantly,” says Yolanda Martí-Mateos, PhD, a postdoctoral scholar in Jain’s lab and first author of the new study. “We looked at muscle, brain, liver—all the usual suspects—but nothing in these organs could explain what was happening.”

Using another imaging technique, the team revealed that red blood cells were the missing “glucose sink”—a term used to describe anything that pulls in and uses a lot of glucose from the bloodstream. The cells, having long been considered metabolically simple, seemed like unlikely candidates.

But further mouse experiments confirmed that red blood cells were indeed absorbing the glucose. In low-oxygen conditions, mice not only produced significantly more red blood cells, but each cell took up more glucose than red blood cells produced under normal oxygen.

To understand the molecular mechanisms of this observation, Jain’s team collaborated with Angelo D’Alessandro, PhD, of the University of Colorado Anschutz Medical Campus, and Allan Doctor, MD, from University of Maryland, who has long studied the function of red blood cells.

The researchers showed how, in low-oxygen conditions, glucose is used by red blood cells to produce a molecule that helps cells release oxygen to tissues—something that’s needed in excess when oxygen is scarce.

“What surprised me most was the magnitude of the effect,” D’Alessandro says. “Red blood cells are usually thought of as passive oxygen carriers. Yet, we found that they can account for a substantial fraction of whole-body glucose consumption, especially under hypoxia.”

A New Path to Diabetes Treatment

The scientists went on to show that the benefits of chronic hypoxia persisted for weeks to months after mice returned to normal oxygen levels.

They also tested HypoxyStat, a drug recently developed in Jain’s lab to mimic the effects of low-oxygen air. HypoxyStat is a pill that works by making hemoglobin in red blood cells grab onto oxygen more tightly, keeping it from reaching tissues. The drug completely reversed high blood sugar in mouse models of diabetes, working even better than existing medications.

“This is one of the first use of HypoxyStat beyond mitochondrial disease,” Jain says. “It opens the door to thinking about diabetes treatment in a fundamentally different way—by recruiting red blood cells as glucose sinks.”

The findings could extend beyond diabetes to exercise physiology or pathological hypoxia after traumatic injury, D’Alessandro notes, where trauma remains a leading cause of mortality in younger populations and shifts in red blood cell levels and metabolism may influence glucose availability and muscle performance.

“This is just the beginning,” Jain says. “There’s still so much to learn about how the whole body adapts to changes in oxygen, and how we could leverage these mechanisms to treat a range of conditions.”

Source: Gladstone Institutes of Science

Categories : Diet and Nutrition Metabolic DisordersTags :

Vegan Diet Helps People With Type 1 Diabetes Cut Insulin Costs by 27%

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Novolog insulin pen. Photo by Dennis Klicker on Unsplash

A low-fat vegan diet that doesn’t limit calories or carbohydrates could help people with type 1 diabetes reduce insulin use and insulin costs, according to new research by the Physicians Committee for Responsible Medicine published in BMC Nutrition.

The new research, which is a secondary analysis of a 2024 Physicians Committee study, compared the effect of a low-fat vegan diet to a portion-controlled diet on insulin use and insulin costs in people with type 1 diabetes. The analysis found that the total dose of insulin decreased by 28%, or 12.1 units, per day in the vegan group, compared to no significant change in the portion-controlled group. The reductions in insulin use in the vegan group likely reflect improved insulin sensitivity, or how well the body responds to insulin. Total insulin costs decreased by 27%, or $1.08 per day, in the vegan group, compared to no significant change in the portion-controlled group.

The 2024 study found that a vegan diet also led to an average weight loss of 11 pounds, improved insulin sensitivity and glycaemic control, and improved cholesterol levels and kidney function in people with type 1 diabetes.

The new research comes as insulin prices in the United States continue to rise. Spending on insulin in the United States tripled in the past 10 years, reaching $22.3 billion in 2022, due to the increased usage and higher price of insulin, according to the American Diabetes Association. The inflation-adjusted cost of insulin increased by 24% from 2017 to 2022.

“As insulin prices continue to rise, people with type 1 diabetes should consider a low-fat vegan diet, which can help improve their insulin sensitivity and reduce the amount of insulin they need, potentially saving them hundreds of dollars a year,” says Hana Kahleova, MD, PhD, the lead author of the study and director of clinical research at the Physicians Committee for Responsible Medicine.

Source: Physicians Committee for Responsible Medicine

Categories : Metabolic DisordersTags :

Oral PCSK9 Inhibitor Offers Cholesterol Control Without the Needle

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Photo by Danilo Alvesd on Unsplash

The results of a phase 3 clinical trial for enlicitide, a novel oral medication designed to lower cholesterol have been reported in a recent New England Journal of Medicine article. The study, involving nearly 3000 adults with existing or at high risk of cardiovascular disease, compared a daily 20mg dose against a placebo over one year.

Researchers found that the drug significantly reduced LDL cholesterol by approximately 57% within 24 weeks, alongside notable decreases in other harmful lipids. These improvements remained consistent and durable throughout the 52-week treatment period. Crucially, the safety profile of the oral inhibitor appeared comparable to the placebo, with no meaningful difference in side effects. The authors conclude that this convenient pill could offer a highly effective alternative to existing injectable therapies for managing heart disease risk.

Listen to a discussion on QuickNews’ podcast!

Categories : Metabolic DisordersTags :

When the Scale Moves Faster than the Body can Adapt: Hair Loss in the Age of GLP-1s

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Photo by Towfiqu barbhuiya

By Dr Kashmal Kalan, Medical Director, Alvi Armani

In 2023, global prescriptions for GLP-1 weight loss medications rose by more than 40%, with drugs like Ozempic and Wegovy moving from specialist clinics into everyday conversation. Alongside this surge, a new concern is appearing more frequently in consultation rooms: unexpected hair loss.

For many patients, the timing is deeply unsettling. After months of discipline and visible progress, they start to notice more hair in the shower, on their pillow, or in their brush. The immediate fear is that something has gone wrong – that the medication is damaging their body, that the weight loss has come at a hidden cost, or something more serious.

In most cases, the reality is more nuanced. At Alvi Armani, we are seeing a consistent pattern: hair loss following rapid weight loss is real, but it is rarely caused by GLP-1 medications alone, despite how often this link is assumed. Instead, it reflects how the body responds to sudden physiological stress.

Hair loss often arrives late

The most common diagnosis in these cases is telogen effluvium, a form of temporary shedding that occurs when a large number of hair follicles shift prematurely into a resting phase. The critical detail is timing – the hair does not fall out immediately but rather sheds months after the original trigger.

This delay is what makes the experience so confusing. By the time hair begins to thin, weight loss may already feel stable, lifestyle changes established, and the initial stress long past. But biologically, the body is only now expressing the shock it absorbed earlier.

In some individuals, this shedding also unmasks an underlying genetic tendency toward pattern hair loss, known as androgenetic alopecia. While rapid weight loss does not create this condition, it can reveal it sooner than expected. What begins as temporary shedding may gradually shift into more persistent thinning – a progression that is emotionally difficult precisely because it feels so unexpected.

Why the body sacrifices hair first

Hair is not essential to survival. When the body experiences stress – whether through rapid fat loss, hormonal shifts, illness, or nutritional restriction – it reallocates resources to protect vital systems. Hair growth is one of the first processes to be downregulated.

Importantly, stress-related shedding does not create a new condition. It accelerates what was already encoded in the body. The hair is not “breaking down”; it is responding to a shift in internal priorities.

The speed of change is critical. Gradual, steady weight loss allows the body time to adapt hormonally and metabolically. Rapid loss, particularly when paired with appetite suppression, elevated stress hormones, or inadequate protein intake, creates a perfect storm for hair disruption.

From a biological perspective, shedding is not a malfunction, but rather an adaptive response. But from a patient’s perspective, it feels personal, visible, and deeply unsettling.

Who tends to notice it most

Women often become aware of thinning first, partly because longer hair makes shedding more obvious, and partly because changes in density carry greater emotional weight. Individuals with a family history of hair loss are also more vulnerable, as are those who lose a significant percentage of body weight in a short period of time.

Nutrition matters more than most realise

Hair is metabolically demanding tissue. It requires consistent access to protein, iron, zinc, and a range of micronutrients to maintain its growth cycle. When intake drops sharply because of appetite suppression, restrictive dieting, or poorly supervised medication use, hair becomes collateral damage.

This is why medically guided weight loss is so important. GLP-1 medications can be powerful tools, but they must be paired with nutritional planning. The body can tolerate change; what it struggles with is deprivation disguised as progress.

Temporary or permanent?

For many patients, telogen effluvium resolves within six to nine months once the body stabilises. Hair regrowth is slow, but it does occur.

However, in those with genetic susceptibility, the episode may mark the beginning of more sustained thinning. This does not mean damage has been done, but it does mean the window for early intervention matters. The earlier changes are recognised, the more options exist to slow or stabilise progression.

When hair loss deserves attention

Shedding should not be ignored if it persists beyond three to six months, if overall density continues to decline, or if there is a strong family history of pattern hair loss. Hair changes are often the first visible signal that the body is struggling to adapt to internal stress.

Early assessment allows for accurate diagnosis, realistic expectations, and far better long-term outcomes.

A final thought on balance

GLP-1 medications have transformed the weight loss landscape, and for many people, they offer genuine health benefits. But transformation should never come at the cost of physiological stability.

Hair is not separate from health. It is one of its most sensitive mirrors. Protecting the body protects the hair. Sustainable change, guided by medical support, remains the most reliable way to achieve results that last – without unexpected consequences.

Categories : Implants and Prostheses Metabolic DisordersTags :

Could a Living Implant End Daily Insulin Injections?

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The development of a self-regulating, implantable living technology that could offer hope for millions with diabetes and other chronic diseases

The crystal capsules developed by the researchers. They made the cover of Science Translational Medicine.

A pioneering study marks a major step toward eliminating the need for daily insulin injections for people with diabetes. The research introduces a living, cell-based implant that can function as an autonomous artificial pancreas, essentially a living drug that is long-term, thanks to a novel crystalline shield technology.

Once implanted, the system operates entirely on its own: it continuously senses blood-glucose levels, produces insulin within the implant itself, and releases the exact amount needed – precisely when it is needed. In effect, the implant becomes a self-regulating, drug-manufacturing organ inside the body, requiring no external pumps, injections, or patient intervention.

One of the study’s most significant breakthroughs addresses the longstanding challenge of immune rejection, which has limited the success of cell-based therapies for decades. The researchers developed engineered therapeutic crystals that shield the implant from the immune system, preventing it from being recognised as a foreign object. This protective strategy enables the implant to function reliably and continuously for several years.

The technology has already been successfully tested in a mouse model for effective and long-term regulation of glucose levels and in non-human primates for cell viability and functionality. These results represent a critical milestone and strongly support the potential for future translation to human patients.

From Postdoctoral Insight to Global Collaboration

The study was led by Assistant Professor Shady Farah of the Faculty of Chemical Engineering at the Technion – Israel Institute of Technology, in co-correspondence with MIT, and in collaboration with Harvard University, Johns Hopkins University, and the University of Massachusetts. Asst Prof Farah began developing the concept with colleagues in 2018 during his postdoctoral fellowship at MIT and Boston Children’s Hospital/Harvard Medical School, under the supervision of Prof Daniel Anderson and Prof Robert (Bob) Langer, a world leader in tissue engineering and co-founder of Moderna.

Today, the research continues in Asst Prof Farah’s laboratory at the Technion, in close collaboration with leading US institutions, including MIT, Harvard, the University of Massachusetts, Boston Children’s Hospital, and the Johns Hopkins University School of Medicine.

A Platform with Far-Reaching Potential

While the immediate focus is diabetes, the researchers emphasise that this implantable, closed-loop platform could be adapted to treat a wide range of chronic conditions requiring continuous delivery of biological therapeutics – including haemophilia and other metabolic or genetic diseases.

If successfully translated to the clinic, this technology could redefine how chronic diseases are treated, shifting from repeated drug administration to living, self-regulating therapies that work seamlessly from within.

To read the full article, click here

Source: TECHNION Israel Institute of Technology

Categories : Metabolic DisordersTags :

Researchers Quantify How Much Obesity Reduction Prevents Common Conditions

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Source: Pixabay CC0

A University of Exeter-led study has quantified the role of obesity in common long-term conditions, showing for the first time the effect of losing weight in preventing multiple diseases.  

Conditions that often occur together may share an underlying cause, which can be key to prevention or treatment. The picture of which conditions co-occur is complex, so researchers paired them together, to allow them to identify shared causes more simply. The study found that obesity is the main shared cause between ten pairs of commonly occurring conditions.   

The research specifically measured how much weight reduction would reduce the risk of the next diagnosis.  In the largest study of its kind, published in Communications Medicine – Nature, the team studied 71 conditions which often occur together, such as type 2 diabetes and osteoarthritis, or kidney disease and chronic obstructive pulmonary disease (COPD).  

The GEMINI study, funded by the UKRI Medical Research Council and supported by the National Institute for Health and Care Research (NIHR), used genetics and healthcare data drawn from a number of large datasets internationally. They found that obesity was part of the cause for  61 of the 71 conditions. They also found that obesity explained all of the genetic overlap in ten pairs of conditions, suggesting it is the main driver for why they frequently occur together.  

Body mass index, or BMI, is a scaled measure of weight – a number over 30 units indicates obesity, while less than 25 indicates “normal” weight. The study quantified how much a reduction in BMI would reduce the risk of both conditions at a population level for people overweight or living with obesity. For example, for every thousand people who have both chronic kidney disease and osteoarthritis, a BMI reduction of 4.5 units would have prevented 17 of them developing both conditions or nine people per thousand with type 2 diabetes and osteoarthritis.  

The team also established the pairs of conditions where obesity is not the main cause and are now investigating other mechanisms.  

Study lead Professor Jack Bowden, at the University of Exeter Medical School: “We’ve long known that certain diseases often occur together, and also that obesity increases the risk of many diseases. This largescale study is the first to use genetics to quantify the role of obesity in causing diseases to occur in the same individuals. We found that for some disease pairings, obesity is the major driving force. Our research provides much more detail about the links between obesity and disease, which will help clinicians target specific advice to patients going forward.”  

Study author Professor Jane Masoli, of the University of Exeter Medical School, who is a Consultant Geriatrician and regional NIHR Ageing lead, said: “Currently nine million people in the UK live with two or more long-term conditions.  Understanding how to prevent diseases accumulating is a key national research and healthcare priority.  This study further strengthens the case to tackle obesity through public health programmes, reinforcing the importance of lifelong obesity management in the NHS strategy on prevention. Our work shows that this could reduce the risk of accumulating multiple health conditions, supporting people to live longer, healthier lives.”  

This research represents another important publication from the GEMINI (Genetic Evaluation of Multimorbidity towards INdividualisation of Interventions) collaborative. Led by the University of Exeter, GEMINI includes people with multimorbidity, health care professionals including those in primary care and experts in statistics and genetics, and was one of six programmes funded by the UKRI strategic priorities fund, an £830 million investment in multimorbidity research. 

The GEMINI team are working to further understand why some conditions more frequently co-occur in the same patients. The team are quantifying the role of other, known modifiable risk factors beyond obesity, and are finding novel genes and pathways that could point to new ways to intervene and improve health. GEMINI data, results, and code are free to download (https://github.com/GEMINI-multimorbidity), and the pairwise genetic and observational correlations can be viewed interactively (https://gemini-multimorbidity.shinyapps.io/atlas/).   

By Louise Vennells

Source: University of Exeter

Categories : Cardiovascular Disease Metabolic DisordersTags :

New Study Explains How Long-term Diabetes Causes Vascular Damage

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Source: CC0

The longer a person has type 2 diabetes, the greater the risk of cardiovascular disease. A new study from Karolinska Institutet, published in the journal Diabetes, shows that changes in red blood cells may be an important explanation, and identifies a specific molecule as a possible biomarker.

People with type 2 diabetes are at increased risk of heart attack and stroke, and the risk increases the longer they have lived with the disease. Previous research has shown that red blood cells can affect blood vessel function in diabetes. Now, a new study shows that the duration of the disease plays a decisive role in when and how these changes occur – and that long-term type 2 diabetes can make red blood cells directly harmful to blood vessels.

The researchers studied both animals and patients with type 2 diabetes. Red blood cells from mice with long-term diabetes and patients who had had the disease for over seven years had a harmful effect on blood vessel function. No such effect was seen in newly diagnosed individuals, but after seven years of follow-up, their blood cells had developed the same harmful properties. When the researchers restored the levels of microRNA-210 in the red blood cells, vascular function improved.

“What really stands out in our study is that it is not only the presence of type 2 diabetes that matters, but how long you have had the disease. It is only after several years that red blood cells develop a harmful effect on blood vessels,” says Zhichao Zhou, associate professor at the Department of Medicine, Solna, Karolinska Institutet, and lead author of the study.

The study points to microRNA-210 in red blood cells as a possible biomarker for early detection of the risk of cardiovascular complications. Researchers are now working to investigate whether this can be used in larger population studies.

“If we can identify which patients are at greatest risk before vascular damage has already occurred, we can also become better at preventing complications,” says Eftychia Kontidou, doctoral student from the same group and the first author of the study.

Source: Karolinska Institutet

Categories : Metabolic Disorders PaediatricsTags :

UK Study Proves Effectiveness of Childhood Type 1 Diabetes Screening

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Photo by Pavel Danilyuk

Thousands of families have taken part in a landmark UK study led by researchers at the University of Birmingham which shows that childhood screening for type 1 diabetes is effective, laying the groundwork for a UK-wide childhood screening programme.

Results from the first phase of the ELSA (Early Surveillance for Autoimmune diabetes) study, co-funded by charities Diabetes UK and Breakthrough T1D, have been published in a research letter in The Lancet Diabetes & Endocrinology today.

The findings mark a major step towards a future in which type 1 diabetes can be detected in children before symptoms appear. Currently, over a quarter of children aren’t diagnosed with type 1 diabetes until they are in diabetic ketoacidosis (DKA), a potentially fatal condition that requires urgent hospital treatment. Early detection can dramatically reduce emergency diagnoses and could give children access to new immunotherapy treatments that can delay the need for insulin for years.

We are working towards a future where type 1 diabetes can be detected in a timely manner

Professor Parth Narendran, lead researcher

Launched in 2022, ELSA is the first UK study of its kind, tested blood samples from 17,931 children aged 3-13 for autoantibodies, markers of type 1 diabetes that can appear years before symptoms.

Children without autoantibodies are unlikely to develop type 1 diabetes, while those with one autoantibody have a 15% chance of developing the condition within 10 years. Having two or more autoantibodies indicates the immune system has already started attacking the insulin-producing cells in the pancreas and it is almost certain these children will eventually need insulin therapy. This is known as early-stage type 1 diabetes.

Among the 17,283 children aged 3-13 years who were screened for type 1 diabetes risk at the time of analysis:

  • 75 had one autoantibody, signaling increased future risk.
  • 160 had two or more autoantibodies but did not yet require insulin therapy, indicating early-stage type 1 diabetes.
  • 7 were found to have undiagnosed type 1 diabetes with all needing to start insulin immediately.

Lead researcher, Parth Narendran, Professor of Diabetes Medicine at the University of Birmingham, said: “We are extremely grateful to all the families who have participated in the study and generously given their time to help understand how a UK-wide screening programme could be developed. Together with Diabetes UK, Breakthrough T1D and the National Institute for Health and Care Research, we are working towards a future where type 1 diabetes can be detected in a timely manner, and families appropriately supported and treated with medicines to delay the need for insulin.

“We are also grateful to partners across the Birmingham Health and Life Sciences District and beyond as well as the NIHR for the support they have provided in getting us to where we are.”

Interventions before diagnosis

Families of children found to have early-stage type 1 diabetes received tailored education and ongoing support to prepare for the eventual onset of type 1 diabetes symptoms and to ensure insulin therapy can begin promptly when needed, reducing the chances of needing emergency treatment. Those with one autoantibody also received ongoing support and monitoring.

Some families were also offered teplizumab, the first ever immunotherapy for type 1 diabetes, which can delay the need for insulin by around three years in people with early-stage type 1 diabetes. The first patient was treated at Birmingham Children’s Hospital. Teplizumab was licensed by the Medicines and Healthcare products Regulatory Agency (MHRA) in the UK in August 2025, and is currently being assessed by the National Institute for Health and Care Excellence (NICE) to determine whether it should be available through the NHS.

As of November 2025, more than 37,000 families have signed up to the ELSA programme. Building on this strong foundation, the second phase of the research, ELSA 2, launches today. ELSA 2 will expand screening to all children in the UK aged 2-17 years, with a focus on younger children (2-3 years) and older teenagers (14-17 years). The research team aims to recruit 30,000 additional children across these new age groups.

ELSA 2 will also establish new NHS Early-Stage Type 1 Diabetes Clinics, providing families taking part with clinical and psychological support and creating a clear pathway from screening to diagnosis, monitoring and treatment.

Case study: Knowing what’s coming … has made an enormous difference

Amy Norman, 44, from the West Midlands, was diagnosed with type 1 diabetes at the age of 13. She recently discovered via the ELSA study that her 11-year-old daughter, Imogen, is in the early stages of type 1 diabetes but has been able to slow its progression as the second child in the UK to access a breakthrough immunotherapy drug – teplizumab. She said: “Being part of the ELSA study has helped us as a family to prepare for the future in a way we never expected. Knowing what’s coming – rather than being taken by surprise – has made an enormous difference to our confidence and peace of mind.

“When I was diagnosed, I had no warning and ended up quite poorly in hospital with diabetic ketoacidosis (DKA). When Imogen’s diagnosis arrives, we hope that having this awareness will reduce her chances of experiencing DKA and the added trauma that comes from a sudden illness.

“Imogen took part in the study to further research and help others, but it has helped her too – being forewarned is being forearmed. She was always going to develop type 1 diabetes, but through ELSA we’ve been able to slow down the process and prepare – we know what is coming, but we’re not scared.”

A game-changer: showing what we can achieve in Birmingham

Professor Neil Hanley, Pro-Vice-Chancellor and Head of the College of Medicine and Health at the University of Birmingham, said, “This is a game-changer. This trial shows we can spare countless children the trauma of an emergency diagnosis, ensure they get early support, and potentially give them access to revolutionary new treatments that could delay or even prevent type 1 diabetes.

“Dr Parth Narendran and his team deserve huge credit; and this breakthrough shows what we can achieve in Birmingham. We have world-class clinicians and scientists working side-by-side, backed by great innovation infrastructure and a vibrant, diverse and affordable city – and, as a result, we are changing lives with next generation diagnostics, therapeutics, and clinical care.”

Rewriting the story of type 1 diabetes

Dr Elizabeth Robertson, Director of Research and Clinical at Diabetes UK, said: “For too many families, a child’s type 1 diabetes diagnosis still comes as a frightening emergency. But that doesn’t have to be the case. Thanks to scientific breakthroughs, we now have the tools to identify children in the very earliest stages of type 1 diabetes – giving families precious time to prepare, avoid emergency hospital admissions, and access treatments that can delay the need for insulin for years.

“The ELSA study, co-funded by Diabetes UK, is generating the evidence needed to make type 1 diabetes screening a reality for every family in the UK. We’re incredibly grateful to the 37,000 families who’ve already signed up and urge others to get involved. Together, we can transform type 1 diabetes care for future generations.”

Rachel Connor, Director of Research Partnerships at Breakthrough T1D, said: “This is about rewriting the story of type 1 diabetes for thousands of families. Instead of a devastating emergency, we can offer time, choices, and hope. By finding children in the earliest stages, we’re not just preparing families, we’re opening the door to treatments that can delay the need for insulin by years. That extra time means childhoods with fewer injections, fewer hospital visits and more normality. Thanks to research like ELSA, what once struck as an unexpected crisis can become an actively managed healthcare process, changing the course of T1D for the better.”

The findings from ELSA’s first phase signal a major step towards a future in which type 1 diabetes can be detected early, managed proactively, and potentially delayed through immunotherapy. ELSA demonstrates that childhood screening in the UK is feasible, acceptable to families, and capable of preventing emergency diagnoses. Continued research through ELSA 2 will assess how screening can be scaled across the NHS and evaluate its cost-effectiveness.

Source: University of Birmingham

Categories : Metabolic DisordersTags :

High Cholesterol and Insulin Resistance are Rising Among Young South Africans – What that Means for Public Health

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Photo by Elizeu Dias on Unsplash

Themba Titus Sigudu, University of the Witwatersrand

In a small mining town in South Africa’s Limpopo province, young people are showing worrying signs of diseases that were once thought to affect only older adults.

These include type 2 diabetes, high blood pressure, high cholesterol, obesity and insulin resistance. This is not unique to Limpopo or South Africa. It reflects a global trend, where young adults in many low- and middle-income countries are increasingly experiencing early-onset metabolic diseases due to rapid urbanisation, lifestyle changes, unhealthy diets and reduced physical activity.

The World Health Organization says non-communicable diseases now account for 75% of all non-pandemic-related deaths globally. Also, 82% of premature deaths before age 70 occur in low- and middle-income countries.

I’m a public health researcher specialising in epidemiology, metabolic health, infectious diseases and environmental health. My colleagues and I conducted a study in the town of Lephalale and found that many young adults there have abnormal cholesterol levels. They also have reduced sensitivity to insulin, a condition known as insulin resistance.

Both are key risk factors for type 2 diabetes and heart disease.

Our findings suggest that these health problems are appearing much earlier in life than expected. This is particularly concerning in communities undergoing rapid social and economic change, where access to health services and screening programmes remains limited.

New jobs, new lifestyles

Lephalale, formerly known as Ellisras, offers a window into these transitions. Once a quiet rural area in the north of South Africa, it has changed rapidly over the past two decades. It is now the site of expanding mining and industrial activities, driven by the expansion of coal mining operations and the development of power stations.

This industrial growth has attracted thousands of workers from surrounding provinces and neighbouring countries, bringing new economic opportunities. It is also reshaping daily life. Increasingly, residents are doing sedentary work and eating energy-dense diets, including fast food. These lifestyle transitions make Lephalale an important setting for studying emerging health risks in young adults.

Long hours sitting at work and reduced physical activity create fertile ground for metabolic disorders. When people eat more processed, high-fat, high-sugar foods and move less, the body begins storing excess energy as fat.

Over time, this can lead to weight gain, elevated blood glucose and abnormal cholesterol levels. These changes make it harder for the body to regulate insulin, causing insulin resistance, the first step towards type 2 diabetes. Also, inactivity and poor diet increase unhealthy cholesterol and triglycerides (types of fat in the blood), raising the risk of heart disease. In rapidly transitioning communities, these health shifts can happen quickly.

Non-communicable diseases such as diabetes, hypertension and heart disease are now among the leading causes of death in South Africa. In 2020, diabetes was reported to be the second biggest underlying cause of death in South Africa, accounting for 6.6% of all deaths.

Our research

We examined 781 young adults aged 18 to 29 years living in Lephalale as part of a long-running study. We have been tracking health patterns in this community since 1992.

Participants provided fasting blood samples that were analysed for glucose, insulin and cholesterol levels. We grouped them into diabetic and non-diabetic categories based on clinical definitions used by the American Diabetes Association.

The results were striking:

  • Diabetic participants had significantly higher total cholesterol, low-density lipoprotein (the “bad” cholesterol) and triglycerides, and lower levels of high-density lipoprotein (the “good” cholesterol) than their non-diabetic peers.
  • Over half (52.7%) of the diabetic group had high total cholesterol, compared with 23% of non-diabetic participants.
  • Insulin resistance, when the body needs more insulin to manage blood sugar, was also much higher among diabetics.
  • Even some non-diabetic participants showed early signs of these metabolic changes.

Unhealthy cholesterol patterns and poor insulin sensitivity tend to occur together, each making the other worse. This combination sets the stage for early heart disease, stroke and diabetes.

Why young adults?

Most public-health strategies focus on older adults because that’s when chronic diseases usually become visible.

But our research adds to growing evidence that the seeds of non-communicable diseases are planted early, often in young adulthood or even adolescence.

Young adults in rural or semi-urban areas may seem healthy, yet many are already developing risks due to diet changes, stress and limited exercise opportunities. The modernisation of small towns, while positive economically, brings hidden health costs.

Without early detection, these individuals may enter middle age already carrying high risk of health problems. This will put pressure on health systems that are already stretched.

What makes this community unique?

Lephalale may be changing, but it still lacks many of the urban services, infrastructure and health resources found in South Africa’s big cities.

Health resources are scarce, and screening for cholesterol or insulin resistance is rare. Public clinics focus on infectious diseases such as HIV or tuberculosis. Silent metabolic disorders go unnoticed until symptoms appear.

Our study shows that rapid industrialisation without parallel investment in public-health education and preventive services risks creating a generation of young adults who are chronically unwell by their thirties.

What can be done?

Three priorities stand out:

Early screening and prevention

Regular cholesterol and glucose testing should be part of routine primary-care visits, especially for adults under 30. Mobile health campaigns, school outreach and workplace screenings could help identify those at risk.

Community-based education

Local awareness campaigns must make the link between diet, physical activity and metabolic health easy to understand. They should show, for example, how frequent consumption of fried or sugary foods contributes to cholesterol build-up and insulin resistance.

Healthy-environment policies

Urban planners and municipalities can support healthy lifestyles by ensuring there are safe spaces for exercise. They must also limit marketing of unhealthy foods, and encourage availability of affordable, nutritious options. Similar “health-in-all-policies” approaches have shown success in other countries. such as Finland’s long-running HiAP strategy, which reduced cardiovascular disease rates and improved population health outcomes.

Young people should be in peak health. Without intervention, today’s young adults risk becoming tomorrow’s chronic-disease patients, burdening families, workplaces and health systems.

Themba Titus Sigudu, Lecturer, University of the Witwatersrand

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

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A Gentle ‘Immune System Reset’ Cured Type 1 Diabetes in Mice

On By ModernMedia

An “immune system reset” cured autoimmune, or Type 1, diabetes in mice in a Stanford Medicine study. The approach may be useful for other autoimmune conditions as well as organ transplants.

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

A combination of blood stem cell and pancreatic islet cell transplant from an immunologically mismatched donor completely prevented or cured Type 1 diabetes in mice in a study by Stanford Medicine researchers. Type 1 diabetes arises when the immune system mistakenly destroys insulin-producing islet cells in the pancreas.

None of the animals developed graft-versus-host disease – in which the immune system arising from the donated blood stem cells attacks healthy tissue in the recipient – and the destruction of islet cells by the native host immune system was halted. After the transplants, the animals did not require the use of immunosuppressive drugs or insulin for the duration of the six-month experiment.

“The possibility of translating these findings into humans is very exciting,” said Seung K. Kim, MD, PhD, professor of developmental biology, gerontology, endocrinology and metabolism. “The key steps in our study – which result in animals with a hybrid immune system containing cells from both the donor and the recipient – are already being used in the clinic for other conditions. We believe this approach will be transformative for people with Type 1 diabetes or other autoimmune diseases, as well as for those who need solid organ transplants.”

Kim, who directs the Stanford Diabetes Research Center and the Northern California Breakthrough T1D Center of Excellence, is the senior author of the study, which published online Nov. 18 in the Journal of Clinical Investigation. Graduate and medical student Preksha Bhagchandani is the lead author of the research.

Setting the table

The findings in the current report dovetail with those from a 2022 study by Kim and collaborators, in which researchers first induced diabetes in mice by destroying insulin-producing cells in the pancreas with toxins. They then cured them with a gentle pre-transplant treatment of immune-targeting antibodies and low-dose radiation, followed by transplantation of blood stem and islet cells from an unrelated donor.

The current study tackled a more complex problem: curing or preventing diabetes caused by autoimmunity, in which the immune system spontaneously destroys its own islet cells. In people this is called Type 1 diabetes. Unlike in the induced-diabetes study — in which the researchers’ goal was to prevent the recipient’s immune system from rejecting donated islet cells — the transplanted islet cells in the autoimmune mice have two targets on their backs: Not only are they foreign, but they are vulnerable to autoimmune attack by a misguided immune system bent on destroying islet cells regardless of their origin.

“Just like in human Type 1 diabetes, the diabetes that occurs in these mice results from an immune system that spontaneously attacks the insulin-producing beta cells in pancreatic islets,” Kim said. “We need to not only replace the islets that have been lost but also reset the recipient’s immune system to prevent ongoing islet cell destruction. Creating a hybrid immune system accomplishes both goals.”

Unfortunately, the inherent features that lead to autoimmune diabetes in these mice also make them more challenging to prepare for a successful blood stem cell transplant.

The solution the researchers found was relatively simple: Bhagchandani and Stephan Ramos, PhD, a postdoctoral fellow and study co-author, added a drug used to treat autoimmune diseases to the pre-transplant regimen the researchers had discovered in 2022. Doing so, then transplanting blood stem cells, resulted in an immune system made up of cells from both the donor and the recipient and prevented development of Type 1 diabetes in 19 out of 19 animals. Additionally, nine out of nine mice that had developed long-standing Type 1 diabetes were cured of their disease by the combined blood stem cell and islet transplantation.

Because the antibodies, drugs and low-dose radiation the researchers administered to the mice are already used in the clinic for blood stem cell transplantation, the researchers believe that translating the approach to people with Type 1 diabetes is a logical next step.

Where the concept began

The study builds on the work of the late Samuel Strober, MD, PhD, a professor of immunology and rheumatology, and his colleagues, including study co-author and professor of medicine Judith Shizuru, MD, PhD. They and other Stanford researchers had shown that a bone marrow transplant from a partially immunologically matched human donor allowed formation of a hybrid immune system in the recipient, and subsequent long-term acceptance of a kidney transplant from the same donor. In some cases, Strober and colleagues showed that transplanted donor kidney function lasted for decades, without the need for drugs to suppress rejection.

A blood stem cell transplant can be used to treat cancers of the blood and immune system, such as leukemia and lymphoma. But in those settings, high doses of chemotherapy drugs and radiation needed to treat the cancer and replace the recipient blood and immune system often result in severe side effects. Shizuru and colleagues have devised a safer, gentler avenue to prepare recipients with non-cancerous conditions such as Type 1 diabetes for donor blood stem cell transplantation — knocking their bone marrow back just enough to provide a foothold for the donated blood stem cells to settle in and develop.

“Based on many years of basic research by us and others, we know that blood stem cell transplants could also be beneficial for a wide range of autoimmune diseases,” Shizuru said. “The challenge has been to devise a more benign pre-treatment process, diminishing risk to the point that patients suffering from an autoimmune deficiency that may not be immediately life-threatening would feel comfortable undergoing the treatment.” 

Judith Shizuru

Judith Shizuru

“Now we know that the donated blood stem cells re-educate the recipient animal’s immune system to not only accept the donated islets, but also not attack its healthy tissues, including islets,” Kim said. “In turn, the donated blood stem cells and the immune system they produce learn to not attack the recipient’s tissues, and graft-versus-host disease can be avoided.”

What comes next?

Challenges remain using this approach to treat Type 1 diabetes. Pancreatic islets can be obtained only after death of the donor, and the blood stem cells must come from the same person as the islets. It is also unclear whether the number of islet cells typically isolated from one donor would be enough to reverse established Type 1 diabetes.

But the researchers are working on solutions, which could include generating large numbers of islet cells in the laboratory from pluripotent human stem cells, or finding ways to increase the function and survival of transplanted donor islet cells.

In addition to diabetes, Kim, Shizuru and their colleagues expect that the gentler pre-conditioning approach they developed could make stem cell transplants a viable treatment for autoimmune disease such as rheumatoid arthritis and lupus, and non-cancerous blood conditions like sickle cell anemia (for which current blood stem cell transplant methods remain harsh), or for transplants of mismatched solid organs.

“The ability to reset the immune system safely to permit durable organ replacement could rapidly lead to great medical advances,” Kim said.

Source: Stanford Medicine