Some researchers said the advice did not go far enough. The panel also declined to recommend extra scans for women with dense breast tissue.Citing rising breast cancer rates in young women, an expert panel on Tuesday recommended starting regular mammography screening at age 40, reversing longstanding and controversial guidance that most women wait until 50.The panel, the U.S. Preventive Services Task Force, finalized a draft recommendation made public last year. The group issues influential advice on preventive health, and its recommendations usually are widely adopted in the United States.In 2009, the task force raised the age for starting routine mammograms to 50 from 40, sparking wide controversy. At the time, researchers were concerned that earlier screening would do more harm than good, leading to unnecessary treatment in younger women, including alarming findings that lead to anxiety-producing procedures that are invasive but ultimately unnecessary.But now breast cancer rates among women in their 40s are on the rise, increasing by 2 percent a year between 2015 and 2019, said Dr. John Wong, vice chair of the task force. The panel continues to recommend screening every two years for women at average risk of breast cancer, though many patients and providers prefer annual screening.“There is clear evidence that starting screening every other year at age 40 provides sufficient benefit that we should recommend it for all women in this country to help them live longer and have a better quality of life,” said Dr. Wong, a primary care clinician at Tufts Medical Center who is the director of comparative effectiveness research for the Tufts Clinical Translational Science Institute.The recommendations have come under harsh criticism from some women’s health advocates, including Representative Rosa DeLauro, Democrat of Connecticut, and Representative Debbie Wasserman Schultz, Democrat of Florida, who say the advice does not go far enough.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

An entirely new approach to inhibiting DNA-cleaving enzymes works through the aggregation of an otherwise non-toxic molecule. This Kobe University discovery may lead to a much-needed method for curbing Streptococcus growth.
Enzymes are the body’s tools to make almost all reactions happen. But the same is true for bacteria like Streptococcus, which causes toxic shock syndrome, a rapidly progressing and deadly condition. When the body’s white blood cells try to capture the bacteria by casting nets made out of their own DNA, Streptococcus uses a DNA-cleaving enzyme to cut through the net. Blocking this enzyme has been a hot target for the development of drugs for the fight against the disease, but nothing has been found that is specific to the DNA-cleaving enzyme and that doesn’t harm the body in other ways.
Kobe University biochemical engineer MARUYAMA Tatsuo thinks he and his team may have found an approach. While doing research on a drug called “Mn007,” they noticed that it had the ability to inhibit a bovine DNA-cleaving enzyme that is functionally very similar to the one used by Streptococcus. Maruyama explains: “It was a coincidence, but we discovered that only aggregates (“clumps”) of Mn007 inhibit the enzyme. This is a completely new mechanism for inhibition and so we decided to investigate if this might be a promising candidate for the treatment of streptococcal infections.”
Their results, published in the journal JACS Au, are promising and curious. They first confirmed that it is really only aggregates that inhibit the enzyme, that the action is specific to this particular DNA-cleaving enzyme, and that it is not mediated by interaction with the DNA or other substances. Next, the Kobe University team made sure that Mn007 could also inhibit the bacterial enzyme. And finally, they tried whether this could, in principle, be applied to Streptococcus infections. Knowing from previous studies that Mn007 is not toxic to the body’s cells, they grew the bacteria in human blood containing white blood cells and added Mn007 to some of the samples. And indeed, when the drug was present, the bacteria showed significantly less growth than without it, indicating that aggregates of Mn007 helped the white blood cells reign in the bacteria’s growth.
These lab studies open an exciting door to further research. First, even though they discovered a completely new mechanism of inhibiting the activity of the DNA-cleaving enzyme, also called a “DNase,” nobody knows yet what this mechanism behind the specific inhibition by the aggregates is. Maruyama says, “Currently, the research group is trying to understand how Mn007 aggregates interact with the DNase and inhibit its enzymatic activity by simulating the behavior of the molecule.”
But a bigger question looms on the horizon: whether the drug can actually be applied as an effective treatment. The researchers write hopefully: “Mn007 would be the first case of a DNase inhibitor applied for therapeutic use. Because Streptococcus pyogenes infections worsen rapidly (within a few days), even temporary suppression of bacterial growth would significantly improve patient outcomes.” They close by saying, “We believe that molecular aggregation will provide a rational approach for the discovery and development of novel inhibitors for those enzymes, leading to a new strategy in drug development.”

A team of researchers from Aarhus University has made a remarkable discovery that could improve cancer treatment and the treatment of a number of other illnesses.
The key lies in regulating cholesterol levels, which can help make existing treatments more effective.
“We’ve identified a new mechanism that can regulate a crucial immune pathway in the fight against cancer, and this gives us a deeper understanding of how we can activate the body’s own defence against the disease,” explains Professor Martin Roelsgaard Jakobsen from the Department of Biomedicine and one of the last three authors of the study.
Special focus on an essential protein
The researchers have focused on the so-called STING protein, an important element of the immune system’s defence against cancer cells.
By manipulating cholesterol levels, the researchers were able to improve the function of the STING protein, thereby opening up new ways of bolstering the body’s natural defences against cancer.
Effective cancer treatment depends on the strength of the patient’s immune system and how well it can be boosted to kill cancer cells.

According to Martin Roelsgaard Jakobsen, cancer treatment requires a combination of treatment strategies that trigger local immune activation in the tumour, attract cytotoxic T cells, and stimulate broader activation of immune cells.
And this is where the new mechanism presents new opportunities.
“The STING protein has already shown promise in cancer treatment, but we haven’t yet discovered how to activate it in a clinical context. Our research provides a new approach to boosting the activity of the STING protein, giving us another way of harnessing the body’s natural defences against cancer,” he explains.
Result of cross-disciplinary collaboration
The study is the result of an interdisciplinary collaboration between researchers at Aarhus University and Aalborg University, including Martin Roelsgaard Jakobsen and Emil Kofod-Olsen, who are specialists in STING signalling and cancer immunology, and Baocun Zhang and Søren Riis Paludan, who have in-depth knowledge of the molecular biology of the STING protein and its role in a number of illnesses.
The combination of different disciplines has been crucial in linking cholesterol levels with immune responses to cancer.

“Our discovery is a direct result of bringing together experts from different fields. The collaboration has created a unique understanding of how we can fight back against cancer more effectively,” says Martin Roelsgaard Jakobsen.
Could pave the way for several drugs
The discovery of how cholesterol affects the STING protein not only opens new doors to cancer treatment. Researchers also expect the mechanism to play a role in the fight against a number of other illnesses.
“Thanks to increased knowledge about both the mechanism of action in the STING protein and how the protein contributes to a number of illnesses, it is now more likely that a number of new drugs against those illnesses can be developed,” says Professor Søren Riis Paludan.
This would include autoimmune diseases and neurodegenerative diseases, in which the immune system also plays a crucial role.

Anticoagulant treatments are crucial for managing many conditions, such as heart disease, stroke and venous thrombosis. Current options, however, carry an inherent risk of serious bleeding due to trauma or unforeseen events. A team from the University of Geneva (UNIGE) and the University of Sydney has developed a new anticoagulant, designed to have an on-demand reversible activity, with a fast-acting ”antidote”. This approach could revolutionise the use of anticoagulants in surgery or other applications. The mechanism of activation and deactivation of the active principle could also be used in immunotherapy. These results are published in Nature Biotechnology.
Anticoagulant therapies are essential for managing many conditions, such as heart disease, stroke, and venous thrombosis. However, current treatment options, such as heparin and warfarin, have major drawbacks, including the need for regular monitoring of blood coagulation and the risk of serious bleeding in the event of overdose or trauma. Around 15% of emergency hospital visits for adverse drug effect are attributable to complication with anticoagulant treatments (an estimated 235 000 case/year in the US), emphasizing the importance of developing new, safer, and more effective therapeutic options.
The group led by Nicolas Winssinger, professor in the Department of organic chemistry at the UNIGE Faculty of Science, in collaboration with Richard Payne, professor at the University of Sydney, has recently developed a new anticoagulant active ingredient with an ”antidote” to reverse its effect rapidly and specifically. This new active ingredient, presented in Nature Biotechnology, consists of two molecules targeting distinct sites of thrombin, a protein whose action is central for blood coagulation. After binding to thrombin, these two molecules combine to inhibit its activity, thereby reducing its coagulant effect. The antidote intervenes by dissociating these two molecules, thus neutralising the action of the active ingredient.
”This breakthrough goes beyond the development of a new anticoagulant and its associated antidote. The supramolecular approach proposed is remarkably flexible and can be easily adapted to other therapeutic targets. It is particularly promising in the field of immunotherapy,” explains Nicolas Winssinger, who directed this research.
A revolution for surgery
This new anticoagulant could offer a more reliable and easier-to-use option for surgical procedures. Heparin, commonly used in this field, is a mixture of polymers of different lengths extracted from pig intestine. The result is a highly variable action, requiring coagulation tests during surgery. The new synthetic anticoagulant developed by UNIGE could help solve the problems of purity and availability associated with heparin.
One of the breakthroughs in this work lies in the use of peptide nucleic acid (PNA) to link the two molecules that bind to thrombin. Two strands of PNA can come together via relatively weak bonds that are easy to break. The research team has shown that by introducing correctly designated strands of free PNA, it is possible to dissociate the two thrombin-binding molecules associated with each other. The free PNA strand thus deactivates the drug’s action. This is a major innovation in the field.
Useful for immunotherapy
Beyond the problem of anticoagulation, this supramolecular concept of activating/deactivating the active principle could be of major interest in the field of immunotherapy, particularly for CAR-T therapies. Although CAR-T therapies are major advances in the treatment of certain cancers in recent years, their use is associated with a significant risk of immune system overreaction (cytokine storm), which can be life-threatening. The ability to rapidly deactivate a treatment with an accessible antidote could therefore represent a crucial advance in improving the safety and efficacy of these therapies.

Queen Mary-led study reveals the most detailed picture yet of genetic contributors to blood pressure. The findings lead to improved polygenic risk scores, which will better predict blood pressure and risk for hypertension.
Researchers led by Queen Mary University of London and supported by the National Institute for Health and Care Research (NIHR) have discovered over a hundred new regions of the human genome, also known as genomic loci, that appear to influence a person’s blood pressure. In total, over 2,000 independent genetic signals for blood pressure are now reported, demonstrating that blood pressure is a highly complex trait influenced by thousands of different genetic variants.
The study, published in Nature Genetics, is one of the largest such genomic studies of blood pressure to date, including data from over 1 million individuals and laying the groundwork for researchers to better understand how blood pressure is regulated.
To understand the genetics of blood pressure, the researchers combined four large datasets from genome-wide association studies (GWAS) of blood pressure and hypertension. After analysing the data, they found over 2,000 genomic loci linked to blood pressure, including 113 new regions. The analyses also implicated hundreds of previously unreported genes that affect blood pressure. Such insights could point to potential new drug targets, and help to advance precision medicine in the early detection and prevention of hypertension (high blood pressure).
From these analyses, the researchers were able to calculate polygenic risk scores, which combine the effects of all genetic variants together to predict blood pressure and risk for hypertension. For example, these risk scores show that individuals with highest genetic risk have mean systolic blood pressure levels which are ~17 mmHg higher than those with lowest genetic risk, and a 7-fold increased risk of hypertension. Therefore, these polygenic risk scores can discriminate between patients according to their hypertension risk, and reveal clinically meaningful differences in blood pressure.
“We have now revealed a much larger proportion of the genetic contribution of blood pressure than was previously known,” says Helen Warren, Senior Lecturer in Statistical Genetics at Queen Mary University of London and senior last author of the study. “We are making our polygenic risk scores data publicly available. There are many different potential applications of genetic risk scores, so it will be exciting to see how our blood pressure scores can be used to address more clinically relevant questions in the future.”
“This large study builds on over 18 years of blood pressure GWAS research. Our results provide new resources for understanding biological mechanisms and importantly new polygenic risk scores for early identification and stratification of people at risk for cardiovascular diseases” says Patricia Munroe, Professor of Molecular Medicine at Queen Mary University of London, also a senior author of the paper.
Polygenic risk scores have potential to serve as a useful tool in precision medicine, but more diverse genomic data is needed for them to be applicable broadly in routine health care. While the collected data was mostly from people of European ancestry (due to limited availability of diverse datasets when the study was started), the researchers found that the polygenic risk scores were also applicable to people of African ancestry, who have previously been underrepresented in genetic studies. This African ancestry result was confirmed through analysing data from the National Institute of Health’s (NIH) All of Us Research Program in the USA, which aims to build one of the largest biomedical data resources and accelerate research to improve human health.
An estimated 30% of adults in the UK have high blood pressure, known as hypertension. High blood pressure often runs in families, meaning that there is a genetic component to developing the condition in addition to environmental contributions such as a high-salt diet, lack of exercise, smoking and stress. When blood pressure is consistently too high, it can damage the heart and blood vessels throughout the body, increasing a person’s risk for heart disease, kidney disease, stroke and other conditions.
The study combined previously published genetic data from the UK Biobank, a large-scale biomedical database and research resource containing genetic and health information from half a million UK participants (N~450,000 individuals); the International Consortium for Blood Pressure (N~300,000 individuals combined from 77 different cohort studies); and the U.S. Department of Veterans Affairs’ Million Veteran Program (N~220,000 individuals), with new data from Vanderbilt University Medical Center’s biorepository, BioVU (N~50,000 individuals).

Researchers have discovered that the smooth muscle cells that line the arteries of people with atherosclerosis can change into new cell types and develop traits similar to cancer that worsen the disease. Atherosclerosis is characterized by a narrowing of arterial walls and can increase risk of coronary artery disease, stroke, peripheral artery disease, or kidney disorders. The findings, supported by the National Institutes of Health (NIH), could pave the way for the use of anti-cancer drugs to counteract the tumor-like mechanisms driving the buildup of plaque in the arteries, the major cause of cardiovascular disease.
“This discovery opens up a whole new dimension for our understanding about therapeutic strategies for the prevention and treatment of atherosclerosis,” said Ahmed Hasan, M.D., Ph.D., program director in the Division of Cardiovascular Sciences at the National Heart, Lung, and Blood Institute, part of NIH. “Previous research has suggested that atherosclerosis and cancer may share some similarities, but this association has not been fully described until now.”
Using a combination of molecular techniques in mouse models and tissue samples taken from patients with atherosclerosis, the researchers of the new study characterized the molecular mechanisms that drive the smooth muscle cells to transition into cancer-like cell types.
The researchers found increased rates of DNA damage and genomic instability — two hallmarks of cancer — in the converted smooth muscle cells of atherosclerotic plaque when compared to healthy tissue. Genomic instability is the increased tendency for DNA mutations and other genetic changes to occur during cell division.
Probing further, they also found that cancer-associated genes became more active as the smooth muscle cells were being reprogrammed into the cells that made up the plaque. Using a mouse model expressing a known cancer mutation accelerated the reprogramming and worsened atherosclerosis. Finally, treating atherosclerotic mice with the anti-cancer drug niraparib, which targets DNA damage, showed potential for preventing and treating atherosclerosis.
“In fact, we saw that niraparib actually shrinks the atherosclerotic plaques in mice,” said Huize Pan, Ph.D., assistant professor of medicine at Vanderbilt University Medical Center, Nashville, Tennessee, and first author of the study.
Muredach Reilly, M.D., professor of Medicine at Columbia University, New York City, and senior author on the study, explained that understanding the molecular mechanisms that are driving the transition of smooth muscle cells can provide opportunities to disrupt tumor-like pathways and change how the cell behaves, in turn preventing or slowing progression of atherosclerosis.

Researchers at the University of Toronto have found a way to better control the preclinical generation of key neurons depleted in Parkinson’s disease, pointing toward a new approach for a disease with no cure and few effective treatments.
The researchers used an antibody to selectively activate a receptor in a molecular signaling pathway to develop dopaminergic neurons. These neurons produce dopamine, a neurotransmitter critical to brain health.
Researchers around the world have been working to coax stem cells to differentiate into dopaminergic neurons, to replace those lost in patients living with Parkinson’s disease. But efforts have been hindered in part by an inability to target specific receptors and areas of the brain.
“We used synthetic antibodies that we had previously developed to target the Wnt signaling pathway,” said Stephane Angers, principal investigator on the study and director of the Donnelly Centre for Cellular and Molecular Biology.
“We can selectively activate this pathway to direct stem cells in the midbrain to develop into neurons by targeting specific receptors in the pathway,” said Angers, who is also a professor in the Leslie Dan Faculty of Pharmacy and the Temerty Faculty of Medicine, and holds the Charles H. Best Chair of Medical Research at U of T. “This activation method has not been explored before.”
The study was recently published in the journal Development.
Parkinson’s disease is the second-most common neurological disorder after Alzheimer’s, affecting over 100,000 Canadians. It particularly impacts older men, progressively impairing movement and causing pain as well as sleep and mental health issues.

Most previous research efforts to activate the Wnt signaling pathway have relied on a GSK3 enzyme inhibitor. This method involves multiple signaling pathways for stem cell proliferation and differentiation, which can lead to unintended effects on the newly produced neurons and activation of off-target cells.
“We developed an efficient method for stimulating stem cell differentiation to produce neural cells in the midbrain,” said Andy Yang, first author on the study and a PhD student at the Donnelly Centre. “Moreover, cells activated via the FZD5 receptor closely resemble dopaminergic neurons of natural origin.”
Another promising finding of the study was that implanting the artificially-produced neurons in a rodent model with Parkinson’s disease led to improvement of the rodent’s locomotive impairment.
“Our next step would be to continue using rodent or other suitable models to compare the outcomes of activating the FZD5 receptor and inhibiting GSK3,” said Yang. “These experiments will confirm which method is more effective in improving symptoms of Parkinson’s disease ahead of clinical trials.”
This research was supported by the University of Toronto Medicine by Design program, which receives funding from the Canada First Research Excellence Fund, and the Canadian Institutes of Health Research.

Researchers at the University of Sydney and University of Geneva have developed a new anticoagulant, whose anticlotting action can be rapidly stopped ‘on demand’. The result could lead to new surgical and post-operative drugs that minimise the risk of serious bleeding.
The research team applied a completely new method to discover the molecule. The anticoagulant combines a short protein molecule (a peptide) from a tsetse fly — a blood-feeding insect — with a second, synthesised peptide. The bonds holding the two peptides together can be broken on demand, providing the anticoagulant ingredient with its own on-off switch.
This new drug-discovery approach is a potential game-changer in surgery and for suppressing blood clots. It could also be applied in other fields such as immunotherapy.
The results are published today in Nature Biotechnology.
In addition to surgical applications, anticoagulant therapies are essential for managing a wide range of conditions, such as heart disease, stroke and venous thrombosis. However, current treatment options, such as heparin and warfarin, have major drawbacks, including the need for regular monitoring of blood coagulation and the risk of serious bleeding in the event of overdose.
About 15 percent of emergency hospital admissions due to adverse drug reactions are attributable to complications from anticoagulant treatments, emphasising the importance of developing new, safer and more effective therapeutic options.
Professor Rich Payne from the School of Chemistry is an NHMRC Investigator Leadership Fellow and Deputy Director of the ARC Centre of Excellence for Innovations in Peptide and Protein Science (CIPPS) and is a coauthor of the research.

He said: “What’s exciting here is that we have applied a completely novel approach to drug discovery. The anticoagulant we have developed uses what we call supramolecular chemistry. This allows the two active molecules needed to suppress coagulation to self-assemble.
“The architecture also means we can apply an antidote that can quickly disassemble the joined molecules, triggering a rapid cessation of the active combination and the anticoagulant effect.
“This has never been done before in drug discovery.”
Research lead, Professor Nicolas Winssinger from the Department of Organic Chemistry at the University of Geneva, said: “This result goes beyond the development of a new anticoagulant and its associated antidote. The supramolecular approach proposed is remarkably flexible and can be easily adapted to other therapeutic targets. It is particularly promising in the field of immunotherapy.”
Revolution for surgery
The new anticoagulant could offer a more reliable and easier-to-use option for surgical procedures. Heparin, commonly used in this field, is a mixture of polymers of different lengths extracted from pig intestine. The use of heparin in the clinic is problematic due to the risk of serious bleeding side effects and requires coagulation tests during surgery. The new synthetic anticoagulant developed by the Geneva and Sydney team could help solve the problems of purity and availability associated with heparin.

One of the breakthroughs in this work lies in the use of a peptide nucleic acid (PNA) to link the two molecules that bind and block the action of thrombin, the enzyme that produces fibrin that makes up our blood clots.
In this case, the tsetse-fly-derived peptide molecule and a synthetic ketobenzothiazole containing peptide bind to two distinct sites on thrombin as a ‘supramolecule’ connected by a PNA double helical linker, similar in shape to DNA.
These two strands of PNA that make up the double helix can come together via relatively weak — non-covalent — bonds that can be broken when needed. The research team has shown that by introducing correctly matched strands of free PNA, it is possible to dissociate the two thrombin-binding molecules. The two free PNA strands are no longer active as anticoagulants. This is a major innovation in the field.
The tsetse fly peptide was developed in laboratories at the University of Sydney. Tests for the efficacy of the supramolecular anticoagulant were also tested at Sydney in human and mouse blood samples and also in vivo in mice.
Useful for immunotherapy
Beyond the problem of anticoagulation, this supramolecular concept of activating and deactivating the active principle could be of significant interest in the field of immunotherapy, particularly for CAR-T therapies.
Although CAR-T therapies are one of the major advances in the treatment of certain cancers in recent years, their use is associated with a significant risk of immune system storm, which can be fatal. The ability to rapidly deactivate treatment with an accessible antidote could be a crucial advance in improving the safety and efficacy of CART-T therapies.

Millions of working parents know the routine: bustle the kids off to childcare in the morning, work all day, then fight the daily traffic jams to get the kids back home. Something to drink, maybe a snack to munch, can help ease the commute.
Understandably, few parents take the time to think about the nutrients or calories involved, but experts at Cincinnati Children’s decided to take a closer look. Their eyebrow-raising findings were published April 27, 2024, in the journal Children’s Health Care.
The researchers took a fresh look at older data contained in daily food journals kept by more than 300 families of children who attended 30 childcare centers that participated in the Preschool Eating and Activity Study (2009-2011). They found that the hour after parents and caregivers picked up their children stood out as a high-calorie, relatively less healthy part of the child’s overall diet.
Overall, these children, ages 3 to 5, consumed more than 1,471 calories across the entire day — an amount on the high end of recommended daily limits. Of that amount, 290 calories, on average, were consumed in the hour after leaving day care. That’s about 20% of the day’s entire calorie intake.
Adding concern: after-care food and drink accounted for about 22% of the day’s added sugar and about one-third of the sweet and salty snack foods the children ate.
“Every parent knows how busy that time of day can feel. Parents can feel stressed, the kids may be cranky, hungry, or tired. There’s nothing wrong with treats once in a while,” says senior author Kristen Copeland, MD, Division of General and Community Pediatrics. “But that car ride home also can be an opportunity to instill healthier habits instead of less healthy ones.”
If busy parents want to try a small change that might make a big difference, consider stocking the car with veggie sticks, cheese, fruit slices, and low-sugar drinks such as water or milk. A few minutes of preparation can make it easier to skip the high-calorie drive-throughs and sugar-loaded packaged snacks.
“Children of preschool age are in a highly habit-forming time of their lives. They thrive on routine,” Copeland says. “Children often look forward to the car ride home, which makes that time an opportunity to start a healthy snacking habit that could last a lifetime.”

Cranberry extracts appear to improve intestinal microbiota and help prevent chronic diseases such as diabetes and cardiovascular diseases. The study of Université Laval and the Institute of Nutrition and Functional Foods (INAF) reported beneficial effects after only four days of use.
Cranberries and berries are associated with multiple health benefits, mainly attributed to their high content of polyphenols, in the form of tannins. They also contain high concentrations of oligosaccharides, small fibres that are thought to contribute to their bioactivity.
The research team, led by Yves Desjardins, professor at the Faculty of Agriculture and Food Sciences, showed that the polyphenols and oligosaccharides present in a cranberry extract boost the genus Bifidobacterium, associated with a reduced risk of diabetes and cardiometabolic diseases. “Normally, these bacteria are stimulated by dietary fibre consumption. We observed the same effect with cranberry extract with a dose almost 20 times lower,” points out Jacob Lessard-Lord, a postdoctoral fellow at INAF.
Cranberry extracts also stimulate the Akkermansia muciniphila bacterium, which plays an important role in the intestinal mucosa, helping to reduce inflammation and strengthen the intestinal barrier.
This is of particular interest when it comes to countering the harmful effects of a Western diet. “This diet alters the microbiota, causes inflammation of the mucosa, and compromises the integrity of the intestinal barrier, which plays a crucial role in protecting the body from bacteria present in the gut. Alteration of the intestinal barrier allows the passage of lipopolysaccharides (LPS) derived from the intestinal microbiota, known as metabolic endotoxemia, and is a crucial factor in the onset and progression of inflammation and metabolic diseases,” explains Yves Desjardins.
“The constant inflammation that results from the presence of LPS in the body can lead to several chronic diseases, including diabetes, and cardiovascular disease,” he explains.
When included into a balanced diet, cranberry extracts could modify the inflammatory pathway and improve the prognosis of a chronic disease. By stimulating Akkermansia muciniphila bacterium and Bifidobacterium, the microbiota regenerates and recreates an anti-inflammatory environment. This results in strengthening the connections between the cells of the intestinal barrier, thereby fortifying it.

In the study, approximately forty participants recruited at INAF were instructed to consume a cranberry supplement in capsule form twice daily, morning and evening, which is equivalent to ingesting 60 grams of fresh cranberries. At the beginning of the experiment and after four days, samples of plasma, urine, and stool were collected from participants. The human study was initiated following promising results in the SHIME in vitro system, which reproduces regions of the intestine.
The research team is now interested in exploring the long-term effects of the extracts. “It’s promising to see a beneficial effect after just four days,” expresses Jacob Lessard-Lord with enthusiasm.
Although cranberries had a beneficial effect on all participants, the results highlighted variability in their responses. Future research will identify which microbiota signatures respond best to the extracts.
The study was conducted as part of the NSERC-Symrise Industrial Research Chair on the prebiotic effect of fruit and vegetable polyphenols (PhenoBio+). Symrise has launched a product based on the team’s findings, Prebiocran, which has been approved in Europe.
The study was published in the scientific journal npj Biofilms & Microbiomes. The authors are Jacob Lessard-Lord, Charlène Roussel, Joseph Lupien-Meilleur, Pamela Généreux, Véronique Richard, Valérie Guay, Denis Roy and Yves Desjardins.