Author: ModernMedia

Pope Leo XIV’s Lung Cancer Highlights Growing Number of Nonsmokers Diagnosed with the Disease – And Younger People Too

By Edgar Beltrán, The Pillar – Own work, CC BY-SA 4.0, Link

Estelamari Rodriguez, University of Miami

When many people think of an average lung cancer patient, they often imagine an older man smoking. But the face of lung cancer has changed. Over the past 15 years, more women, never smokers and younger people are being diagnosed with lung cancer.

In fact, lung cancer is the leading cause of cancer death among women, and more women die from lung cancer than breast, ovarian and colorectal cancer each year. The American Lung Association reports that while lung cancer rates have risen by 79% for women over the last 44 years, they decreased by 43% for men. And for the first time in history, there are more young women than men diagnosed with lung cancer.

News about Pope Leo XIV’s lung cancer diagnosis on Oct. 13, 2026, sparked discussion about increasing rates of the disease among people who have never smoked. Leo reportedly is not a smoker. Potential causes for the disease include environmental exposures and genetics, and recognising the diverse factors that can increase someone’s risk of lung cancer – regardless of their smoking history – is essential for timely and appropriate screening and treatment.

Cancer that is found at the earliest stages, like that of the pope, can be treated with surgery and cured for both smokers and nonsmokers. The challenge is that people who have never smoked are not currently included in lung cancer screening guidelines, and tumours are often only found by chance.

As a thoracic oncologist, I have seen many younger women and never smokers walk into my clinic with a new diagnosis of lung cancer. Particularly for never smokers, lung cancer is unexpected for both patients and their doctors, which can often lead to delays in diagnosis. Researchers have described this trend of increasing lung cancer rates among women in different parts of the world and are starting to understand why cases are on the rise.

Lung cancer in women

The first explanation of why rates of lung cancer in women have increased is that many started smoking later than men, pushing back their peak in smoking-related lung cancer diagnoses.

Women also started smoking in the years when filtered cigarettes were most commonly used. This led to an increased risk of a type of cancer called adenocarcinoma due to the way cigarette filters distribute tobacco smoke to the outer parts of the lungs. Some studies suggest that women are more susceptible to the carcinogenic effects of exposure to tobacco and cigarette smoke, including second-hand smoke, and may develop lung cancer after fewer years of smoking compared to men.

However, it is important to note that most people diagnosed today with lung cancer are not active smokers. About 20% of women with lung cancer have never smoked – higher than for men with lung cancer who’ve never smoked. An increasing number of lung cancer diagnoses are among people who never smoked.

Lung cancer risk factors

Besides smoking and secondhand smoke, there are several other lung cancer risk factors. These include a family history of cancer and exposure to asbestos, radon and air pollution.

Exposure to carcinogens in the workplace in the form of inhaled chemicals such as arsenic, beryllium, cadmium, silica and nickel is still a concern in some parts of the world. The potential lung cancer risk of e-cigarette and marijuana smoke is still under study but of potential concern.

Recently, researchers have also found that genetics can play a role in lung cancer risk in some patients with a strong history of lung cancer. Studies of these families have helped identify potential susceptibility genes for lung cancer and environmental risk factors.

Like BRCA1 and BRCA2 in breast cancer, alterations in genes that promote or protect against tumour development can contribute to lung cancer development. Researchers have yet to identify specific mutations that may predispose individuals to lung cancer. However, studying familial genetic predispositions can help elucidate how lung cancer develops and lead to new biomarkers for early cancer detection in high-risk groups.

Lung cancer screening

In 2021, the United States Preventive Services Task Force updated its lung cancer screening guidelines to include younger patients with less smoking history. Now, lung cancer screening is recommended for adults ages 50 to 80 who have smoked at least one pack per day for 20 years, current smokers and former smokers who quit smoking within the last 15 years. Women at risk for lung cancer can talk to their doctors about ordering a low-dose CT scan for lung cancer screening.

Nationwide, more than 70% of eligible women undergo breast cancer screening but less than 6% of all eligible smokers pursue lung cancer screening. Researchers estimate that these new screening guidelines will increase the number of women eligible for lung cancer screening by 40% by including those at a younger age who have less smoking exposure.

A low-dose CT scan can help with early detection of lung cancer. In this image, the tumour is the white nodule in the upper right corner of the black space. Atlas of Pulmonary Pathology/Flickr, CC BY-SA

Lung cancer diagnosis

In recent years, increasing understanding of the genetic changes that can lead to cancer and how to harness the immune system to treat cancer has led to new targeted therapies and immunotherapies that have improved the prognosis of patients with lung cancer. Women tend to have a better lung cancer prognosis than men, especially if they never smoked and have tumours with molecular changes that can be treated with targeted therapies.

However, lung cancer symptoms may go unrecognised in women. Symptoms of lung cancer can include coughing, shortness of breath, overwhelming fatigue and pain in the back, chest or shoulder, which could be confused for other ailments. Because women tend to be slightly younger when diagnosed than men, patients may be able to tolerate symptoms longer and delay seeking medical attention. Physicians also might not attribute these symptoms to lung cancer due to a patient’s younger age.

Recognising the early symptoms of lung cancer, expanding lung cancer screening eligibility and testing for genetic biomarkers to select the best therapy are some of the steps that could help address the global epidemic of lung cancer in women.

This is an updated version of an article published on Feb. 1, 2023.

Estelamari Rodriguez, Associate Director of Community Outreach in Thoracic Oncology, University of Miami

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

Researchers Explore Gut & Brain Health Link for People with HIV

Irritable bowel syndrome. Credit: Scientific Animations CC4.0

Oregon Health & Science University researchers have secured a $5.8 million, five-year federal award to investigate whether damage to the gastrointestinal tract contributes to neuroinflammation in people living with HIV – raising the potential for new treatments to preserve brain function in people with HIV and older adults.

“Even though antiretroviral drugs are very successful at suppressing the virus, we’ve seen people living with HIV have neurocognitive disorders similar to what happens when people age,” said co-lead investigator Afam Okoye PhD (professor, OHSU Vaccine & Gene Therapy Institute). “If we can show a dynamic relationship between inflammation in the gut and the brain, this line of research could then lead to new treatments to reduce neuroinflammation.”

The award from the National Institute of Mental Health of the National Institutes of Health will enable researchers to align nonhuman primate models with human autopsy tissues to better understand the interplay between inflammation in the gut and brain health among people living with HIV.

Scientists have long associated inflammation in the gastrointestinal tract with impaired cognition in the brain. People with inflammatory bowel disease are at increased risk for Parkinson’s and Alzheimer’s disease, for example.

This problem disproportionately affects people living with HIV.

Researchers surmise this may be related to the fact that the initial infection of the virus – even when it’s subsequently held in check by antiretroviral therapies – causes lasting damage to immune cells in the GI tract. The research team will include pathologists at OHSU and infectious disease specialists at the NIH to better characterise how exactly inflammation in the gut is linked to brain function.

The research also will involve nonhuman primates at OHSU’s Oregon National Primate Research Center.

“Neuroinflammation in people with HIV is very hard to study,” said Okoye (also Division of Pathobiology and Immunology, ONPRC). “These are very challenging studies to do, but we have expertise and experience in the nonhuman primate model. It’s high risk but also high reward.”

Ultimately, it may be possible to develop targeted therapies that tamp down harmful or runaway inflammation while retaining the beneficial effects of a strong immune system.

“Inflammation in and of itself is not bad,” said co-lead investigator Jacob Estes PhD (professor and director of the VGTI). “It’s part of the immune system’s response to mediate infection. Ultimately, this research could lead to precision targets that would limit pathology that harms brain function but doesn’t completely shut off the immune system’s ability to do the things it needs to do to promote health.”

Source: Oregon Health & Science University

New Research on Botticelli’s Venus Uncovers a Pituitary Tumour

By Sandro Botticelli – Adjusted levels from File:Sandro Botticelli – La nascita di Venere – Google Art Project.jpg, originally from Google Art Project. Compression Photoshop level 9., Public Domain, Link

New evidence supporting the theory that Botticelli’s Venus died from a pituitary tumour was published on Monday.

The Medical Humanities paper published by the BMJ is the third in a series of papers led by Professor Paolo Pozzilli, in which he has set out his research on the Renaissance aristocrat Simonetta Vespucci, Sandro Botticelli’s muse, who died at just 23 from suspected tuberculosis.

Simonetta Vespucci (c. 1453–1476), born Simonetta Cattaneo in Genoa, was a Renaissance beauty dubbed “La Bella Simonetta.” Married at 16 to Marco Vespucci, she captivated Florence’s elite, including the Medici family.

Botticelli painted her in both The Birth of Venus and Primavera, and was so devoted to her that he asked to be buried at her feet. The “Venus squint” made famous in her paintings was copied by other artists and became a hallmark of Renaissance beauty.

Professor Paolo Pozzilli’s previous examination of documents about her death, and of the portraits, suggested an expanding pituitary tumour led to pituitary apoplexy, an acute condition ending in bleeding and death. This may have been sparked by dancing, or a violent rape – both suggested by the historical record.

In the latest paper, Pozzilli’s team examines Botticelli’s depiction of Vespucci’s eyes in the famous Birth of Venus, and in other portraits of her.

The findings support the original hypothesis. They describe swelling around the woman’s eyes, particularly her left eye. The tissue covering the white part of the eye is loose or folded, and the tissue underneath is swollen with fluid.

These changes, together with a squint (where the eyes do not point in the same direction), may be associated with a large tumour of the pituitary gland. There is also some swelling around her right eye.

Paolo Pozzilli (Honorary Professor of Diabetes and Clinical Research, Queen Mary University of London) said: “Sandro Botticelli was a brilliant artist who depicted his subjects with great realism. So it is not surprising that he’s left medical evidence in his paintings that we are able to read centuries later. The squint (‘strabismus’) of Venus in Simonetta Vespucci’s portraits embodies a poignant paradox: once exalted as the epitome of divine allure in Renaissance art and copied by artists like Bronzino, it now reveals itself as a subtle harbinger of her doom.”

Source: Queen Mary University London

Prescriptions for Nature Could Fight the ‘Epidemic of Loneliness’

Photo by Henry Xu on Unsplash

About one in three Americans and one in six people worldwide feel lonely on a regular basis, a troubling reality that has prompted some public health officials to declare an ‘epidemic of loneliness’.

A new global study presents a novel remedy. It found that nature-based social prescribing – clinicians literally prescribing things like gardening, hiking or birdwatching – can significantly reduce loneliness. Spending time in nature with others works even better, particularly for the loneliest among us, the study found.

“There has been a lot of passion about nature-based prescriptions, but not a lot of evidence,” said corresponding author Jill Litt (professor of environmental health, CU Boulder; principal investigator, RECETAS project).

Thus far, all the trials have shown promising results. The latest findings, looking at 320 lonely adults in Barcelona, appear in the October issue of Lancet Regional Health.

“We now have randomised controlled trials showing this works and the impacts last,” said Litt.

Loneliness is not about being physically isolated. Rather, it is a “subjective disconnect between one’s expectations of their social relationships and one’s reality.”

“I’ve heard people describe it like a knot in their stomach, like something is just not right,” said Litt. “You could be in a room full of people and still feel lonely.”

Chronic loneliness can increase risk of cardiovascular disease, dementia, stroke, depression and anxiety. It can also burden the healthcare system, as people suffering from loneliness tend to visit their doctor more and are more likely to visit the emergency department with vague complaints on Friday afternoons – a phenomenon known as “Friday afternoon syndrome.”

Due to stigma, people are often reluctant to admit or don’t recognise they are lonely and assume the physical symptoms they feel are due to something else.

“Once clinicians really start to drill down to the root causes, they discover that loneliness is a big factor and the solutions may lie outside the traditional medical system,” said Litt (also a researcher with the Barcelona Institute for Global Health).

RECETAS (Re-imagining Environments for Connection and Engagement) was launched in 2021 with a $5.6 million grant from the European Union. It has since conducted randomised controlled trials in Barcelona, Spain; Prague, Czech Republic; and Helsinki, Finland; and quasi-experimental studies in Marseille, France; Cuenca, Ecuador; and Melbourne, Australia.

The newest findings centre around the site in Barcelona.

The study included 320 lonely older adults from 12 low-income neighbourhoods. Half were placed in a group of 8–10, which spent two hours weekly for nine weeks together doing things like gardening, birdwatching or nature-based art programmes along with two trained facilitators. The other half were provided the same menu of free, easily accessible nature-based activities that they could do on their own. Both strategies worked. Participants on average showed an 11% reduction in loneliness scores at three months; 12% at six months; and 17% at one year. For those who started with lower emotional wellbeing, the group intervention worked better.

Litt said that nature, with its vivid sounds, smells and sights, can act as an “additional facilitator,” augmenting therapeutic benefits.

Even being in nature alone can alleviate loneliness, the research suggests.

“Being out in nature forms this kind of reservoir of calm that we can return to later in life during stressful times,” said Louise Chawla (environmental psychologist and professor emerita, CU Boulder), who recently co-authored another paper with Litt about the role that nature can play in fostering social connections. “It’s not just restorative when you are in a place but also when you go back to it in memory.”

Public health agencies in Spain have already begun to recognise the Friends in Nature model as a best-practice for addressing the loneliness epidemic. Litt is now working to bring similar trials to the US in hopes that someday, insurers might cover things like a membership in a community garden or birdwatching club.

“We have nature in our cities and investment in our green infrastructure,” she said. “Now we need a mechanism to bridge these resources with our health systems to offer person-centred care that leverages the power of nature for healing and wellbeing.”

RECETAS project: https://www.recetasproject.eu/

Source: University of Boulder Colorado

Smoking May Affect Fertility in Both Men and Women, New Study Finds

Photo by Sara Kurfess on Unsplash

New research has shed light on how exposure to cigarette smoke could affect reproductive health in both men and women, identifying changes in biological processes involved in ovarian function and sperm production.

The study, led by researchers from the Universities of Nottingham and Sheffield and published in Frontiers, provides new insight into potential mechanisms linking smoking with reproductive health.

Infertility affects a significant proportion of people of reproductive age worldwide. According to the World Health Organization, approximately one in six people globally experience infertility at some point during their reproductive years.

In this study, researchers used a mouse model to examine the effects of different levels of cigarette-smoke exposure on the ovaries and testes, focusing on changes to reproductive tissues and the activity of genes involved in their normal function.

In females, the number and structure of ovarian follicles showed relatively little change following exposure, even at higher levels. However, researchers identified clear changes in the activity of numerous genes.

Genes involved in cell division and metabolism became less active, while genes associated with protein production became more active. The pattern of gene activity showed similarities with biological processes previously associated with ovarian ageing and reduced ovarian function.

In males, higher levels of smoke exposure were associated with changes to structures within the testes, including enlargement of the seminiferous tubules. Researchers also identified changes in the activity of genes involved in sperm production, immune responses and cell signalling.

Some genes associated with sperm production became more active, while others involved in immune function became less active. The findings suggest that cigarette-smoke exposure may alter biological processes important for normal testicular function and sperm development.

The researchers say the findings add to existing evidence about the potential impact of smoking on reproductive health and highlight the need to better understand the biological mechanisms involved.

Professor Lucy Fairclough (School of Life Sciences, University of Nottingham), co-author, said: “Our study has identified potential biological mechanisms that could help explain the link between smoking and reproductive health in both men and women.

“In females, we identified changes in gene activity associated with biological processes that have previously been linked to ovarian ageing and reduced ovarian function. In males, we found changes in genes involved in sperm production and testicular function.

“These findings are important because they help us understand how exposure to cigarette smoke could affect reproductive health. Further research will be needed to establish how these biological changes relate to fertility in humans.”

Dr Adam Watkins (University of Sheffield) said: “While it is well-established that smoking is harmful for your reproductive health, the exact mechanisms are not fully understood. Our mouse study has enabled us to explore how the ovaries and testes respond following exposure to cigarette smoke. Interestingly, our study shows that the ovary and testis respond differently to the cigarette smoke. We observed that while the structure of the ovary was unaltered, the testis showed measurable changes in its morphology. Within the ovary, we identified changes in genes that regulate cell proliferation and the synthesis of proteins, while in the testis, genes regulating sperm production were altered.

“While our study only assessed the effects of cigarette smoke on the ovaries and testes, it does provide new mechanistic insight into how parental smoking shapes their reproductive health.”

Source: University of Sheffield

SGLT-2 Inhibitors Lower CVD-Linked Inflammation

Photo by Towfiqu barbhuiya

For the first time in a human trial, SGLT2 inhibitors have been shown to reduce circulating inflammatory cells linked to cardiovascular disease, in addition to their established effects on glycaemia and body weight. The findings were published in Circulation.

“There had been some suggestive studies in animals with these medications indicating they might be modulating the immune system – affecting inflammation – but that hadn’t really been shown in humans,” said Dr Mona Mashayekhi (Division of Diabetes, Endocrinology and Metabolism, Vanderbilt Health). “This study provides the first direct evidence of SGLT2 inhibitors altering human immune cells which may potentially reduce cardiovascular risk.

“This finding is significant because it’s the first time this medication has been shown to have an immune effect at the cellular level with some specificity. If we understand how these medicines are reducing obesity-associated inflammation and heart disease and kidney disease, then we can identify the best patient for this treatment or discover other drug targets in that pathway that could really be beneficial.”

The research team enrolled 16 women with obesity and prediabetes and treated them with empagliflozin. Baseline assessments were performed, followed by three months of treatment. Immune changes were also reviewed in a comparator cohort of women who followed a low-calorie diet for three months. Measurements were taken at two weeks and at three months.

Using genetic sequencing and cellular imaging, investigators found that monocyte–platelet aggregates (MPAs) were significantly decreased. Individuals receiving empagliflozin showed a significant reduction in MPAs within two weeks, with a further decrease by week 12. Only the medication group exhibited reduced MPAs, indicating effects beyond weight loss.

Investigators also documented metabolic reprogramming of circulating monocytes, which shifted from a hyper-inflammatory state toward a more stable phenotype oriented toward normal cellular energy metabolism.

Mashayekhi and colleagues have begun a randomised placebo-controlled trial (planned n = 74) of participants with obesity and metabolic syndrome, currently recruiting at Vanderbilt Health. Immune measures will be assessed over three months as in the pilot; adipose tissue will also be sampled and analysed.

By Jill Clendening

Source: Vanderbilt University Medical Center

What’s the Best Way to Avoid Weight Regain After Stopping GLP-1 Therapy?

Photo by I Yunmai on Unsplash

Glucagon-like peptide-1 (GLP-1) receptor agonists are effective treatments for obesity, but discontinuation is common due to cost, insurance coverage limitations, side effects, patient preference, and other factors – commonly leading to rapid weight regain. Results from a pilot randomised trial, which are published in Obesity Science & Practice, suggest that structured support may attenuate early weight gain after GLP-1 cessation.

In the trial, 39 adults with prior GLP-1-induced weight loss were randomised to usual care, a digital wellness application, or medically tailored meals at the time of GLP-1 cessation, continuing for 4 months.

Surveys showed that diet quality, perceived health, adherence, and satisfaction did not differ significantly by group, though some estimates suggested possible trends favouring the wellness application. Relative to the control group, the other groups experienced less weight gain. Over 4 months, participants in the control group gained an estimated 10.75% body weight, compared with 3.60% in the wellness application group and 3.58% in the medically tailored meals group.

“People invest significant time and effort in improving their health and achieving weight loss,” said corresponding author Kelseanna Hollis-Hansen, PhD, MPH, of Tufts University Food is Medicine Institute. “We need evidence-based strategies to support them if and when they discontinue GLP-1 medication, so they can maintain those gains and continue building long-term health, vitality, and well-being.”

Source: Wiley

Pig Kidney Xenotransplant Successfully Bridges Patient to Human Transplant

Photo by César Badilla Miranda on Unsplash

In January 2026, Tim Andrews, who had received a genetically edited pig kidney in January 2025, became the recipient of a human kidney. A new Mass General Brigham paper, published in The Lancet, details Andrews’ experience and how xenotransplantation could bridge the gap between end-stage kidney failure and a human transplant, allowing a patient to forgo dialysis in the meantime.

Authors report that Andrews, 66 at the time of xenotransplantation, successfully lived with the genetically edited kidney for 271 days – during which he did not need dialysis – before receiving a human kidney from a donor. His case represents the longest dialysis-free survival following porcine kidney xenotransplantation in a living human and the first transition to human kidney transplantation.

A record-setting bridge transplant

“The organ shortage is the greatest crisis we have right now in transplantation,” said lead author Leonardo Riella, MD, PhD, of the Center for Transplantation Sciences and the Division of Nephrology at Mass General Brigham.

“We know that the best treatment option for patients with end-stage kidney disease who have developed renal failure is transplantation, but we simply don’t have enough human organs to transplant in a timely manner. Our vision is that xenotransplantation could help address this gap – initially as a bridge to get patients off dialysis while they wait for a human donor kidney, and potentially, as we establish long-term safety and durability, as a destination therapy in its own right.”

How the pig kidney performed

The world’s first porcine kidney xenotransplant to a living human recipient occurred in 2024 at Massachusetts General Hospital, with the patient surviving 52 days before death from cardiac causes unrelated to the transplant. No previous studies have documented xenograft survival beyond two months, a successful “bridge” to receipt of a human organ, or the mechanisms leading to late xenograft failure in living recipients.

Andrews received the genetically engineered pig kidney under an FDA Expanded Access Investigational New Drug application. He was then monitored for kidney function, rejection, antibody development and potential pig-to-human infection. The kidney functioned immediately. An early episode of T-cell-mediated rejection resolved with treatment, no pig pathogen transmission was detected, and the patient was able to go without dialysis for 271 days.

After approximately six months, immunosuppression was reduced in the setting of infection. The xenotransplant subsequently developed microvascular injury and inflammation that progressed to organ failure. The patient then received a deceased-donor human kidney, with immediate graft function and no evidence of sensitization during follow-up.

Lessons from late graft failure

The findings illustrate both the promise and areas for improvement for xenotransplants as a bridge for patients awaiting human kidneys. Importantly, the microvascular injury to the porcine kidney has implications for the development of immunosuppressive strategies, donor genetic engineering and monitoring in future clinical transplantation studies.

“Mass General Brigham has a strong history of kidney transplantation, beginning with the first live donor kidney transplant in 1954,” said senior author Tatsuo Kawai, MD, PhD, director of the Legorreta Center for Clinical Transplantation Tolerance at Mass General Brigham. “Our findings continue that history by both furthering what we know about xenotransplants and generating knowledge that could be applied to other organ transplantation work.”

“The patients are the true pioneers here,” added Riella. “By stepping forward and being willing to participate in these early-stage studies, they are advancing the science. Without their trust and courage, we would not be able to do what we do.”

Source: Mass General Brigham

Atypical B Cells Found to Switch Roles During Infection

Scanning electron micrograph of a B cell. Credit: NIH

Researchers at Karolinska Institutet have mapped how so-called atypical B cells develop and change function over time. The study, published in The EMBO Journal, shows that the cells do not constitute a uniform group but instead follow several developmental pathways that converge on a common end stage. The findings may help explain why atypical B cells have previously been linked to different roles in the immune system.

B cells are an important part of the immune system and help the body recognise and fight infections. A group of B cells known as atypical B cells has attracted considerable interest among researchers in recent years. They occur in several infections, but also in connection with vaccinations and certain inflammatory diseases. Despite extensive research, it has long remained unclear how these cells arise and what function they serve. 

In the new study, the researchers analysed blood samples from people who had experienced malaria as well as from healthy blood donors. By combining several advanced methods, they were able to track the development of individual B cells and examine how their properties changed over time. 

Atypical B cells develop in several stages

The results show that atypical B cells are not a distinct cell type but rather exist along a continuum with early, intermediate and late developmental stages. The researchers identified three cell-surface markers, CD11c, CD24 and CD27, which made it possible to follow this progression. 

“We show that atypical B cells can be understood as a continuous developmental process rather than as a fixed and clearly defined group of cells,” says Christopher Sundling, researcher at the Department of Medicine, Solna, Karolinska Institutet, and corresponding author of the study. 

The study also shows that the function of the cells changes as they develop. The early stages had a greater capacity to develop into antibody-producing cells and to produce cytokines, signalling molecules that help different parts of the immune system communicate with one another. 

In the later stages, the cells instead acquired characteristics suggesting that they are better able to capture and present foreign substances to other immune cells. The researchers also found that the late-stage cells had a greater capacity to associate with microbial particles. 

May have different origins

Another important observation was that atypical B cells may have several different origins. The researchers found evidence that they arise from different types of memory B cells that follow parallel developmental pathways but eventually reach a similar late stage. 

“Our results show that the function of these cells changes gradually during development. This may help explain why previous studies have described atypical B cells in different ways and assigned them different roles in the immune system,” says Alan-Dine Courey-Ghaouzi, doctoral student and first author of the study. 

The researchers emphasise that the study was carried out in the context of malaria, but that the findings are likely to reflect general principles of how atypical B cells develop in other infections and inflammatory conditions as well. 

Source: Karolinska Institutet

Study may Explain why IBD Patients React to Previously Tolerated Foods

Gut inflammation may alter how bacteria process food.

Irritable bowel syndrome. Credit: Scientific Animations CC4.0

A new study published in Gastroenterology finds that gut inflammation can change how gut bacteria break down food, possibly triggering immune reactions to foods that were previously tolerated. The findings may help explain why many people with IBD react adversely to foods such as dairy or gluten, even in remission.

About two-thirds of patients with IBD report food intolerances. Dairy, wheat and fibre are the most frequently blamed triggers, but the mechanisms have remained unclear.

The gut microbiota may hold the answer. Prior research has shown that patients with IBD often have an altered microbiota. This study identifies a novel mechanism by which that alteration drives food reactions.

“The microbiome acts as a metabolic organ, helping us digest food components, including those that can trigger gut reactions,” said Dr Alberto Caminero. “Our study shows that inflammation impairs this microbial digestive capacity, potentially contributing to adverse food reactions and opening new possibilities for microbiome-based therapies to restore this function in patients with IBD.”

Other key authors from McMaster University Medical Centre included Dr Bruna Barbosa and senior clinical collaborators Dr Neeraj Narula and Dr Premysl Bercik.

Using two mouse models of colitis, researchers found that inflammation made animals more prone to developing food sensitivities. After inflammation, exposure to dairy or gluten triggered an allergic-type immune response in the colon; reintroducing those foods later caused heightened gut sensitivity and worse colitis symptoms.

The cause traced back to the microbiota: inflammation depleted the specific bacteria that normally break down these food triggers. That shift alone was enough to increase sensitisation risk – transferring gut bacteria from inflamed mice into germ-free mice made those mice more prone to sensitisation to the same foods, while restoring the missing bacteria reduced these effects.

The pattern held in humans, too. Among patients with IBD, those who self-reported food intolerances were more likely to have both a reduced ability to break down common trigger foods and lower levels of the bacteria responsible for that job.

The researchers note that microbiota disruption is likely just one piece of a larger picture that also includes genetics, infections and stress – all of which need further research.

Together, the findings point to a possible mechanism behind food sensitivities in IBD: inflammation disrupts the gut bacteria that normally process certain foods, and this disruption – not the foods themselves – helps trigger the immune reactions patients experience.

Source: American Gastroenterological Association