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How Antibiotics in Infancy may Increase Diabetes Risk

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Gut Microbiome. Credit Darryl Leja National Human Genome Research Institute National Institutes Of Health

Exposure to antibiotics during a key developmental window in infancy can stunt the growth of insulin-producing cells in the pancreas and may boost risk of diabetes later in life, new research in mice suggests. The study, published this month in the journal Science, also pinpoints specific microorganisms that may help those critical cells proliferate in early life.

The findings are the latest to shine a light on the importance of the human infant microbiome—the constellation of bacteria and fungi living on and in us during our first few years. The research could lead to new approaches for addressing a host of metabolic diseases.

“We hope our study provides more awareness for how important the infant microbiome actually is for shaping development,” said first author Jennifer Hill, assistant professor in molecular, cellular and developmental biology at CU’s BioFrontiers Institute. “This work also provides important new evidence that microbe-based approaches could someday be used to not only prevent but also reverse diabetes.”

Something in the environment

More than 2 million U.S. adults live with Type 1 diabetes. The disease typically emerges in childhood, and genetics play a strong role. But scientists have found that, while identical twins share DNA that predisposes them to Type 1 diabetes, only one twin usually gets the disease.

“This tells you that there’s something about their environmental experiences that is changing their susceptibility,” said Hill.

For years, she has looked to microbes for answers.

Previous studies show that children who are breastfed or born vaginally, which can both promote a healthy infant microbiome, are less likely to develop Type 1 diabetes than others. Some research also shows that giving babies antibiotics early can inadvertently kill good bugs with bad and boost diabetes risk.

The lingering questions: What microbes are these infants missing out on?

“Our study identifies a critical window in early life when specific microbes are necessary to promote pancreatic cell development,” said Hill.

A key window of opportunity

She explained that human babies are born with a small amount of pancreatic “beta cells,” the only cells in the body that produce insulin. But some time in a baby’s first year, a once-in-a-lifetime surge in beta cell growth occurs.

“If, for whatever reason, we don’t undergo this event of expansion and proliferation, that can be a cause of diabetes,” Hill said.

She conducted the current study as a postdoctoral researcher at the University of Utah with senior author June Round, a professor of pathology.

They found that when they gave broad-spectrum antibiotics to mice during a specific window (the human equivalent of about 7 to 12 months of life), the mice developed fewer insulin producing cells, higher blood sugar levels, lower insulin levels and generally worse metabolic function in adulthood.

“This, to me, was shocking and a bit scary,” said Round. “It showed how important the microbiota is during this very short early period of development.”

Lessons in baby poop

In other experiments, the scientists gave specific microbes to mice, and found that several they increased their production of beta cells and boosted insulin levels in the blood. The most powerful was a fungus called Candida dubliniensis.

The team used faecal samples from The Environmental Determinants of Diabetes in the Young (TEDDY) study to make what Hill calls “poop slushies” and fed them to the mice.

When the researchers inoculated newborn mice with poop from healthy infants between 7 to 12 months in age, their beta cells began to grow. Poop from infants of other ages did not do the same. Notably, Candida dublineinsis was abundant in human babies only during this time period.

“This suggests that humans also have a narrow window of colonisation by these beta cell promoting microbes,” said Hill.

When male mice that were genetically predisposed to Type 1 diabetes were colonised with the fungus in infancy, they developed diabetes less than 15% of the time. Males that didn’t receive the fungus got diabetes 90% of the time.

Even more promising, when researchers gave the fungus to adult mice whose insulin-producing cells had been killed off, those cells regenerated.

Too early for treatments

Hill stresses that she is not “anti-antibiotics.” But she does imagine a day when doctors could give microbe-based drugs or supplements alongside antibiotics to replace the metabolism-supporting bugs they inadvertently kill.

Poop slushies (faecal microbiota transplants) have already been used experimentally to try to improve metabolic profiles of people with Type 2 diabetes, which can also damage pancreatic beta cells.

But such approaches can come with real risk, since many microbes that are beneficial in childhood can cause harm in adults. Instead, she hopes that scientists can someday harness the specific mechanisms the microbes use to develop novel treatments for healing a damaged pancreas—reversing diabetes.

She recently helped establish a state-of-the-art “germ-free” facility for studying the infant microbiome at CU Boulder. There, animals can be bred and raised entirely without microbes, and by re-introducing them one by one scientists can learn they work.

“Historically we have interpreted germs as something we want to avoid, but we probably have way more beneficial microbes than pathogens,” she said. “By harnessing their power, we can do a lot to benefit human health.”

Source: University of Colorado at Boulder

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Social Skills not as Relevant for Autism Diagnosis than Thought

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Photo by Peter Burdon on Unsplash

People with autism are typically diagnosed by clinical observation and assessment. To deconstruct the clinical decision process, which is often subjective and difficult to describe, researchers used a large language model (LLM) to synthesize the behaviours and observations that are most indicative of an autism diagnosis. Their results, publishing in the Cell Press journal Cell, show that repetitive behaviours, special interests, and perception-based behaviours are most associated with an autism diagnosis.

These findings have potential to improve diagnostic guidelines for autism by decreasing the focus on social factors – which the established guidelines in the DSM-5 focus on but the model did not classify among the most relevant in diagnosing autism.

“Our goal was not to suggest that we could replace clinicians with AI tools for diagnosis,” says senior author Danilo Bzdok of the Mila Québec Artificial Intelligence Institute and McGill University in Montreal. “Rather, we sought to quantitatively define exactly what aspects of observed behaviour or patient history a clinician uses to reach a final diagnostic determination. In doing so, we hope to empower clinicians to work with diagnostic instruments that are more in line with their empirical realities.”

The scientists leveraged a transformer language model, which was pre-trained on about 489 million unique sentences. They then fine-tuned the LLM to predict the diagnostic outcome from a collection of more than 4000 reports written by clinicians working with patients considered for autism diagnosis. The reports, which were often used by multiple clinicians, included accounts of observed behaviour and relevant patient history but did not include a suggested diagnostic outcome.

The team developed a bespoke LLM module that pinpointed specific sentences in the reports that were most relevant to a correct diagnosis prediction. They then extracted the numerical representation of these highly autism-relevant sentences and compared them directly with the established diagnostic criteria enumerated in the DSM-5.

“Modern LLMs, with their advanced natural language processing capabilities, are natively suited to this textual analysis,” Bzdok says. “The key challenge we faced was in designing sentence-level interpretability tools to pinpoint the exact sentences, expressed by the healthcare professional themselves, that were most essential to a correct diagnosis prediction by the LLM.”

The researchers were surprised by how clearly the LLM was able to distinguish between the most diagnostically relevant criteria. For example, their framework flagged that repetitive behaviours, special interests, and perception-based behaviour were the criteria most relevant to autism. While these criteria are used in clinical settings, current criteria focus more on deficits in social interplay and lack of communication skills.

The authors note that there are limitations to this study, including a lack of geographical diversity. Additionally, the researchers did not analyse their results based on demographic variables, with the goal of making the conclusions more broadly applicable.

The team expects their framework will be helpful to researchers and medical professionals working with a range of psychiatric, mental health, and neurodevelopmental disorders in which clinical judgement forms the bulk of the diagnostic decision-making process.

“We expect this paper to be highly relevant to the broader autism community,” Bzdok says. “We hope that our paper motivates conversations about grounding diagnostic standards in more empirically derived criteria. We also hope it will establish common threads that link seemingly diverse clinical presentations of autism together.”

Source: ScienceDaily

Categories : Diet and NutritionTags : Leave a comment

Why Does Obesity Takes Away the Pleasure of Eating?

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Photo by Jonathan Borba

The pleasure we get from eating junk food — the dopamine rush from crunching down on salty, greasy chips and a luscious burger — is often blamed as the cause of overeating and rising obesity rates in our society. But a new study suggests that pleasure in eating, even eating junk food, is key for maintaining a healthy weight in a society that abounds with cheap, high-fat food.

Paradoxically, anecdotal evidence suggests that people with obesity may take less pleasure in eating than those of normal weight. Brain scans of obese individuals show reduced activity in pleasure-related brain regions when presented with food, a pattern also observed in animal studies.

Now, University of California, Berkeley, researchers have identified a possible underlying cause of this phenomenon — a decline in neurotensin, a brain peptide that interacts with the dopamine network — and a potential strategy to restore pleasure in eating in a way that helps reduce overall consumption.

The study, published in Nature, reveals an unsuspected brain mechanism that explains why a chronic high-fat diet can reduce the desire for high-fat, sugary foods, even when these foods remain easily accessible. The researchers propose that this lack of desire in obese individuals is due to a loss of pleasure in eating caused by long-term consumption of high-calorie foods. Losing this pleasure may actually contribute to the progression of obesity.

“A natural inclination toward junk food is not inherently bad — but losing it could further exacerbate obesity,” said Stephan Lammel, a UC Berkeley professor in the Department of Neuroscience and a member of the Helen Wills Neuroscience Institute.

The researchers found that this effect is driven by a reduction in neurotensin in a specific brain region that connects to the dopamine network. Importantly, they demonstrate that restoring neurotensin levels — either through dietary changes or genetic manipulations that enhance neurotensin production — can reinstate the pleasure in eating and promote weight loss.

“A high-fat diet changes the brain, leading to lower neurotensin levels, which in turn alters how we eat and respond to these foods,” Lammel said. “We found a way to restore the desire for high-calorie foods, which may actually help with weight management.”

While findings in mice don’t always translate directly to humans, this discovery could open new avenues for addressing obesity by restoring food-related pleasure and breaking unhealthy eating patterns.

“Imagine eating an amazing dessert at a great restaurant in Paris — you experience a burst of dopamine and happiness,” said Neta Gazit Shimoni, a UC Berkeley postdoctoral fellow. “We found that this same feeling occurs in mice on a normal diet, but is missing in those on a high-fat diet. They may keep eating out of habit or boredom, rather than genuine enjoyment.”

Gazit Shimoni and former UC Berkeley graduate student Amanda Tose are co-first authors, and Lammel is senior author of the study, which will be published March 26 in the journal Nature.

Solving a long-standing puzzle in obesity research

For decades, doctors and researchers have struggled to understand and treat obesity, as countless fad diets and eating regimens have failed to produce long-term results. The recent success of GLP-1 agonists like Ozempic, which curb appetite by increasing feelings of fullness, stands out among many failed approaches.

Lammel studies brain circuits, particularly the dopamine network, which plays a crucial role in reward and motivation. Dopamine is often associated with pleasure, reinforcing our desire to seek rewarding experiences, such as consuming high-calorie foods.

While raising mice on a high-fat diet, Gazit Shimoni noticed a striking paradox: While in their home cages, these mice strongly preferred high-fat chow, which contained 60% fat, over normal chow with only 4% fat, leading them to gain excessive weight. However, when they were taken out of their home cages and given free access to high-calorie treats such as butter, peanut butter, jelly or chocolate, they showed much less desire to indulge than normal-diet mice, which immediately ate everything they were offered.

“If you give a normal, regular-diet mouse the chance, they will immediately eat these foods,” Gazit Shimoni said. “We only see this paradoxical attenuation of feeding motivation happening in mice on a high-fat diet.”

She discovered that this effect had been reported in past studies, but no one had followed up to find out why, and how the effect connects to the obesity phenotype observed in these mice.

Restoring neurotensin reverses obesity-related brain changes

To investigate this phenomenon, Lammel and his team used optogenetics, a technique that allows scientists to control brain circuits with light. They found that in normal-diet mice, stimulating a brain circuit that connects to the dopamine network increased their desire to eat high-calorie foods, but in obese mice, the same stimulation had no effect, suggesting that something must have changed.

The reason, they discovered, was that neurotensin was reduced so much in obese mice that it prevented dopamine from triggering the usual pleasure response to high-calorie foods.

“Neurotensin is this missing link,” Lammel said. “Normally, it enhances dopamine activity to drive reward and motivation. But in high-fat diet mice, neurotensin is downregulated, and they lose the strong desire to consume high-calorie foods — even when easily available.”

The researchers then tested ways to restore neurotensin levels. When obese mice were switched back to a normal diet for two weeks, their neurotensin levels returned to normal, dopamine function was restored, and they regained interest in high-calorie foods.

When neurotensin levels were artificially restored using a genetic approach, the mice not only lost weight, but also showed reduced anxiety and improved mobility. Their feeding behaviour also normalised, with increased motivation for high-calorie foods and a simultaneous reduction of their total food consumption in their home cages.

“Bringing back neurotensin seems to be very, very critical for preventing the loss of desire to consume high-calorie foods,” Lammel said. “It doesn’t make you immune to getting obese again, but it would help to control eating behaviour, to bring it back to normal.”

Toward more precise treatments for obesity

Although directly administering neurotensin could theoretically restore feeding motivation in obese individuals, neurotensin acts on many brain areas, raising the risk of unwanted side effects. To overcome this, the researchers used gene sequencing, a technique that allowed them to identify specific genes and molecular pathways that regulate neurotensin function in obese mice.

This discovery provides crucial molecular targets for future obesity treatments, paving the way for more precise therapies that could selectively enhance neurotensin function without broad systemic effects.

“We now have the full genetic profile of these neurons and how they change with high-fat diets,” Lammel said. “The next step is to explore pathways upstream and downstream of neurotensin to find precise therapeutic targets.”

Lammel and Gazit Shimoni plan to expand their research to explore neurotensin’s role beyond obesity, investigating its involvement in diabetes and eating disorders.

“The bigger question is whether these systems interact across different conditions,” Gazit Shimoni said. “How does starvation affect dopamine circuits? What happens in eating disorders? These are the questions we’re looking at next.”

Source: University of California – Berkeley

Categories : Cardiovascular DiseaseTags : Leave a comment

Possible Link Between Medication and Unexpected Blood Clots

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Thrombophilia. Credit: Scientific Animations CC4.0.

Why do medications that are supposed to help patients with chronic inflammatory diseases sometimes lead to blood clots? This is one of the questions that a team of researchers from Aarhus University has sought to answer in a study that has just been published in the journal Inflammopharmacology.

The study suggests that disturbances in the JAK-STAT signalling pathway, an important communication pathway in the body, may contribute to this side effect.

“In the study, we uncover the potential links between components of the JAK-STAK signalling pathway, blood markers in patients with blood clots, and the genetic factors that contribute to the risk of blood clots in patients. This helps improve our understanding of why we see an increased risk of blood clots when using JAK inhibitors,” explains Stine Rabech Haysen, former medical student at the Department of Biomedicine at Aarhus University, who is the first author of the publication. 

The potential of the study

In the study, researchers used publicly available data from a number of published studies about patients with blood clots and compared them with a healthy control group.

They found no direct genetic explanation, but they did find a statistically significant enrichment of genes that are subject to regulatory control of the JAK-STAT signalling pathway among genes whose expression is altered in patients with blood clots.

“Although we cannot draw definitive conclusions about the mechanistic link between the use of JAK inhibitors and the risk of blood clots, our study demonstrates the potential of using data mining to identify and shed light on possible mechanisms of drug side effects,” says one of the study’s senior authors, associate professor at the Department of Biomedicine Per Qvist.

What does this mean for patients?

Although JAK inhibitors rarely lead to blood clots, it’s important to understand the mechanism behind them so that the risk can be reduced.

“For the average person, our study means that we’re getting closer to understanding why some drugs can have dangerous side effects like blood clots. And going forward, our method could help identify and prevent serious side effects, potentially making drug treatment safer,” explains the other senior author of the study, associate professor at the Department of Biomedicine Tue Wenzel Kragstrup.

The researchers will now test the method on other types of medication to see if it can be used to detect side effects more widely.

Source: Aarhus University

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New Cannabis Formula will Help Epilepsy, Multiple Sclerosis Sufferers

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Photo by Kindel Media on Unsplash

Scientists at the University of South Australia have come up with an innovative solution to improve the effectiveness of cannabidiol to treat epilepsy, multiple sclerosis and other neurodegenerative diseases.

Cannabidiol (CBD), a non-psychoactive cannabis compound, is widely prescribed for its analgesic, anti-inflammatory and neuroprotective properties, but its clinical applications to date have been limited by its poor water solubility and absorption in the human body.

By developing a phospholipid complex – a class of lipids (fats) that contain phosphorus – UniSA researchers have increased the solubility of cannabidiol by up to six times and improved its absorption in the gastrointestinal tract.

Lead researcher Professor Sanjay Garg says the breakthrough, reported in the International Journal of Molecular Sciences, means that patients could experience more consistent and effective results with lower doses of oral CBD medications.

Currently, only a small fraction of orally ingested CBD reaches the bloodstream, limiting its therapeutic effects.

“For this reason, a number of different formulations have been explored, including the production of synthetic CBD, self-emulsifying delivery systems, and encapsulating CBD in gelatine matrix pellets, but all of them have only resulted in minor improvements in bioavailability,” Prof Garg says.

His research team identified the optimal phospholipid composition to form nanosized CBD-PLC particles. Compared to pure CBD, the phospholipid complex improved dissolution rates from 0% to 67.1% within three hours, demonstrating a significant enhancement in drug release.

In cellular uptake studies, CBD-PLC exhibited 32.7% higher permeability than unmodified CBD, ensuring greater absorption through the intestinal wall.

Another critical advantage of this new delivery system is its stability. Traditional CBD formulations degrade over time when exposed to heat, light or oxygen, reducing potency and shelf life.

However, testing over 12 months showed that CBD-PLC retained its performance under varied storage conditions, making it a more reliable option for pharmaceutical applications.

The study’s first author, UniSA PhD candidate Thabata Muta, says the discovery has significant implications for the future of CBD-based therapeutics.

“Improved bioavailability means that lower doses can achieve the same therapeutic effect, potentially reducing side effects and making treatment more cost effective,” Thabata says.

The research team believes that this innovation could be applied beyond CBD, providing a blueprint for enhancing the absorption of other poorly water-soluble drugs.

With the global CBD market projected to grow from USD 7.59 billion in 2023 to USD 202.45 billion by 2032, the findings of this study come at a crucial time, according to the study authors.

The team is now exploring opportunities for commercialisation and clinical trials to validate their new formulation.

Source: University of South Australia

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Do Seizures in Newborns Increase Children’s Risk of Developing Epilepsy?

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Seizures in newborns are one of the most frequent acute neurological conditions among infants admitted to neonatal care units. A study published in Developmental Medicine & Child Neurology indicates that newborns experiencing such neonatal seizures face an elevated risk of developing epilepsy.

For the study, investigators analysed data on all children born in Denmark between 1997 and 2018, with the goal of comparing the risk of epilepsy in children with and without neonatal seizures.

Among 1,294,377 children, the researchers identified 1,998 who experienced neonatal seizures. The cumulative risk of epilepsy was 20.4% among children with neonatal seizures compared with 1.15% among children without. This indicates that 1 in 5 newborns with neonatal seizures will develop epilepsy.

Epilepsy was diagnosed before 1 year of age in 11.4% of children with neonatal seizures, in an additional 4.5% between 1 and 5 years, 3.1% between 5 and 10 years, and 1.4% between 10 and 22 years. Stroke, hemorrhage, or structural brain malformations in newborns, as well as low Apgar scores, were associated with the highest risks of developing epilepsy.

“Our study highlights that there are risk factors that may be used to identify infants for tailored follow-up and preventive measures,” said corresponding author Jeanette Tinggaard, MD, PhD, of Copenhagen University Hospital – Rigshospitalet. “Importantly, four out of five neonatal survivors with a history of neonatal seizures did not develop epilepsy, and we suggest future studies to explore a potential genetic predisposition.”

Source: Wiley

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A Novel Pathway with Potential to Slow the Progression of Pulmonary Fibrosis

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Credit: Scientific Animations CC4.0

Researchers have found a potential new way to slow the progression of lung fibrosis and other fibrotic diseases by inhibiting the expression or function of Piezo2, a receptor that senses mechanical forces in tissues including stress, strain, and stiffness. The new study in The American Journal of Pathology, published by Elsevier, sheds light on the underlying mechanisms of pulmonary fibrotic diseases and identifies potential new targets and options for therapy to improve patients’ outcomes.

Pulmonary fibrotic diseases are a group of conditions that cause significant morbidity and sometimes mortality. Idiopathic pulmonary fibrosis (IPF) is a devastating progressive fibrotic lung disease with a median survival of 2.9 years from diagnosis. Lung fibrosis results in dramatic mechanical changes including increased stiffness in the tissue that cells can sense and respond to, making it difficult for the lungs to expand and contract properly during breathing.

Piezo channels are a newly discovered receptor that are sensitive to mechanical signals. Since the 2021 Nobel Prize in Medicine was awarded to Dr Ardem Patapoutian for the discovery of Piezo channels in 2010, interest has increased in their role in tissue homeostasis and disease outside of neuronal signalling, however, little has been published on their possible role in fibrotic lung diseases. A group of researchers driven to understand how mechanical forces in lung tissue contribute to and drive pulmonary fibrosis investigated the role of Piezo2 in pulmonary fibrosis using donor tissue from patients with IPF, mouse models of lung fibrosis, cell culture investigation of lung cells (fibroblasts) that create the fibrosis lesions, and by examining publicly available RNAseq datasets from other research groups.

Investigators found that:

  • Piezo2 is highly expressed in human lung tissue from patients with IPF and in multiple (different) mouse models of lung fibrosis.
  • Piezo2 is highly expressed in primary human lung fibroblasts in culture, the cells that are believed to play key roles in producing fibrosis in tissues (by proliferating and laying down matrix proteins, creating scar-like features).
  • Lung fibroblasts grown on stiffer substrates are reprogrammed to be more profibrotic, by proliferating, producing extra matrix proteins, and differentiating to scar-forming myofibroblasts.
  • Inhibition of Piezo2 with either RNA silencing or a peptide inhibitor, to prevent them from sensing the stiffness of their environment, reduces profibrotic programming.

Lead investigator Patricia J. Sime, MD, Division of Pulmonary Disease and Critical Care Medicine, Virginia Commonwealth University, says, “We are excited to report that this research that suggests inhibiting expression or function of Piezo2 could be a potential new therapeutic route to treating lung fibrosis and other fibrotic diseases. This is especially important as there is an unmet need for additional therapies for fibrotic diseases.”

Despite the introduction of nintedanib and pirfenidone for therapy of some fibrotic lung diseases, pulmonary fibrosis can remain challenging to effectively treat. This is in part because lung cells can be driven to a profibrotic phenotype by multiple pathways that reinforce each other, so that targeting one pathway alone may not be effective to slow or stop disease progression.

First author Margaret A.T. Freeberg, PhD, Division of Pulmonary Disease and Critical Care Medicine, Virginia Commonwealth University, continues, “Some types of lung fibrosis have been very difficult to treat. For example, IPF is a form of pulmonary fibrosis that often progresses. While there have been advances in therapy, the approved medications for IPF can slow, but do not always halt progression. One of the reasons that fibrosis can be difficult to effectively treat may be explained by the multiple profibrotic disease pathways that reinforce each other. Blocking Piezo2 signaling to prevent fibroblast reprogramming represents a new pathway we can target in our fight against fibrosis.”

Dr. Sime concludes, “This research identifies mechanical forces and a new specific target (Piezo2) that we can block to prevent fibrotic reprogramming of some lung cells. We believe this points to Piezo2 as an important new therapeutic target that might (by itself or in combination with other therapies) slow the progression of pulmonary fibrosis in our patients. Many new investigational drugs that target pulmonary fibrosis receive orphan drug designation from the FDA, and this may accelerate development and increase interest from pharmaceutical partners.”

Source: Elsevier

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New Evidence for a Chronic Disease Link with Microplastics

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Tiny fragments of plastic have become ubiquitous in our environment and our bodies. Higher exposure to these microplastics, which can be inadvertently consumed or inhaled, is associated with a heightened prevalence of chronic noncommunicable diseases, according to new research being presented at the American College of Cardiology’s Annual Scientific Session (ACC.25).

Researchers said the new findings add to a small but growing body of evidence that microplastic pollution represents an emerging health threat. In terms of its relationship with stroke risk, for example, microplastics concentration was comparable to factors such as minority race and lack of health insurance, according to the results.

“This study provides initial evidence that microplastics exposure has an impact on cardiovascular health, especially chronic, noncommunicable conditions like high blood pressure, diabetes and stroke,” said Sai Rahul Ponnana, MA, a research data scientist at Case Western Reserve School of Medicine in Ohio and the study’s lead author. “When we included 154 different socioeconomic and environmental features in our analysis, we didn’t expect microplastics to rank in the top 10 for predicting chronic noncommunicable disease prevalence.”

Microplastics—defined as fragments of plastic between 1 nanometre and 5 millimetres across—are released as larger pieces of plastic break down. They come from many different sources, such as food and beverage packaging, consumer products and building materials. People can be exposed to microplastics in the water they drink, the food they eat and the air they breathe.

The study examines associations between the concentration of microplastics in bodies of water and the prevalence of various health conditions in communities along the East, West and Gulf Coasts, as well as some lakeshores, in the United States between 2015-2019. While inland areas also contain microplastics pollution, researchers focused on lakes and coastlines because microplastics concentrations are better documented in these areas. They used a dataset covering 555 census tracts from the National Centers for Environmental Information that classified microplastics concentration in seafloor sediments as low (zero to 200 particles per square meter) to very high (over 40 000 particles per square metre). 

The researchers assessed rates of high blood pressure, diabetes, stroke and cancer in the same census tracts in 2019 using data from the U.S. Centers for Disease Control and Prevention. They also used a machine learning model to predict the prevalence of these conditions based on patterns in the data and to compare the associations observed with microplastics concentration to linkages with 154 other social and environmental factors such as median household income, employment rate and particulate matter air pollution in the same areas.

The results revealed that microplastics concentration was positively correlated with high blood pressure, diabetes and stroke, while cancer was not consistently linked with microplastics pollution. The results also suggested a dose relationship, in which higher concentrations of microplastic pollution are associated with a higher prevalence of disease. However, researchers said that evidence of an association does not necessarily mean that microplastics are causing these health problems. More studies are required to determine whether there is a causal relationship or if this pollution is occurring alongside another factor that leads to health issues, they said.

Further research is also needed to determine the amount of exposure or the length of time it might take for microplastics exposure to have an impact on health, if a causal relationship exists, according to Ponnana. Nevertheless, based on the available evidence, it is reasonable to believe that microplastics may play some role in health and we must take steps to reduce exposures, he said. While it is not feasible to completely avoid ingesting or inhaling microplastics when they are present in the environment, given how ubiquitous and tiny they are, researchers said the best way to minimise microplastics exposure is to curtail the amount of plastic produced and used, and to ensure proper disposal.

“The environment plays a very important role in our health, especially cardiovascular health,” Ponnana said. “As a result, taking care of our environment means taking care of ourselves.”

In a separate study presented at ACC.25, researchers from a different group reviewed the scientific literature and found that studies showed a strong correlation between microplastics in plaques in the heart’s arteries and the risk of adverse cardiovascular events, suggesting that the presence of microplastics could play a role in the onset or exacerbation of serious heart problems.

Source: American College of Cardiology

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New Non-surgical Contraceptive Implant is Delivered Through Small Gauge Needles

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Mass General Brigham and MIT investigators have developed a long-acting contraceptive implant that can be delivered through tiny needles to minimise patient discomfort and increase the likelihood of medication use.

Their findings in preclinical models provide the technological basis to develop self-administrable contraceptive shots that could mimic the long-term drug release of surgically implanted devices.

The new approach, which would reduce how often patients need to inject themselves and prove valuable for patients with less access to hospitals and other medical care providers, is described in Nature Chemical Engineering. 

“Needle size and liquid viscosity are crucial considerations for commercial translation of injectables,” said senior author Giovanni Traverso, MD, PhD, MBBCH, of the Division of Gastroenterology in the Department of Medicine at Brigham and Women’s Hospital. “Our engineering challenge was finding a way to maximise comfort for patients by using smaller needles, which cause less bruising or bleeding, and to make the viscosity low enough for easy application with the syringe by hand.” 

Traditional contraceptive implants are small, flexible rods that are surgically inserted under the skin to slowly deliver drugs over time, removing the hassle of remembering to take a pill. But the surgery required for implants makes them less accessible to some patients.

Traverso’s team developed a new approach to deliver the contraceptive drug levonorgestrel (LNG) through Self-assembling Long-acting Injectable Microcrystals (SLIM). SLIM act like tiny puzzle pieces that, once injected inside the body, undergo solvent exchange to assemble into a single solid implant that slowly releases the drug as the surface erodes. Unlike similar self-administering technologies, the solvent exchange assembly enables delivery by much smaller needles. 

The researchers will continue their work to optimize the dosing, duration, and injectability of the SLIM system, including understanding how it performs in the human body. The design could also be applied to other hydrophobic drugs, which make up most new pharmaceuticals. The researchers plan to investigate how different drug properties impact the SLIM system’s effectiveness.

 “We anticipate that SLIM could be a new addition to the current suite of family planning options available to women, especially for people in low-resource settings where options for contraception and health care facilities are limited,” said Traverso.

Source: Mass General Brigham

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A Citrus Remedy Quenches Dry Mouth in Cancer Patients

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Photo by Diana Polekhina on Unsplash

A natural citrus oil from oranges, lemons, and limes is proving highly effective in relieving dry mouth, and when combined with a new lipid formulation, new research suggests it may be effective without significant side effects.

Developed by the University of South Australia in collaboration with the Medical School at Stanford University, this world first formulation uniquely combines limonene (a citrus essential oil) with a lipid-based drug delivery system to treat dry mouth (xerostomia), a common side effect of radiotherapy.

The new formula demonstrated 180-fold better solubility than pure limonene in lab experiments and boosted relative bioavailability by over 4000% compared to pure limonene in pre-clinical trials.

Dry mouth is the most reported side effect following radiotherapy for the treatment of head and neck cancer, affecting up to 70% of patients due to salivary gland damage. It can lead to difficulty speaking and swallowing, significantly reducing quality of life.

Limonene has protective effects on saliva production during radiotherapy, but its poor solubility means high doses are needed to take effect, and these cause indigestion, abdominal discomfort and unpleasant ‘citrus burps’.

Lead researcher, Professor Clive Prestidge says UniSA’s new limonene-lipid combination creates a ‘super-solubilising’ treatment that reduces dry mouth at lower dose and without uncomfortable side effects.

“The therapeutic benefits of limonene are well known. It’s used as an anti-inflammatory, antioxidant, and mood-enhancing agent, and can also improve digestion and gut function. But despite its widespread use, its volatility and poor solubility have limited its development as an oral therapy,” Prof Prestidge says.

“As limonene is an oil, it forms a film on the top of the stomach contents, causing significant stomach pain and discomfort.

“Our novel formulation combines limonene with healthy fats and oils – called lipids – to create a super-solubilising compound that the body can easily absorb with reduced uncomfortable side effects.

“This increases the dispersion of limonene in the stomach, boosts absorption, and controls biodistribution – all while increasing a patient’s saliva production and reducing dry mouth.”

Co-researcher Dr Leah Wright says the formulation has the potential to significantly improve the quality of life for cancer patients and others suffering dry mouth conditions.

“Cancer patients undergoing radiotherapy and other medical treatments regularly experience dry mouth, which not only prevents them from comfortably swallowing, but can also have other negative and potentially life-threatening outcomes,” Dr Wright says. 

“While limonene can be ingested directly, it’s not well tolerated, especially by those with dry mouth. Plus, its poor absorption prevents it from effectively reaching the salivary glands – the target site.

“This inventive and highly impactful limonene-lipid formulation could provide a simple, effective oral solution for dry mouth, offering cancer patients long-lasting relief and comfort, improved oral health, and a higher quality of life during a difficult time.”

Clinical trials for the new formula are ongoing, with next steps to be announced soon.

Source: University of South Australia