UNESCO warns there’s close to a 100% chance of a Mediterranean tsunami

 On the French Riviera, a tsunami could arrive before a warning reaches people on the beach. In some local scenarios, the first waves could reach shore in under 10 minutes. France's national warning center, meanwhile, is designed to send its initial alert to authorities within 15 minutes of a potentially dangerous earthquake. Those two timelines leave no room for delay.

That is why researchers and local officials around Nice are doing more than improving alerts. They are mapping walking routes, identifying refuge sites, and helping residents and visitors recognize when they need to leave the coast immediately. The goal is to make the first decisions before an emergency begins, rather than after the sea starts behaving strangely.

What UNESCO's Mediterranean Tsunami Warning Means

The Mediterranean is often treated as an unlikely setting for a tsunami. UNESCO has warned against that assumption. On June 22, 2022, the organization stated that "the probability of a tsunami wave exceeding 1 meter in the Mediterranean in the next 30 years is close to 100%."

The details matter. That estimate concerned an event somewhere in the Mediterranean basin over the following three decades, roughly through 2052. It was not a prediction of an imminent disaster, a guarantee that the French Riviera would be struck, or a forecast that every Mediterranean coastline would experience the same waves.

Nevertheless, the region has the ingredients needed to generate dangerous tsunamis. Earthquakes can occur along active faults in the Ligurian Sea, near the French and Italian coasts. Farther south, the movement of the African and Eurasian plates creates another source of potentially powerful earthquakes off North Africa. Underwater landslides provide an additional, sometimes much more local, trigger.

The Danger Is Not Just a Giant Wave

A tsunami begins when a large volume of water is suddenly displaced, often by an earthquake, landslide, or volcanic eruption. The disturbance spreads outward, potentially traveling long distances before reaching the coast. Historically called tidal waves, raz-de-marée in France or maremoti in Italy, tsunamis can bring both sudden flooding and extremely powerful currents.

They do not always resemble the towering wall of water people imagine. A tsunami can appear as a rapid rise or retreat of the sea, followed by repeated surges. Flooding can range from centimeters to several meters, while fast currents can exert forces equivalent to several tons per square meter against coastal structures. The first wave is not necessarily the largest.

Even relatively small tsunamis deserve attention. Italy's National Institute of Geophysics and Volcanology notes that a tsunami with an amplitude of just 50 centimeters can be dangerous because of the energy and sustained movement of the water, which can behave more like a rushing torrent than ordinary surf.

Globally, tsunamis have killed more than 250,000 people since 1970. The December 26, 2004, Indian Ocean disaster and the March 11, 2011, tsunami in Japan account for much of that devastating toll.

The French Riviera Has Been Hit Before

The Montpellier researchers describe the Mediterranean as having the largest historical tsunami record after the Pacific. Along the French Riviera, they cite roughly 20 reported events between the 16th century and the early 2000s, including waves exceeding two meters. Several episodes show how differently the danger can unfold.

On February 23, 1887, an earthquake in the Ligurian Sea, with an estimated magnitude between 6.5 and 6.8, triggered a tsunami along the coast. Historical accounts describe the sea falling by about one meter in Antibes and Cannes, leaving fishing boats stranded. Waves approaching two meters then swept over the beaches.

A very different event occurred on October 16, 1979. Part of the construction site for a new commercial port in Nice (Alpes-Maritimes), beside the airport, collapsed into the sea. The resulting landslide and tsunami caused eight deaths, according to a reconstruction published in Natural Hazards. Effects were reported in Nice, Antibes, and Cannes, with disturbances observed in Antibes for about half an hour. The later study found that water reached elevations of 3.5 meters locally and flooded as far as 150 meters inland.

The May 21, 2003, Boumerdès earthquake (Algeria) demonstrated that the trigger could also lie across the Mediterranean. Its effects reached the Riviera about 75 minutes later. Investigators documented abrupt sea level drops (from 50 cm to 1.5 m), partially emptied harbor basins, swirling water, strong currents, and damaged boats in eight marinas. Harbor resonance, in which the shape of a basin reinforces the water's oscillations, helped explain why neighboring ports experienced different effects.

Mediterranean tsunamis are not confined to those older events. On December 4, 2022, a flow of hot volcanic material entered the sea at Stromboli and generated a small tsunami, activating the island's warning system. Italy's geological institute reported no damage, but the event provided another reminder that the region's tsunami activity is real and ongoing.

Why an Alert May Not Be Enough

France has operated its national tsunami warning center, the Centre d'alerte aux tsunamis (Cenalt), since July 2012. Working within the international system coordinated by UNESCO, it monitors earthquakes that could generate tsunamis and sends initial messages to French emergency authorities and other warning centers.

The warning then has to reach the public. In France, the chain includes the interdepartmental crisis management operational center (Cogic), followed by authorities responsible for issuing instructions. One channel is FR-Alert, which can send notifications to mobile phones in the threatened area. Detecting an earthquake and getting people moving are therefore separate steps.

Distance makes a crucial difference. A tsunami generated off North Africa may take less than 90 minutes to reach the Riviera. A nearby source in the Ligurian Sea, between Corsica and the Italian coast, can leave far less time. Local landslides are particularly challenging because their effects can develop quickly and may not be preceded by a felt earthquake. A functioning warning system cannot always overcome such a short travel time.

Mapping a Way Off the Beach

Planning starts with identifying where evacuation may be necessary. French government agencies and the University of Montpellier have defined a coastal evacuation zone using elevation, distance from the sea, and historical information. It generally covers land below five meters in elevation and within 200 meters of the shoreline. Around river mouths, the distance extends to 500 meters from the estuary. These are planning boundaries, not a prediction that a future wave will be five meters high.

Across the French Mediterranean coast, including Corsica, that zone encompasses about 1,700 kilometers of coastline, 187 towns, and at least 164,000 residents. At the height of summer, planners must also consider an estimated 835,000 beach users. Those figures describe the scale of potential evacuation planning, not a forecast that one tsunami would affect everyone at once.

In the Nice Côte d'Azur metropolitan area, dense development and heavy tourism make the challenge especially demanding. The research team used photographs and computer modeling to estimate beach attendance (between 10,000 and 87,000 people on the beaches, depending on the season and time of day).

Source: ScienceDaily

Wasps are disappearing this summer, and scientists are worried

 Summer can be lovely – until a wasp turns up. Whether they present as an irritating picnic visitor or an uninvited loft guest, common social wasps are as much a part of our summer as festivals, sun cream and the growing despair of how to entertain children who’ve forgotten how to be bored.

But summer 2026 is breaking the norm, and there don’t seem to be many wasps about. As a wasp biologist, I’ve noticed it acutely, because my students need wasps for their experiments, and we simply can’t find them.

A second sign that something is wrong is the absence of wasp stories in the media. Wasps tend to be more active in warmer weather. Their colonies grow faster and bigger, and they end up making news headlines by bothering humans. This time last year – also a warm spring and hot summer – the media airwaves were filled with “plagues of wasps” stories. Now, even professional pest-controllers tell me it’s a quiet year with very few requests to remove wasp nests.

Admittedly, these are anecdotes not data: the Big Wasp Survey – the only national wasp monitoring survey – is yet to start sampling this summer. But the signs are not good.

If data back this up, their absence worries me greatly because – love them or hate them – wasps are important in ecosystems as pest-controllers, pollinators and decomposers.

So, what’s happening?

Spring started well for wasps. In the warm, dry spring a glut of glorious foundresses – new queens – emerged from hibernation to start their nests alone, carrying out all the nest building, egg laying, foraging and brood rearing. This nest-founding period is a risky time. If a new queen survives until her first brood emerges as adult workers, though, then the odds are in her favour as she no longer needs to undertake risky foraging.

But spring 2026 was strange: the warm, dry start should have been good. Warm, dry spring weather improves a nest’s chance of survival as it ensures a good nectar supply for the queen to develop her ovaries and good prey populations for her to feed the brood. But we experienced unprecedented heat for the time of year, punctuated by cold, damp days and followed by unexpectedly chilly nights.

Such weather extremes may have caused queens to abandon their nests or die, reducing the initial spring queen bounty to a more modest population.

Temperature tolerance

And then came the heatwave. And another. And another. Some insects may benefit from this. Wildlife charity Butterfly Conservation is hoping 2026 could be a “bumper summer of butterflies” because warm, dry days mean uninterrupted foraging, mating and egg-laying.

But all insects have a thermal tolerance called critical thermal maximum (CTmax). If their CTmax is exceeded, insects succumb to desiccation, muscle spasms and eventual stupor.

For honeybees, this is around 49°C – which might sound high, yet ground surfaces exceeded 50°C in the UK heatwaves this summer. But the temperature doesn’t need to reach an animal’s CTmax to affect their productivity and behaviour. For example, bumblebee cognition and foraging efficiency are impaired by heatwaves of 32°C.

Bumblebee Conservation Trust raised concerns that 2026 may exacerbate a declining trend in bumblebee populations as flowers wither and bees fail to forage effectively.

Wasps are thought to be quite resilient to extreme weather. They are one of the most successful invasive species around the globe. And as a social insect, their thermoregulation behavior (such as wing fanning to cool the larvae) and nest architecture (which has insulating envelopes surrounding the brood combs) may help buffer any environmental perturbations.

Insects also have waxy molecules called cuticular hydrocarbons that coat their exoskeletons protecting them from desiccation. Social wasp cuticular hydrocarbons change structure in response to heat, better protecting them from desiccation in excessive heat.

Their varied diets should also buffer them from imbalances in prey populations. However, their CTmax may be lower than other social insects – at around 45°C (113°F) – which may have made them especially vulnerable to the high ground temperatures of the 2026 heatwaves.

Why are the wasps so small?

There’s something else that I’ve noticed: the few wasps I’ve seen are rather small. The adult size of many insects is fixed during their development, depending on the quality and quantity of food they receive as larvae. Wasps don’t get bigger once they’ve pupated.

The first workers to emerge in spring are usually small because the queen is limited in how much food she can provide for them alone. But by early August, the foraging capacity of the colony has increased exponentially, brood are better fed and the emerging workers are substantially larger.

Source: ScienceDaily

Global warming is breaking a 400-year climate link between two oceans

  A new study suggests that the climate connection between the tropical Indian and Pacific oceans can be disrupted by major volcanic eruptions, while human-caused greenhouse gas emissions may now be driving an even more unusual breakdown in that relationship.

Researchers at the Woods Hole Oceanographic Institution (WHOI) combined paleoclimate evidence with climate model simulations to examine how closely the two ocean basins have behaved over the past several centuries.

Their findings indicate that volcanism can temporarily weaken the climate link between the Indian and Pacific oceans. More recently, however, human-driven climate forcing has produced what the researchers describe as an "exceptional" shift in the way climate variability in the two regions is connected.

The study was published in Nature Communications under the title "Coupling of Pacific and Indian Ocean variability disrupted by 19th century volcanism."

A Climate Connection That Usually Moves in Step

Climate conditions across the Indian Ocean often respond to changes occurring in the Pacific Ocean. This connection helps shape broad patterns of rainfall, temperature, and atmospheric circulation across the tropics.

Since the 1980s, however, scientists have noticed that this relationship has weakened. The Indian Ocean has increasingly behaved differently from what would normally be expected based on conditions in the Pacific, a change that researchers have linked to climate warming.

One challenge is that reliable instrumental climate records cover less than a century. That makes it difficult to determine whether the recent change is truly unusual or simply part of a longer natural cycle.

To look further back in time, the WHOI team turned to tropical paleoclimate records preserved in corals, tree rings, and stalagmites. These natural archives allowed the researchers to reconstruct Indian and Pacific Ocean climate conditions back to the early 1600s.

Volcanoes Disrupted the Ocean Link in the 1800s

The paleoclimate evidence shows that the Indian and Pacific oceans remained closely connected through most of the past 400 years.

One period stood out.

Between 1810 and 1850, the relationship between the two ocean basins changed significantly. Researchers linked that disruption to a series of major tropical volcanic eruptions, which appear to have weakened the Pacific Ocean's usual influence over climate conditions in the Indian Ocean.

Computer simulations covering the past thousand years supported that interpretation.

The strength of the disruption depended on both the size of the volcanic eruptions and the background climate conditions that existed at the time.

"This is one of the first studies to examine the breakdown in the connection between the Pacific and Indian oceans using evidence from past climates, modern observations, and climate models," said co-author Caroline Ummenhofer, a senior scientist at WHOI.

Modern Changes Appear Far More Unusual

The volcanic connection was only part of what the researchers uncovered. By comparing the modern climate with several centuries of past conditions, they were also able to judge how unusual the current weakening of Indian and Pacific Ocean coupling really is.

"The modern data we have is limited and doesn't go back far enough. With climate models and paleo-records, we are now able to say with more confidence that the recent changes we are seeing are really quite exceptional," said lead author Shawn Wang.

Wang is a former WHOI graduate student and postdoctoral researcher, and he is currently a postdoc at the University of Colorado Boulder.

The findings suggest that although volcanic eruptions can temporarily interrupt the connection between the two ocean basins, the modern breakdown appears to be driven by a different force.

"A key finding is that global warming and human emissions are now overwhelming the Pacific's natural influence on the Indian Ocean," Ummenhofer said.

Why the Indian Ocean Matters for Climate Predictions

Understanding how strongly the Indian and Pacific oceans influence each other is important for climate forecasting.

Connections between ocean basins can help scientists anticipate shifts in rainfall and other major climate patterns. If those relationships weaken or change, forecasts based on historical behavior may become less reliable.

Much past research has examined major ocean basins separately. This study instead focuses on the ways they interact, and on what happens when those connections begin to weaken.

Source: ScienceDaily

Scientists find hidden pathways pancreatic cancer uses to spread

 A new study from Brazil, published in the journal Molecular and Cellular Endocrinology, sheds light on how pancreatic cancer gains the ability to spread at an early stage. Researchers found that a protein called periostin, along with stellate cells in the pancreas, plays a crucial role in helping cancer cells invade nearby nerves. This early nerve invasion raises the risk of metastasis and is closely tied to how aggressive the disease becomes. The findings also highlight potential targets for more precise and personalized cancer treatments.

The research shows that pancreatic tumors do not act alone. Instead, they alter parts of the surrounding healthy tissue, effectively reprogramming it to support cancer invasion. This process helps explain why pancreatic cancer is so difficult to control once it begins to spread.

A Rare Cancer With a Deadly Impact

The most common form of pancreatic cancer is adenocarcinoma, which develops in the glandular cells that produce pancreatic juice. This type accounts for about 90% of all pancreatic cancer diagnoses. While pancreatic cancer is not among the most frequently diagnosed cancers, it is known for being especially aggressive. Its death rate nearly matches its diagnosis rate.

Worldwide, there are roughly 510,000 new pancreatic cancer cases each year, with nearly the same number of deaths reported annually.

In Brazil, estimates from the National Cancer Institute (INCA) point to about 11,000 new cases and 13,000 deaths each year. "It's an aggressive cancer that's difficult to treat. Around 10% of patients have a chance of long-term survival, such as five years after diagnosis," says Pedro Luiz Serrano Uson Junior, an oncologist and one of the study's authors.

Why Nerve Invasion Matters

One reason pancreatic cancer is so dangerous is a process known as perineural invasion. This occurs when cancer cells move into and spread along nerves. The process can cause severe pain and also helps the tumor reach other parts of the body more easily. "Perineural invasion is a marker of cancer aggressiveness," Uson explains.

Because nerves connect different regions of the body, cancer cells that enter these pathways gain new routes for expansion.

Mapping the Tumor's Hidden Support System

The research was carried out at the Center for Research on Inflammatory Diseases (CRID), one of FAPESP's Research, Innovation, and Dissemination Centers (RIDCs). The study was led by researcher Carlos Alberto de Carvalho Fraga, with Helder Nakaya serving as principal investigator. Nakaya is also a senior researcher at Einstein Israelite Hospital and a professor at the University of São Paulo's School of Pharmaceutical Sciences.

To uncover how nerve invasion occurs, the team used advanced tools that analyze the activity of thousands of genes in individual cells while mapping their exact locations within tumor tissue. "We were able to integrate data from dozens of samples with extremely powerful resolution," Nakaya says.

The researchers examined 24 pancreatic cancer samples and found that the stroma, the connective tissue that supports the tumor, plays an active role in cancer progression rather than serving as a passive structure.

The Role of Periostin and Tissue Remodeling

One of the study's most important findings involved pancreatic and stellate cells that produce large amounts of periostin. This protein is known for its ability to reshape the extracellular matrix - the structure that organizes and maintains healthy tissue.

Tumor cells rely on major changes to this matrix in order to push through tissue and reach nearby nerves. This remodeling process involves specialized enzymes and widespread tissue disruption. "Periostin participates in this remodeling, paving the way for tumor cells to invade," Nakaya explains. Once cancer cells reach a nerve, it can act like a "road" that helps them spread further.

Why Treatments Struggle to Reach the Tumor

As the tumor environment changes, it triggers a desmoplastic reaction. This involves the buildup of dense, fibrous tissue around the tumor, made up of cells and proteins that stiffen and inflame the area. The hardened tissue makes it harder for chemotherapy and immunotherapy drugs to penetrate the tumor.

This protective microenvironment allows cancer cells to survive and continue spreading. "That's why pancreatic cancer is still so difficult to treat," says Uson.

Early Spread Leads to Poor Outcomes

According to Uson, the tumor's ability to infiltrate surrounding tissue is a major reason for the poor outlook faced by many patients. "Perineural invasion is a sign that cancer cells have gained mobility. They escape the tumor mass, travel through healthy tissue, and reach nerve and lymphatic bundles, which carry them to other regions of the body, facilitating the development of metastases."

More than half of pancreatic cancer cases already show signs of perineural invasion at an early stage. However, this spread is usually discovered only after surgery. "Unfortunately, we discover this perineural invasion after it's already occurred. It's only seen in the surgical specimen when it goes for biopsy," Uson says.

Source: ScienceDaily

Scientists find the genetic switch that makes pancreatic cancer resist chemotherapy

 Researchers at Duke-NUS Medical School have discovered a molecular "switch" that determines whether pancreatic cancer cells respond to chemotherapy or resist it. The finding points to a way to potentially shift some of the most treatment resistant tumors into a state where existing drugs can work more effectively.

The study, published in the Journal of Clinical Investigation, explains how this switch operates at a molecular level. The results suggest that pairing targeted therapies with standard chemotherapy may improve outcomes for patients whose tumors no longer respond to treatment.

Why Pancreatic Cancer Is So Difficult to Treat

Pancreatic cancer is one of the deadliest cancers worldwide. In Singapore, it ranks as the ninth most common cancer but the fourth leading cause of cancer related death. Because symptoms often appear late and current treatments have limited impact, most patients depend on chemotherapy, which typically provides only modest benefit.

Over the past decade, scientists have identified two main molecular subtypes of pancreatic cancer, classical and basal. Tumors in the classical subtype tend to be more organized at the cellular level, and patients with this form are more likely to respond to treatment. In contrast, basal subtype tumors are more disorganized and aggressive, and they are often resistant to chemotherapy.

Importantly, pancreatic cancer cells are not fixed in one subtype. They can shift between these states, moving from a more treatable form to a more resistant one. This flexibility is known as cancer cell plasticity.

The Role of GATA6 in Tumor Behavior

The research team focused on a gene called GATA6, which helps maintain pancreatic cancer cells in the more structured and less aggressive classical state. When GATA6 levels are high, tumors tend to grow in a more organized way and are more likely to respond to chemotherapy. When GATA6 levels fall, cells lose that structure, become more aggressive, and are harder to treat.

Professor David Virshup of Duke-NUS's Programme in Cancer & Stem Cell Biology, the study's lead author, said:

"We have known that pancreatic cancer cells can switch between these two states. What we didn't understand was the mechanism driving that switch. By identifying the pathway that suppresses GATA6, we now have a clearer picture of how tumors become resistant -- and potentially how to reverse that process."

KRAS and ERK Pathway Drive the Switch

The researchers traced the switch to a chain of signals inside pancreatic cancer cells. A gene called KRAS, which is mutated in nearly all pancreatic cancers, sends constant growth signals that drive tumor development. KRAS passes these signals through a partner protein known as ERK, which relays the instructions further inside the cell.

When the ERK pathway becomes highly active, it protects another protein that interferes with the production of GATA6. As GATA6 levels drop, cancer cells lose their organized structure, shift toward the more aggressive basal state, and become much less responsive to chemotherapy.

Using genetic screening, molecular analysis in cancer cells, and drug treatments, the team demonstrated that blocking the KRAS and ERK pathway lifts this suppression. When that happens, GATA6 levels rise again. The cancer cells then shift back toward the more organized state and regain sensitivity to chemotherapy.

Combination Therapy Shows Stronger Effects

The study also found that higher levels of GATA6 on their own made pancreatic cancer cells more responsive to treatment. When drugs that inhibit the KRAS and ERK pathway were combined with standard chemotherapy, the anti cancer effects were stronger than with either approach alone. However, this enhanced benefit occurred only when GATA6 was present, highlighting its central role in determining which patients might benefit most from combination therapy.

These findings help clarify why patients with higher GATA6 levels often respond better to certain chemotherapy regimens. They also provide a scientific foundation for ongoing clinical trials that are testing new treatments aimed at KRAS and related pathways.

Professor Lok Sheemei, Duke-NUS' Interim Vice-Dean for Research, said:

"Pancreatic cancer remains one of the toughest cancers to treat. These findings provide a mechanistic explanation for why tumors respond poorly to chemotherapy and offers a rational strategy for combining targeted therapies with existing drugs."

Broader Implications for Other KRAS Driven Cancers

The implications may extend beyond pancreatic cancer. Many other cancers fueled by KRAS mutations show similar shifts in cell behavior and treatment response. Understanding how cancer cells transition between different states could help researchers address therapy resistance in additional cancer types.

Professor Patrick Tan, Dean and Provost's Chair in Cancer and Stem Cell Biology at Duke-NUS, commented:

"This work demonstrates how basic science can uncover actionable insights into treatment resistance. Understanding how cancer cells switch states gives us a more strategic way to design combination treatments."

Duke-NUS Medical School is internationally recognized for its leadership in medical education and biomedical research, combining fundamental discoveries with translational expertise to improve health outcomes in Singapore and beyond.

Source: ScienceDaily

Scientists discover sleep switch that builds muscle, burns fat, and boosts brainpower

 Deep sleep does more than help you feel rested. It actively rebuilds your body, strengthening muscles, supporting bone growth, and helping burn fat. For teenagers, it is also essential for reaching full height potential.

At the center of all this is growth hormone, which surges during sleep. But scientists have long puzzled over why poor sleep, especially the early deep stage known as non-REM sleep, leads to lower levels of this critical hormone.

Scientists Discover the Brain Circuit Behind It

Researchers at the University of California, Berkeley, have now uncovered the answer. In a study published in Cell, they mapped the brain circuits that control growth hormone release during sleep and identified a new feedback system that keeps those levels in balance.

This discovery offers a clearer understanding of how sleep and hormones work together. It may also open the door to new treatments for sleep disorders linked to metabolic diseases like diabetes, as well as neurological conditions such as Parkinson's and Alzheimer's.

"People know that growth hormone release is tightly related to sleep, but only through drawing blood and checking growth hormone levels during sleep," said study first author Xinlu Ding, a postdoctoral fellow in UC Berkeley's Department of Neuroscience and the Helen Wills Neuroscience Institute. "We're actually directly recording neural activity in mice to see what's going on. We are providing a basic circuit to work on in the future to develop different treatments."

Lack of sleep does more than leave you tired. Because growth hormone helps control how the body processes sugar and fat, poor sleep can increase the risk of obesity, diabetes, and heart disease.

The Brain Regions Driving Growth Hormone

The system behind this process is buried deep in the hypothalamus, an ancient part of the brain shared by all mammals. Here, specialized neurons release signals that either trigger or suppress growth hormone.

Two key players are growth hormone releasing hormone (GHRH), which stimulates release, and somatostatin, which inhibits it. Together, they coordinate hormone activity across the sleep-wake cycle.

Once growth hormone enters the system, it activates the locus coeruleus, a brainstem region that controls alertness, attention, and cognitive function. Disruptions in this area are linked to a wide range of neurological and psychiatric disorders.

"Understanding the neural circuit for growth hormone release could eventually point toward new hormonal therapies to improve sleep quality or restore normal growth hormone balance," said Daniel Silverman, a UC Berkeley postdoctoral fellow and study co-author. "There are some experimental gene therapies where you target a specific cell type. This circuit could be a novel handle to try to dial back the excitability of the locus coeruleus, which hasn't been talked about before."

How Sleep Stages Control Hormone Release

To study this system, researchers recorded brain activity in mice by inserting electrodes and stimulating neurons with light. Because mice sleep in short bursts throughout the day and night, they provided a detailed view of how growth hormone changes across sleep stages.

The team found that GHRH and somatostatin behave differently depending on whether the brain is in REM or non-REM sleep.

During REM sleep, both hormones increase, leading to a surge in growth hormone. During non-REM sleep, somatostatin drops while GHRH rises more modestly, still boosting hormone levels but in a different pattern.

A Surprising Feedback Loop in the Brain

The researchers also uncovered a feedback loop that links growth hormone to wakefulness. As sleep continues, growth hormone gradually builds up and stimulates the locus coeruleus, nudging the brain toward waking.

But there is a twist. When this brain region becomes too active, it can actually trigger sleepiness instead, creating a delicate balance between sleep and alertness.

"This suggests that sleep and growth hormone form a tightly balanced system: Too little sleep reduces growth hormone release, and too much growth hormone can in turn push the brain toward wakefulness," Silverman said. "Sleep drives growth hormone release, and growth hormone feeds back to regulate wakefulness, and this balance is essential for growth, repair and metabolic health."

Why It Matters for Brain and Body

This balance does more than affect physical growth. Because growth hormone works through brain systems that control alertness, it may also influence how clearly you think and how focused you feel.

"Growth hormone not only helps you build your muscle and bones and reduce your fat tissue, but may also have cognitive benefits, promoting your overall arousal level when you wake up," Ding said.

Funding and Research Team

The research was supported by the Howard Hughes Medical Institute (HHMI) and the Pivotal Life Sciences Chancellor's Chair fund. Yang Dan holds the Pivotal Life Sciences Chancellor's Chair in Neuroscience. The study also included collaborators from UC Berkeley and Stanford University.

Source: ScienceDaily

One fat helped pancreatic cancer grow while another cut disease in half

 For years, the common assumption has been simple: eating less fat may help lower cancer risk. New research suggests the picture is much more complicated.

Scientists report that when it comes to pancreatic cancer, the specific type of fat in the diet may be more important than the total amount consumed.

The findings, published in Cancer Discovery, a journal of the American Association for Cancer Research, indicate that different fats can have dramatically different effects on cancer development.

"It's really the type of fat that you're consuming, not just total fat content," says Christian Felipe Ruiz, PhD, an associate research scientist in Yale School of Medicine's Department of Genetics and lead author of the study. "Depending on the type of fat that you consume, it can go completely different ways. We found that some fats promote cancer, as we would expect, while other fats are really good at suppressing cancer."

Oleic Acid Linked to Faster Tumor Growth

One of the study's most unexpected findings involved oleic acid, the primary fatty acid found in olive oil.

Researchers found evidence that oleic acid may encourage tumor growth in pancreatic cancer, a result that surprised the team because of the fatty acid's long-standing reputation as a heart-healthy dietary fat.

"It's traditionally been considered a healthy type of fat for cardiovascular health," Ruiz says.

The cancer examined in the study was pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer and one of the deadliest cancers overall. Only about 13% of people diagnosed with PDAC survive for five years.

"More than 65,000 people are expected to be diagnosed with PDAC in the U.S. this year, with over 50,000 deaths," Ruiz notes. "At the moment, effective treatment options are limited, especially for advanced disease. Therefore, prevention strategies are sorely needed to move the needle on PDAC mortality."

Although previous research has linked high-fat diets to a greater risk of PDAC, scientists have struggled to identify exactly how dietary fat influences the disease. The new study, led by senior author Mandar Deepak Muzumdar, MD, associate professor of genetics and of internal medicine at YSM, sought to answer that question.

Muzumdar is also a member of Yale Cancer Center and the Yale Cancer Biology Institute at West Campus.

Comparing Different Types of Dietary Fat

To isolate the effects of specific fats, the researchers created 12 different high-fat diets. Each diet contained the same number of calories, with the only difference being the source of fat. The diets were designed to reflect common patterns of fat consumption in the modern American diet.

According to Ruiz, many earlier studies relied on a simpler approach.

For decades, researchers commonly "gave mice very high levels of fat in their diet, often using a single fat source." In many cases, those diets derived 60% of calories from lard, which does not accurately reflect typical human eating habits and makes it difficult to determine the effects of individual fatty acids.

"Exactly what components of dietary fat cause cancer has remained a mystery," Ruiz adds.

The results were striking. Mice carrying a genetic mutation that produces a disease closely resembling human PDAC developed tumors more rapidly when fed diets rich in oleic acid. Oleic acid is a monounsaturated fatty acid (MUFA) found in foods such as olive oil, high-oleic safflower oil, high-oleic sunflower oil, peanuts, and lard.

In contrast, diets rich in polyunsaturated fatty acids (PUFAs) slowed cancer development. The strongest protective effects were seen with omega-3 fatty acids, including those found in fish oil.

"When we fed mice diets enriched with fish oil, we saw a 50% reduction in disease compared with mice fed a standard fat diet."

How Dietary Fats Affect Cancer Cell Survival

The findings led researchers to investigate ferroptosis, a form of programmed cell death caused by lipid oxidation.

When fatty acids become part of pancreatic cell membranes, their chemical characteristics influence how easily those cells can be damaged by oxidation. PUFAs are more prone to oxidation, making cancer cells more vulnerable to ferroptosis and death. MUFAs are more resistant to oxidation, helping protect cancer cells from this process.

"Monounsaturated fats really protect the cancer cells from lipid oxidation," Ruiz explains. "Because oxidation is reduced, they're less likely to undergo ferroptosis."

The researchers observed a direct relationship between fat composition and disease severity.

"When we increased the ratio of MUFAs to PUFAs in the diet, disease burden increased. Conversely, when we decreased the ratio, disease burden was reduced."

Source: ScienceDaily