Category: Metabolic Disorders

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GLP-1 Medications May Also Help with Symptoms of Anxiety and Depression

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GLP-1 medications used to treat diabetes and obesity were associated with a reduced need for hospital care and sickness absence due to psychiatric reasons, a new study shows. The large register-based study was carried out in collaboration between the University of Eastern Finland, Karolinska Institutet in Stockholm and Griffith University in Australia.

Diabetes and obesity are associated with an increased risk of mental health symptoms, and similarly, individuals with mental disorders have an elevated risk of metabolic diseases such as obesity and diabetes. Researchers have long been interested in the connections between these conditions and in how pharmacological treatments may affect both metabolic and mental health disorders.

The present study, published in The Lancet Pyschiatry, included nearly 100 000 participants, over 20 000 of whom had used GLP-1 medications. Participants were followed through Swedish national registers between 2009 and 2022.

The risk of substance use was also reduced

The results showed that the use of GLP-1 medications – particularly semaglutide – was associated with a reduction in sickness absence and hospital care due to psychiatric reasons. During periods of semaglutide use, the reduction was 42% compared with periods when GLP-1 medications were not used. For depression, the risk was 44% lower, and for anxiety disorders, 38% lower. 

In addition, semaglutide use was associated with a lower risk of substance use disorders: hospital care and sickness absence related to substance use were 47% lower during periods of semaglutide use compared with periods without GLP-1 medication. The use of GLP-1 receptor agonists was also associated with a reduced risk of suicidal behaviour.

One of the study’s authors, Professor Mark Taylor from Griffith University, says such results were to be expected: “An earlier study examining Swedish registers found the use of GLP-1 medications to be associated with a reduced risk of alcohol use disorder. Alcohol-related problems often have downstream effects on mood and anxiety, so we expected the effect to be positive on these as well.”

However, the magnitude of the association surprised the researchers:
“Because this is a registry-based study, we cannot determine exactly why or how these medications affect mood symptoms, but the association was quite strong. It is possible that, in addition to factors such as reduced alcohol consumption, weight loss-related improvements in body image, or relief associated with better glycaemic control in diabetes, there may also be direct neurobiological mechanisms involved – for example, through changes in the functioning of the brain’s reward system,” says Research Director, Docent Markku Lähteenvuo from the University of Eastern Finland.

Other recent evidence on the effects of GLP-1 medications on anxiety and depressive disorders has been somewhat inconsistent, but it has been largely based on small studies.

Source: University of Finland

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Could a New Type of Weight‑loss Pill Shake up the Market? Here’s What to Know About Orforglipron

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Martin Whyte, University of Surrey

A new type of daily pill has proven more effective for weight loss and blood sugar control than its currently available counterparts, according to a recent trial. The drug, known as orforglipron, could be a game-changer in the rapidly expanding oral weight-loss drug market.

The advent of the injectable weight-loss drug semaglutide (known better by its brand names Wegovy and Ozempic) marked a distinct shift in the weight-loss drugs market when it became available just a few years ago.

Semaglutide is a class of glucagon-like peptide-1 (GLP-1) medication. These drugs mimic the gut hormone GLP-1, which is released soon after eating. This hormone signals fullness to the brain, slowing digestion and stimulating the release of insulin. By replicating the action of this hormone, GLP-1 drugs have proven highly effective at managing type 2 diabetes and promoting weight loss.

Although semaglutide is widely used, a key issue with the drug is that it needs to be injected into the belly, thighs or back of the arm. This can make it difficult for patients with needle phobia or who don’t want to self-inject due to the inconvenience.

Another logistical issue with injectable GLP-1 drugs is that they require refrigeration throughout the supply chain. This can pose a challenge in low- and middle-income countries.

It’s for these reasons that researchers and developers have started investigating the efficacy of oral versions of semaglutide.

Based on current research, it appears that oral semaglutide is very effective. However, it must be taken on an empty stomach – and users must wait 30 minutes before eating or drinking.

Alongside being expensive to produce, it also has poor bioavailability compared with injectable semaglutide. This means only about 1% of the ingested drug is absorbed and able to exert its effects.

But a recent phase 3 clinical trial has shown that a new type of oral weight-loss pill may have overcome these issues – proving to be more effective than the current oral semaglutide products on the market.

Oral weight-loss pill

The recent 52-week phase 3 trial involved 1,698 adults with type 2 diabetes across six countries. It set out to compare current oral semaglutide products against orforglipron, which is also taken as a daily tablet.

The primary measure researchers were looking for was a reduction in HbA1c. This blood test reflecting average blood sugar levels over three months is the standard indicator of diabetes control. Diabetes is present if HbA1c is 6.5% or more.

From a baseline average HbA1c of 8.3%, it was found that after 52 weeks, orforglipron was able to reduce this value by an average of 1.71–1.91%. In comparison, oral semaglutide only reduced HbA1c by 1.47%.

Not only did orforglipron meet the trial’s goals of proving it was as effective to oral semaglutide, it proved it was superior for lowering blood sugar. The participants who took orforglipron also lost more weight – an average of 6.1kg-8.2kg, compared with 5.3kg in those taking semaglutide.

However, a key issue highlighted by the trial was one of tolerability.

GLP-1 drugs can cause gastrointestinal side-effects such as nausea, vomiting, diarrhoea and constipation. In this latest trial, around 59% of participants on orforglipron reported such symptoms, compared with 37–45% on semaglutide.

The reason for this difference may be the more prominent, daily peak drug concentrations with orforglipron. The consequence was that around 10% of orforglipron participants discontinued treatment due to adverse effects. Just 4-5% of those taking semaglutide discontinued treatment.

Future studies may want to look at how orforglipron compares with injectable semaglutide. Photo by Haberdoedas on Unsplash

No head-to-head trials have been done of injectable GLP-1 versus orforglipron. However, the weight loss seen in this study of people with type 2 diabetes is broadly comparable with that previously observed with injectable GLP-1.

Market implications

The trial’s results show that orforglipron, which was developed by Eli Lilly, can be considered one of semaglutide’s most credible challengers.

Another remarkable thing about orforglipron is that it belongs to a new category of drugs called small-molecule drugs. This means it’s a synthetic chemical compound small enough to be absorbed directly through the gut wall. There, it’s able to act on GLP-1 receptors, even though it isn’t of a similar structure to a GLP-1 hormone.

Oral semaglutide, on the other hand, is a peptide drug. This means the structure of its amino acids (one of the building blocks of protein) closely resembles that of the natural GLP-1 hormone.

As a small-molecule drug, orforglipron is cheaper and simpler to manufacture than peptide-based drugs such as semaglutide.

And as with oral semaglutide, it requires no refrigeration. This gives it a logistical advantage over injectable GLP-1 formulations – a potentially important consideration for expanding access in low- and middle-income countries, where cold chain infrastructure is unreliable.

It remains to be seen, however, how orforglipron will perform against oral semaglutide in the broader market.

Although this latest trial has shown it is superior for controlling blood sugar and aiding weight loss, its higher rate of side-effects and treatment discontinuation may temper enthusiasm. In a crowded and competitive market, long-term adherence – shaped as much by tolerability as by efficacy – is probably a critical differentiator.

Orforglipron is still undergoing trials in patients with obesity but without diabetes.

Martin Whyte, Associate Professor of Metabolic Medicine, University of Surrey

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

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Study Finds Low Response Rate by Clinicians to Elevated Levels of Lp(a)

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Elevated Lipoprotein(a) [Lp(a)] is an independent, genetically determined risk factor for atherosclerotic cardiovascular disease (ASCVD), with levels >50mg/dL affecting 20–30% of the global population. Despite therapeutic limitations, interest in Lp(a) has increased, driven by its prognostic value and the emergence of targeted therapies. However, with increasing guideline-directed Lp(a) testing, clinician response to elevated concentrations, especially in the absence of guideline-based treatment indications, remains unclear.

In a new study and presentation at the American College of Cardiology, researchers found that elevated Lp(a) was associated with earlier and more frequent initiation of preventive pharmacotherapy.  These response rates were modest in a low-risk, primary prevention study population.

Specifically, nearly 80% of patients with elevated Lp(a) > 50mg/dL did not initiate lipid-lowering therapy in the absence of other ASCVD risk factors. Drugs that drastically lower “bad” LDL cholesterol (PCSK9 inhibitors) and aspirin initiation was even less common, suggesting selective rather than systematic responses to elevated Lp(a). Together, these findings suggest that elevated Lp(a) appears to only occasionally influence prescribing behaviour – behaviour consistent with previous reports.

“While not currently a standard indication for statin therapy alone, elevated Lp(a) is increasingly used by clinicians as a “risk enhancer” to guide more aggressive, albeit often unstandardised, preventive measures,” says corresponding author Sheilah A. Bernard MD, associate professor of medicine at Boston University Chobanian & Avedisian School of Medicine.

The researchers conducted a multicentre retrospective observational cohort study evaluating initiation of preventive pharmacotherapy following Lp(a) measurement among nearly 15 000 patients at low risk for ASCVD. Within 90 days of Lp(a) measurement, lipid-lowering therapy initiation was uncommon but more frequent among patients with elevated Lp(a) compared to those with non-elevated Lp(a). PCSK9 inhibitor initiation was rare but more frequent among patients with elevated Lp(a). Similarly, aspirin initiation was uncommon but more frequent among patients with elevated Lp(a).

According to the researchers, these findings should not be interpreted as indicating that such prescribing is guideline-directed. “Current recommendations recognise Lp(a) as a risk-enhancing factor rather than as a treatment target, and no therapy is approved solely for Lp(a) elevation. Our analysis describes contemporary practice rather than appropriate management,” adds Bernard who also is a cardiologist at Boston Medical Center.

The findings also appear online in the American Journal of Preventive Cardiology.

Source: EurekAlert!

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How do GLP-1 Agonists Improve Pancreatic Beta Cell Health?

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Salk Institute researchers find protein that connects GLP-1 agonist drugs to long-term, broad genomic responses that can promote pancreatic health and resilience

Small (left) and large (right) condensates of the Mediator complex inside nuclei of a pancreatic beta cell-derived cell line. Salk researchers discovered that GLP-1s interact with the multi-protein complex called Mediator to cause a broad genomic response.
Click here for a high-resolution image.
Credit: Salk Institute

GLP-1s are building a reputation as “wonder drugs.” First characterised for their ability to improve insulin release and treat diabetes, the drugs were later found to promote weight loss and improve cardiovascular health. In addition to these surprising bonus benefits is the ability of GLP-1 drugs to improve pancreatic beta cell health. But how, exactly, are they doing that?

Salk Institute researchers are burrowing down into the mechanistic details behind how GLP-1 drugs promote viability and stress resistance in pancreatic beta cells. Since cellular performance adaptations arise from gene expression changes, the team screened for regulatory proteins that can flip “on” advantageous gene programs during prolonged GLP-1 use. They identified a protein called Med14, part of a larger protein complex called Mediator, that was enabling the GLP-1-dependent changes in gene expression that lead to pancreatic health benefits.

The study was published in Proceedings of the National Academy of Sciences on March 4, 2026, and was funded by federal research grants from the National Institutes of Health and private philanthropy.

“The broad salutary effects of GLP-1 drugs in diabetes, cardiovascular disease, and obesity have sparked a wave of exciting scientific research at the mechanistic level. We’re left wondering,  ‘How are GLP-1s causing these effects?’” asks senior author Marc Montminy, MD, PhD, a biochemist, physiologist, and distinguished professor emeritus at Salk. “We were able to single out a protein, Med14, whose activation downstream of GLP-1 helps reprogram pancreatic beta cell gene expression to improve the cells’ viability and insulin production.”

What are GLP-1 drugs?

Often simply called “GLP-1 drugs” or “GLPs,” glucagon-like peptide-1 receptor agonists work by mimicking a hormone our bodies naturally make. The hormone, called glucagon-like peptide-1, helps regulate blood sugar.by promoting the secretion of insulin. They do so by attaching to corresponding GLP-1 receptors on pancreatic beta cells, which then produce and release insulin into the body.

But GLP-1 drugs differ in one significant way from their natural counterpart: Unlike human-made GLP-1 hormones that appear and disappear quickly around mealtimes, artificial GLP-1 receptor agonists can stick around much longer. The Salk researchers suspect this longer-term presence may explain some of the “wonder drug” benefits of GLP-1 drugs. But what, exactly, on the molecular level, are GLP-1 drugs doing when they stick around? And how does their staying power turn into effects like lower risk of stroke or improved osteoarthritis?

“The fact that these drugs based off our hormones are stable seems to be important to the longer-term effects we’re witnessing in pancreatic beta cells and other tissues,” says first author Sam Van de Velde, PhD, a staff scientist in Montminy’s lab. “To understand how we are getting these longer-term effects, we need to study these drugs on a longer time scale – and that’s exactly what we did.”

How do GLP-1 drugs influence pancreatic health?

When the hormone GLP-1 finds a pancreatic beta cell, the ensuing chain of signals, proteins, and gene expression changes that lead to insulin secretion is very well documented. On the other hand, the mechanisms and changes on the longer-term GLP-1 drug scale are poorly understood.

So, the researchers set out on a molecular fishing expedition in a pancreatic beta cell line. The team was hoping to hook a protein (or proteins) that, post-GLP-1 activation, had a particular chemical modification called phosphorylation. And that’s exactly what they found in Med14.

Med14 is a subunit in a multi-protein complex called Mediator, which is a well-described general regulator of gene expression throughout the genome. To confirm whether Med14 was an integral link between GLP-1 drugs and ultimate changes in gene expression and pancreatic beta cell behavior, the researchers decided to mutate Med14, making the protein resistant to phosphorylation.

The gene expression patterns associated with prolonged GLP-1 drug exposure disappeared in a Med14 mutant pancreatic beta cell line and in beta cells of a Med14 mutant mouse model. With working Med14, the helpful gene programs were activated – supercharging pancreatic beta cells to grow and better handle sugar-rich environments after meals.

How else might GLP-1 drugs affect the body?

None of the Salk team’s experiments were conducted in humans, yet the relevance remains. For example, some of the genes regulated by Med14 phosphorylation are known to be linked to type 2 diabetes susceptibility in humans.

“Our findings unexpectedly reveal that phosphorylation of just a small part of the Med14 protein plays a significant role in the response to GLP-1 drugs – and in the metabolic response to hormones more broadly,” says Reuben Shaw, PhD, a professor and holder of the William R. Brody Chair at Salk, and director of the National Cancer Institute-Designated Salk Cancer Center. “Now there are many new questions to answer, from validating our findings in human tissues to seeing whether Med14 has a similar role in other cells and organs.”

The team is especially curious about the effects of prolonged GLP-1 exposure beyond pancreatic beta cells. One of the messenger molecules between GLP-1 and Med14, called cAMP, is a commonly used messenger molecule in many other situations that don’t include GLP-1. With that in mind, could other drugs or hormones activate genetic programs similar to GLP-1? And what’s going on in other metabolically intensive tissues, like fat?

The questions keep coming for the so-called “wonder drug,” and Salk scientists are enthusiastically working to answer them.

Source: Salk Institute

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Can GLP-1 Agonists ‘Change the Weather’ for Osteoarthritis?

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Photo by Towfiqu barbhuiya

For GPs, solutions for treating osteoarthritis are frustratingly limited – it’s like the weather, everyone talks about it but nobody does anything about it. While standard care can relieve symptoms, there is currently no way to regenerate the actual lost cartilage in the joints. Some experimental treatments have proven successful in animal models and in petri dishes, but those are still many years away from being approved and available on the market.

But what if there was a currently available drug that could be repurposed? Since overweight and obesity worsen osteoarthritis symptoms by placing excess strain on weight-bearing joints, GLP-1 agonists such as semaglutide have proven that they can help by promoting rapid weight loss, as demonstrated by the STEP-9 trial.

Research into GLP-1s has now revealed that they may offer a whole constellation of other benefits, such as a potential reduction in stroke risk. Now, it appears that GLP-1 agonists may have a direct effect on osteoarthritis independent of weight loss. In our podcast, we look at a recently published article in Cell Metabolism that suggests that GLP-1 agonists might go beyond just the weight loss – promote actual cartilage regrowth by jumpstarting the joint cells’ energy processing pathways. We also explore some of the caveats of potentially using GLP-1 agonists in this way, such as a lack of understanding of the long term effects, as well as the well-documented occurrence of muscle loss.

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Specific Brain Signals Rapidly Eliminate Body Fat in Mice

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Researchers at WashU Medicine have identified a potent pathway that begins in the brain and leads to loss of all body fat without reducing food intake. The study is reported in Nature Metabolism.

The team – led by senior author Erica L. Scheller, DDS, PhD, an associate professor in the Division of Bone and Mineral Diseases in the Department of Medicine; Xiao Zhang, PhD, a former graduate student in Scheller’s lab who is now a postdoctoral fellow at the University of Pennsylvania School of Medicine; and Sree Panicker, a graduate student in Scheller’s lab – was inspired by a unique population of fat cells located deep within the skeleton.

“About 70% of our bone marrow is filled with fat that doesn’t respond to diet or exercise,” said senior author Scheller. “We wanted to figure out why.”

The team found that these special cells, called constitutive bone marrow adipocytes, expressed high levels of proteins that inhibit fat breakdown. This causes resistance to fat loss in day-to-day settings. “We call these cells stable adipocytes,” said Zhang, the study’s first author. In mice, sustained injection of leptin, a hormone, into the brain was able to unlock the stable adipocytes by putting the body into a state of low glucose and insulin. This reduced the inhibitors of fat breakdown, causing complete loss of body fat within days, even though the mice were still eating normally.

This pathway is so powerful that the scientists caution against using it in humans until it is better understood. Stable adipocytes occur in places like the bone marrow, in the hands and feet, and around important glands. In severe wasting disorders, loss of fat within these cells is associated with bone fractures and reduced quality of life. Scheller’s team hopes to prevent this loss and preserve health in patients with severe wasting disorders by defining the mechanisms of stable fat loss. Conversely, methods to activate fat loss from stubborn adipocytes may support future treatments for obesity. This work was funded by the National Institutes of Health (NIH).

By Jaci McDonald

Source: Washington University

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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

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Oral PCSK9 Inhibitor Offers Cholesterol Control Without the Needle

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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!

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

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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.