Author: ModernMedia

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

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

Scientists Discover a Gut Bacterium Linked to Muscle Strength

Photo by Jonathan Borba on Unsplash

Ageing naturally weakens our muscles, but a new study published in the journal Gut have found a gut bacterium that may help turn the tide. The researchers Leiden University Medical Center and the Universities of Granada and Almería, found that Roseburia inulinivorans is linked to stronger muscles in both people and mice. The discovery hints at the potential for new probiotics to support muscle strength and healthy ageing.

While exercise and good nutrition remain important for maintaining muscle strength, scientists are now turning their attention to a lesser‑known player: the gut. “The bacteria living in our intestines help us process nutrients, regulate inflammation and manage energy,” Patrick Rensen, professor at the division of Endocrinology, notes. “All of these processes are essential for keeping our muscles healthy as we age.”

A gut bacterium linked to stronger muscles

In their new work, the researchers identified one particular gut bacterium, Roseburia inulinivorans, that appears to be linked to stronger muscles across the lifespan. “When we compared young adults aged 18 to 25 with older adults aged 65 and above, we noticed clear differences,” postdoc Borja Martínez-Téllez says. “Older adults who carried this bacterium had 29 percent stronger handgrip strength than those who didn’t.” In young adults, higher levels of Roseburia inulinivorans were associated with stronger muscles and better overall fitness. “It was remarkable to see the same pattern in both age groups,” Martínez-Téllez adds.

Testing the bacterium in mice

To find out whether this link was more than coincidence, the researchers carried out a series of experiments in mice. “We wanted to understand whether this bacterium actually causes improvements in muscle strength,” Rensen explains. After clearing the mice’s gut bacteria using antibiotics, they introduced human strains of Roseburia inulinivorans for eight weeks.

“The results were striking,” Rensen says. “The mice became 30 percent stronger, developed larger muscle fibres and produced more fast‑twitch fibres.”

The team also found that the bacterium changed how the muscles used certain building blocks and activated energy‑related pathways inside the muscle. “These metabolic changes may help explain why the muscles grew stronger,” according to Martínez-Téllez.

From discovery to potential probiotic treatment

Another key observation is that levels of Roseburia inulinivorans naturally decline with age. “This could partly explain why muscle strength drops as we get older,” Martínez-Téllez says. “If this bacterium supports muscle metabolism, then restoring it might one day help preserve muscle function later in life.”

Together, the findings suggest that Roseburia inulinivorans could become a future probiotic, developed into a safe, supplement‑like product aimed at preventing age‑related muscle‑wasting conditions. “A nutraceutical approach – using food‑based or naturally derived products – could offer a gentle and non‑invasive way to support healthy ageing,” Martínez-Téllez explains.

The researchers however caution that considerable work needs to be done before these findings can be turned into a treatment for humans.

Source: Leiden University Medical Center

How Body’s ‘Cold Sensor’ Works – and Why Menthol Tricks it

First-ever molecular snapshots show the body’s “cold sensor” in action, with implications for treating pain, migraines, and dry eye

Using cryo-electron microscopy, researchers captured multiple conformational snapshots of the cold sensing channel, TRPM8, as it transitions from closed to open.

When you step outside on a winter morning or pop a mint into your mouth, a tiny molecular sensor in your body springs into action, alerting your brain to the sensation of cold. Scientists have now captured the first detailed images of this sensor at work, revealing exactly how it detects both actual cold and the perceived cool of menthol, a compound derived from mint plants. The research was presented at the 70th Biophysical Society Annual Meeting in San Francisco from February 21–25, 2026.

The study focused on a protein channel called TRPM8. “Imagine TRPM8 as a microscopic thermometer inside your body,” said Hyuk-Joon Lee, a postdoctoral fellow from Seok-Yong Lee’s laboratory at Duke University. “It’s the primary sensor that tells your brain when it’s cold. We’ve known for a long time that this happens, but we didn’t know how. Now we can see it.”

TRPM8 sits in the membranes of sensory neurons innervating the skin, oral cavity, and eyes. It responds to cold temperatures – roughly between 8°C and 28°C – by opening up and allowing ions to flow into the cell, which triggers a nerve signal to the brain. It’s also the reason menthol, eucalyptus, and certain other compounds produce that characteristic cooling sensation.

“Menthol is like a trick,” Lee explained. “It attaches to a specific part of the channel and triggers it to open, just like cold temperature would. So even though menthol isn’t actually freezing anything, your body gets the same signal as if it were touching ice.”

Using cryo-electron microscopy – a technique that images flash-frozen proteins with an electron beam – Lee and colleagues captured multiple conformational snapshots of TRPM8 as it transitions from closed to open. They discovered that cold and menthol activate the channel through shared yet distinct allosteric networks: cold primarily triggers changes in the pore region (the part that actually opens to let ions through), while menthol binds a different part of the protein and induces shape changes that propagate to the pore.

“When cold is combined with menthol, the response is enhanced synergistically,” Lee said. “We used this combination to capture the channel in its open state – something that hadn’t been achieved with cold by itself.”

The findings have medical implications. When TRPM8 doesn’t function properly, it has been linked to conditions including chronic pain, migraines, dry eye and certain cancers. Acoltremon, a drug that activates TRPM8, is an FDA-approved eye drop for dry eye disease. As a menthol analogue, it works by activating the cooling pathway to stimulate tear production and soothe irritated eyes.

The researchers also identified what they call a “cold spot” – a specific region of the protein that is uniquely important for sensing temperature and helps prevent the channel from becoming desensitised during prolonged cold exposure.

“Previously, it was unclear how cold activates this channel at the structural level,” Lee said. “Now we can see that cold triggers specific structural changes in the pore region. This gives us a foundation for developing new treatments that target this pathway.”

The work offers the first molecular definition of how cold and chemical stimuli are integrated to create the sensation of coolness – answering a fundamental question in sensory biology that has puzzled scientists for decades.

Source: Biophysical Society

“Two-for-one” C-section and Tummy Tuck Idea Alarms Surgeons

Photo by Jonathan Borba on Unsplash

The ‘mommy makeover’ is trending, and a growing number of patients are now asking whether cosmetic procedures such as a tummy tuck, liposuction, or breast augmentation can be performed at the same time as a Caesarean section. But surgeons warn that combining elective cosmetic surgery with a C-section can sharply escalate risk during an already vulnerable period for the body.

Professor Chrysis Sofianos, a triple-board certified plastic surgeon and Academic Head of the Division of Plastic and Restorative Surgery at the University of the Witwatersrand, says procedures such as a tummy tuck should only be considered once the body has adequately recovered after childbirth – typically around six months after delivery, depending on individual healing.

“Our practice is seeing a growing number of patients ask whether body-contouring surgery can be performed while they are already in theatre for a C-section. But this reflects a dangerous misunderstanding of surgical safety and postpartum physiology.

“While the idea may appear efficient or financially attractive, pairing medically necessary obstetric surgery with elective cosmetic procedures significantly increases operative risk at a time when the patient is physiologically vulnerable.”

Combining surgeries and compounding risks

C-sections account for around 75% of private sector hospital births in South Africa. Professor Sofianos notes that because there is often an overlap between women accessing private medical care and those who may later consider elective cosmetic procedures, more patients are likely to ask whether these operations can be combined.

“However, the more important question is whether they should. And the simple answer is no,” he says. “A C-section is already a major abdominal operation. Introducing additional surgical trauma before the body has recovered would introduce excessive strain and substantially raise the risk of complications.”

Pregnancy and the immediate postpartum period are associated with a hypercoagulable state, meaning the blood has an increased tendency to clot. Postpartum women therefore face a markedly elevated risk of venous thromboembolism, particularly in the first six weeks after delivery. Prolonging operative time and increasing tissue disruption may further elevate this risk by contributing to immobility, tissue stress, and inflammatory response.

A C-section on its own carries recognised complications, including haemorrhage, infection, anaesthetic complications, and clotting risk. Adding abdominoplasty (tummy tuck) can introduce additional risks such as bleeding, fluid accumulation, wound breakdown, delayed healing, and blood clots.

Liposuction also introduces risks, such as fluid imbalance, internal injury, infection, and, in rare but serious cases, fat embolism – a potentially life-threatening condition in which fat enters the bloodstream and compromises vital organs.

The false economy of combining procedures

Professor Sofianos also notes that combining procedures rarely provides the financial or practical advantages patients may assume.

“There is a common a misconception that theatre and anaesthetic fees can be consolidated if surgeries are combined into a single session. In reality, longer operative times, greater monitoring requirements, and the potential for complications may result in far higher medical costs. More importantly, financial reasoning should never supersede patient safety.”

He adds that the combined recovery period can also be far more demanding than patients anticipate.

“Recovery after a C-section already places significant physical, emotional, and psychological demands on a new mother. Adding major cosmetic surgery to that recovery period can complicate mobility, wound care, and pain management at a time when the patient must also care for a newborn.

“A more intensive recovery process may further require extended postoperative care, closer medical oversight, and additional support at home, all of which can add to the existing financial burden.”

Finally, he warns that operating during the immediate postpartum period might not produce the optimal long-term aesthetic result a patient may be looking for, and could expose them to unnecessary revision surgery later.

“Medically and ethically, I do not believe combined C-section and ‘mommy makeover’ surgeries should ever be considered. No responsible surgeon should minimise the compounded risks associated with performing such procedures. Ultimately, safe, staged care remains the gold standard for medical care, or allowing the body to recover fully before elective cosmetic surgery is undertaken.”

Reducing Sodium in Everyday Foods may Yield Heart-health Benefits Across Populations

Credit: Pixabay CC0

Lowering sodium in packaged and prepared foods could significantly improve cardiovascular health and prevent many cases of heart disease, stroke and deaths in the general population in France and the U.K., according to two new research studies published in Hypertension, an American Heart Association journal.

Consuming too much sodium is a major risk factor for hypertension, also known as high blood pressure, which can lead to health complications such as heart attack, stroke, chronic kidney disease, dementia and other forms of cardiovascular disease, according to the American Heart Association.

To address the global concern about excessive sodium consumption many countries have implemented salt-reduction strategies to improve public health and reduce health costs.

Two studies – one in France involving salt-reduction targets for baguettes and other bread products in 2025, and the other in the United Kingdom focusing on 2024 goals for takeaway and packaged foods – estimated the potential impact on the general population if those salt-reduction targets were met. The projections calculated in these two studies indicate that minor adjustments in sodium content to some of the most common prepared foods in each country would require no effort from people to change their eating habits, yet may produce significant public health benefits.

“This approach is particularly powerful because it does not rely on individual behaviour change, which is often difficult to achieve and sustain. Instead, it creates a healthier food environment by default,” said Clémence Grave, M.D., lead author of the study from France and epidemiologist and public health physician at the French National Public Health Agency, headquartered in Saint-Maurice near Paris.

The World Health Organization recommends adults should consume less than 2,000 milligrams (mg) of sodium per day, however, global intake is much higher. The American Heart Association recommends daily intake of no more than 2300mg of sodium a day – equal to about 1 teaspoon of table salt; but also says the ideal limit is no higher than 1500 mg per day for most adults, especially for those with high blood pressure.

Sodium reduction in bread (France)

In 2019, France set a national public health goal to reduce salt consumption by 30%. In 2022, a voluntary agreement was signed between the government and bread producers to lower salt content by 2025. Bread, especially the baguette, is a culturally and nutritionally central food in France, yet it can be high in salt– traditionally contain about 25% of total daily recommended intake of salt. By 2023, most breads made in France already met the new sodium standards.

To understand the potential impact of the agreement on public health, researchers used national data and a mathematical model to estimate how many cases of cardio-cerebrovascular disease (conditions and diseases that affect both the heart and the brain’s blood vessels), kidney disease and dementia could be prevented if the salt-reduction targets met full compliance.

The analysis found that with bread consumption remaining the same and sodium-reduction targets fully met, less salt in baguettes and bread would decrease daily intake by 0.35 g per person, leading to slightly lower blood pressure across the population.

“This salt-reduction measure went completely unnoticed by the French population – no one realised that bread contained less salt,” Grave said. “Our findings show that reformulating food products, even with small, invisible changes, can have a significant impact on public health.”

Sodium reduction in packaged foods and take-out meals (United Kingdom)

For the study in the U.K., researchers used national survey data to estimate the amount of salt people consumed from pre-prepared packaged and take-out meals. They then estimated daily sodium intake if all relevant food categories met the 2024 sodium-reduction targets.

Sales-weighted average and maximum salt content targets were set for 84 grocery food categories – including bread, cheeses, meats, and snacks – and, for the first time, 24 out-of-home categories such as burgers, curries, and pizza. The modelling also covered how these changes could affect heart disease, stroke, quality of life and health care costs.

The research found that fully meeting the sodium reduction goals could have reduced average salt intake from about 6.1 g to 4.9g per day – translating to an estimated average of 17.5% less salt consumed per person per day. Men would experience slightly larger reductions than women because they tend to consume more salt in general.

Even this small, daily reduction in salt would lower blood pressure modestly across the population, and the improvements could add up.

Source: American Heart Association

Family Dinners May Reduce Substance Use Risk for Many Adolescents

Regular bonding over meals may help prevent kids from using alcohol, cannabis, and e-cigarettes, but those with significant stress or trauma need additional support

Photo by Vanessa Loring on Pexels

Anew study from researchers at Tufts University School of Medicine finds that regular family dinners may help prevent substance use for a majority of US adolescents, but suggests that the strategy is not effective for youth who have experienced significant childhood adversity.

The findings provide important insights for practitioners looking to help families prevent substance use, as well as for researchers aiming to develop interventions that better account for adolescents’ unique experiences.  

For the study, published January 19 in the Journal of Aggression, Maltreatment & Trauma, researchers analysed online survey data from 2090 US adolescents ages 12 to 17 and their parents. Participants from around the country were asked about the quality of their family meals – including communication, enjoyment, digital distractions, and logistics – as well as adolescents’ alcohol, e-cigarette, and cannabis use in the previous six months.

The researchers then examined how these patterns differed based on adolescents’ experiences of household stressors and exposure to violence, as reported by both the children and parents. Instead of counting each adverse experience equally, the researchers created a weighted score based on how strongly the different experiences are linked to substance use in prior research and this national sample.

Higher family dinner quality was associated with a 22% to 34% lower prevalence of substance use among adolescents who had either no or low to moderate levels of adverse childhood experiences. 

“These findings build on what we already knew about the value of family meals as a practical and widely accessible way to reduce the risk of adolescent substance use,” said Margie Skeer, the study’s lead author, professor and chair of the Department of Public Health and Community Medicine at the School of Medicine.  

“Routinely connecting over meals – which can be as simple as a caregiver and child standing at a counter having a snack together – can help establish open and routine parent-child communication and parental monitoring to support more positive long-term outcomes for the majority of children,” added Skeer. “It’s not about the food, timing, or setting; it’s the parent-child relationship and interactions it helps cultivate that matter.”

Adverse childhood experiences reported by participants in the study included parents being divorced; a family member being diagnosed with a substance-use disorder; someone in the family having a mental-health disorder; the adolescent witnessing violence; the adolescent often being teased about their weight; a parent using non-prescribed drugs daily; or the adolescent experiencing sexual or physical dating violence.  

The study found that family meals offered little protection for adolescents whose adversity score reached the equivalent of four or more experiences – a population that encompasses nearly one in five U.S. high school students younger than 18, according to a study of the most recent Youth Risk Behavior Survey data.  

“While our research suggests that adolescents who have experienced more severe stressors may not see the same benefits from family meals, they may benefit from more targeted and trauma-informed approaches, such as mental health support and alternative forms of family engagement,” said Skeer.  

She added that future research should explore whether other supportive routines – beyond shared meals or outside the family environment – can help protect adolescents exposed to highly stressful or traumatic childhood experiences. 

Source: Tufts University

Revealing How Transplanted Neural Stem Cells Preserve Vision

Photoreceptor cells in the retina. Credit: Scientific Animations

Cedars-Sinai investigators working to optimise a cell-based treatment for retinitis pigmentosa have uncovered how transplanted neural stem cells interact with host retinal cells to preserve vision. The findings, published in Nature Communications, may guide future research toward strategies to treat degenerative eye disease.

“We used single-cell analysis to show that neural stem cells can protect vision in several ways, including providing protective proteins, restoring retinal cells to a healthier state, reducing cellular stress, and maintaining retinal integrity,” said Clive Svendsen, PhD, executive director of the Board of Governors Regenerative Medicine Institute and co-corresponding author of the study.

Investigators transplanted neural stem cells into the retinas of laboratory rats with retinal degeneration. Previous studies have shown the transplants significantly reduced vision loss in the animals for up to 180 days, the equivalent of about 20 years in humans. In this study the team examined interactions between the transplanted cells and diseased retinal cells to better understand the neural stem cells’ protective effects.

“Our study reveals that the interaction between neural stem cells and host retinal cells dynamically changes over time,” said Shaomei Wang, MD, PhD, professor of Biomedical Sciences and co-corresponding author of the study.  “Through a better understanding of this process, we may be able to develop more powerful approaches to treat eye diseases in the future.”

Investigators are now evaluating the use of neural stem cells engineered to express key protective proteins identified in this study to further improve the host retinal environment. 

Additional Cedars-Sinai authors include Saba Shahin, Shaughn Bell, Bin Lu, Hui Xu, Jason Chetsawang, Stephany Ramirez, Jorge S. Alfaro, Alexander Laperle and Soshana Svendsen.

Other authors include Somanshu Banerjee and Vivek Swarup.

Source: Cedars-Sinai Medical Center

Trial Results Show Daily Multivitamin Use May Slow Biological Ageing

Photo by Diana Polekhina on Unsplash

An analysis led by Mass General Brigham investigators found slower aging in older adults after two years of a daily multivitamin, with greater benefits for those who began the trial with accelerated biological age.

‘Biological age’, age on a cellular level, can differ from chronological age. Using data from a large randomised clinical trial of older adults, researchers at Mass General Brigham evaluated the effects of taking a daily multivitamin over the course of two years on five measures of biological ageing and found a slowing equivalent to about four months of ageing. The benefits were increased in those who were biologically older than their actual age at the start of the trial. Their results are published in Nature Medicine.

“There is a lot of interest today in identifying ways to not just live longer, but to live better,” said senior author Howard Sesso, ScD, MPH, associate director of the Division of Preventive Medicine in the Mass General Brigham Department of Medicine. “It was exciting to see the benefits of a multivitamin linked with markers of biological ageing. This study opens the door to learning more about accessible, safe interventions that contribute to healthier, higher-quality ageing.”

Epigenetic clocks estimate biological ageing based specific sites in our DNA that regulate gene expression (known as DNA methylation) and change naturally as we get older, helping track mortality and the pace of ageing. This study, which uses data from the well-established COcoa Supplement Multivitamins Outcomes Study (COSMOS), analysed DNA methylation data from blood samples of 958 randomly selected healthy participants with an average chronological age of 70.

The study participants were randomised to take a daily cocoa extract and multivitamin; daily cocoa extract and placebo; placebo and multivitamin; or placebos only. Samples were analysed for changes in five epigenetic clocks from the start of the trial and at the end of the first and second years. Compared to the placebo only group, people in the multivitamin group had slowing in all five epigenetic clocks, including statistically significant slowing seen in the two clocks that are predictive of mortality. The changes equated to about four months less biological ageing over the course of two years. Additionally, people who were biologically older than their actual age at the start of the trial benefited the most.

“We plan to do follow-up research to determine if the slowing of biological ageing – observed through these five epigenetic clocks, and additional or new ones – persists after the trial ends,” said co-author and collaborator Yanbin Dong, MD, PhD, director of Georgia Prention Institute, Medical College of Georgia at Augusta Univeristy.

Further studies are also needed to determine how improvements in biological aging may explain reductions in clinical outcomes. The COSMOS team plans to investigate how the effects of a daily multivitamin on biological aging may extend to different outcomes they have seen evidence of benefits for, such as improvements in cognition and reductions in cancer and cataracts.

“A lot of people take a multivitamin without necessarily knowing any benefits from taking it, so the more we can learn about its potential health benefits, the better,” said Sesso. “Within COSMOS, we are fortunate and excited to build upon a rich resource of biomarker data to test how two interventions may improve biological aging and reduce age-related clinical outcomes.”

Source: Mass General Brigham

Mental Health Issues Before Surgery can Affect Memory and Cognition

Photo by JD Mason on Unsplash

Depression and other psychological factors may be linked to the risk of postoperative confusion in older adults. This is shown in a new systematic review from Karolinska Institutet, published in the British Journal of Anaesthesia. The study summarises results from more than 6700 patients.

Older individuals undergoing surgery face an increased risk of developing cognitive complications, such as postoperative delirium. Delirium is characterised by sudden changes in attention and awareness, and can lead to longer hospital stays and reduced functioning. The new study analyses 30 previously published works in which researchers examined whether preoperative psychological factors, such as depression, anxiety, stress, and personality traits, may influence these complications.

Depression most common

The review identified four groups of psychological factors. Depression was the most common and appeared in nearly all studies. In the statistical meta-analysis, no clear association between depression and delirium was observed, but when the researchers used alternative statistical synthesis methods, they found evidence suggesting that psychological factors play a role.

“Our results show that depression is the most consistently reported psychological risk factor, even though the pooled statistical analyses did not demonstrate a significant effect,” says Anahita Amirpour, PhD at the Department of Neurobiology, Care Sciences and Society.
“At the same time, we saw that anxiety, stress, and personality traits may also play a role, although the research base there is more limited.”

Postoperative delirium

In total, the study included 6714 patients from 16 different countries. Postoperative delirium was the most common outcome measure and occurred in between 9 and 55% of patients, depending on the study. Very few studies examined other cognitive complications, such as long-term effects on memory and attention.

The researchers emphasise that the results should be interpreted with caution. Many of the included studies varied greatly in how they measured both psychological factors and cognitive outcomes, and only two studies examined time periods extending beyond the immediate postoperative phase.

Source: Karolinska Institutet

Copper Peptides: These Powerful Molecules are Worth the Skincare Hype

Picture by Macrovector on Freepik

Ahmed Elbediwy, Kingston University and Nadine Wehida, Kingston University

Peptides have become one of the skincare industry’s most popular ingredients. It’s no wonder why, with evidence showing these powerful molecules hold the secret to healthier, firmer and more radiant skin.

But out of the many peptides that exist, one in particular has been gaining attention lately in the beauty industry: copper peptides.

It’s not surprising that copper peptides are garnering so much attention. This peptide is special because of its ability to multitask – with research showing that not only does it help make the skin firmer and more supple, it also protects the skin from damage.

The human body naturally produces many types of peptides. Each supports vital body functions, acting like tiny building blocks of life. Many help form the foundation of essential proteins – such as collagen and elastin, which help keep skin healthy and youthful.

The three main types of peptides in cosmetics are: carrier peptides, signal peptides and neurotransmitter-inhibiting peptides.

Carrier peptides aid in wound repair by physically transporting important minerals into the cells to initiate repair.

Signal peptides can prevent ageing by stimulating the activation of the skin’s fibroblasts – specialised skin cells that produce substances such as collagen, a protein which helps maintain the skin’s elasticity.

Neurotransmitter-inhibiting peptides act like botulinum toxin, relaxing facial muscles by blocking the signals that make them contract. This may reduce wrinkles.

Copper peptides are actually a type of carrier peptide. They’re produced naturally by your body. But as we age, the concentration of copper peptides in our bodies drops. Applying synthetic, lab-made versions – found in creams, serums and masks – can help replenish these molecules and help your skin.

Copper peptides were first discovered in 1973. Research found that these molecules aided wound healing, which is why the first commercialised carrier peptide in 1985 was designed to deliver copper into wounded tissue.

After gaining research attention for this role, further studies examined what other functions copper peptides had on the skin. Researchers found that they had anti-ageing, anti-inflammatory and renewing properties and also supported hair growth.

Copper peptides act as little helpers that tell your skin cells to repair and rebuild themselves. They do this by boosting collagen and elastin, key proteins that keep your skin feeling smooth and firm.

Copper peptides have been also found to reduce inflammation and calm skin redness, too. But perhaps most crucially, they have been found to act as antioxidants, fighting damage caused by pollution and the sun’s ultraviolet rays.

On top of that, copper peptides improve wound healing. This is why they’re often used after cosmetic treatments – such as face and neck lifts and micro-needling – that can damage the skin. Copper infused wound dressings are also used to help chronic wounds heal faster.

Overall, skin cell studies have shown that copper peptides increase collagen production, improve skin thickness and skin elasticity. Clinical trials and lab tests confirm these benefits, making copper peptides one of the most researched anti-ageing ingredients.

For best results, you might want to try applying it twice a day – first in the morning so it can act as a potent antioxidant, then in the evening so it can replenish collagen overnight.

Copper peptides can also penetrate the skin more effectively when delivered with microneedles, which makes them even more useful in advanced skincare products.

Copper peptides v other peptides

Other peptides do work well on the skin – such as palmitoyl-based peptides and acetyl hexapeptide-8 peptide – both of which fight wrinkles. But these both work differently to copper peptides.

Palmitoyl peptides signal the skin to make more collagen, while acetyl hexapeptide-8 relaxes facial muscles to reduce expression lines, acting like a less expensive version of botulinum toxin.

Copper peptides stand out among these other peptides because they can do the work of multiple peptides in one. Copper peptides boost collagen, improve skin healing and fight oxidative stress. This appears to make them better at preventing the signs of ageing.

Some skin cell studies show they work even better when combined with other well known skincare ingredients, such as hyaluronic acid (which boosts hydration).

However, some combinations of peptides can cause copper peptides to be unstable – making them fall apart. This could increase skin sensitivity, especially when combined with peptides, such as vitamin A and C.

Copper peptides themselves can also cause, in a few people, some skin irritation and mild allergic reactions. If you find you experience these symptoms after using copper peptides, stop use immediately.

Copper peptides are more than just a trend – they’re backed by science. They help keep skin healthy and speed up healing. They might even play a role in future cancer treatments.

Research has shown copper peptides turn on genes that tell damaged cancer cells to shut themselves down and stop replicating. They’ve also been shown to fix other genes that control cell growth and repair.

If you’re curious about skincare, copper peptides may be worth incorporating into your daily routine. Just remember that good, healthy skin also needs other measures – such as sunscreen, hydration and a healthy lifestyle.

Ahmed Elbediwy, Senior Lecturer in Cancer Biology & Clinical Biochemistry, Kingston University and Nadine Wehida, Senior Lecturer in Genetics and Molecular Biology, Kingston University

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