Now, in a Commentary published in Med, Emily Hoedt and Nicholas Talley at the University of Newcastle in Callaghan, Australia, argue that effective treatment of IBD requires an approach combining tailored donors, microbiota analysis, and diet. “To move forward, we must embrace a more nuanced, personalized approach,” they say.

Because disruptions to gut microbes are common in conditions such as IBD, including ulcerative colitis and Crohn’s disease, therapies aimed at restoring the microbiota have gained increasing attention. Fecal microbiota transplants have shown promise, particularly in ulcerative colitis, but responses remain variable, and success appears to depend on donor characteristics. 

Diet, especially fiber intake, is thought to support microbial recovery, yet clinical results are inconsistent. While certain fibers can promote beneficial bacteria such as Faecalibacterium prausnitzii, many patients do not to improve or even experience worse symptoms. 

These mixed outcomes suggest that microbial presence alone may not be sufficient for treating disease, and that the functional capacity of the gut microbiota—such as the ability to degrade dietary fiber—may be critical, the authors say. However, they add, “mechanistic understandings of how food components influence disease activity are limited.”

Microbial function

Recent studies suggest that successful microbiota-based therapies depend not only on introducing beneficial microbes, but also on restoring microbial function. Fiber supplements, rather than improving outcomes for all patients, may have counterproductive effects if the recipient’s microbiota lacks the enzymes needed to degrade it or converts it into inflammatory metabolites.

The authors emphasize that beneficial clinical effects arise when engrafted microbes actively produce protective metabolites—such as short-chain fatty acids—and interact appropriately with the host’s immune system. This suggests that matching donors and recipients is important.

Beyond bacteria, also fungi and viruses may influence outcomes, indicating that microbial composition alone is less important than microbial functionality and host-microbe interactions for therapeutic success.

Lasting remission 

Supporting beneficial microbes while limiting inflammation can improve the effectiveness of microbiota-based therapies, the authors say. In the future, they add, larger studies will be essential to identify responders and guide precision nutrition.

Hoedt and Talley conclude that microbiota-based therapies such as fecal microbiota transplants cannot be optimized through a one-size-fits-all approach. Long-term remission in IBD and related conditions likely relies on personalized strategies combining donor selection, microbiota profiling, and tailored diet, the authors say.

“This will require interdisciplinary collaboration across microbiology, nutrition, immunology, and clinical medicine,” they add. “Only then can we unlock the full potential of microbiome-based therapies and achieve lasting remission for patients with chronic gastrointestinal diseases.”

The findings, published in Cell Host & Microbe, reveal a gut-testis interplay that may explain why low oxygen environments reduce male fertility at high altitudes.

In addition to low air pressure and oxygen levels, gut imbalances, diet, and microbial metabolites can also affect sperm. However, how gut changes at high altitudes cause sperm damage—and which bacteria and metabolites are involved—remains unclear.

So, researchers led by Jianchun Zhou at the Army Medical University in Chongqing, China, set out to study how sperm quality is affected by high-altitude low-oxygen conditions.

High-altitude conditions

In experiments with mice, males living at the equivalent of 5,800 meters produced fewer pregnancies when mated, had smaller testes, lower sperm concentration and motility, and showed structural damage in the sperm-producing tubules compared to males living at lower altitutdes. 

High-altitude low-oxygen conditions increased the levels of a bacterium called Clostridium symbiosum, which produces a metabolite called succinate. Giving mice either C. symbiosum or succinate lowered sperm quality, while a modified version of the bacterium that cannot make succinate did not. 

Succinate travels from the gut to the testis and harms sperm development by activating a type of immune cells that promote inflammation. These immunce cells release inflammatory molecules that trigger cell death in sperm-producing cells and boost inflammation, the researchers found.-

Improving sperm quality 

The gut microbiota from people living at high altitudes had higher levels of C. symbiosum and succinate than the microbiota of people living at low altitudes. And mice receiving gut microbiota from people living at high altitudes showed higher succinate levels, more inflammatory immune cells in their testes, and reduced sperm quality compared to mice receiving gut microbiota from people living at lower altitudes.

However, removing inflammatory immune cells or reducing succinate levels prevented sperm damage in mice, the researchers found.

The findings reveal a “gut-testis immune axis” and suggest that gut bacteria can indirectly harm sperm through immune signaling, the authors say. The results, they add, “provide insights into the potential targets for improving male sperm quality in [high-altitude] regions.”

Falcone explains that her group has identified alterations in microbiota-derived metabolites in patients with multiple sclerosis and has also shown that the gut microbiota can directly promote the activation of autoreactive T cells, which then migrate to peripheral organs and contribute to disease onset and progression. These findings open important clinical and therapeutic perspectives. Current strategies under investigation include the use of probiotics, dietary interventions, and fecal microbiota transfer, not only from healthy donors but potentially also from patients who respond well to immunoregulatory therapies.

For generations, one might say, we carpet-bombed the mouth with antiseptic mouthwash, marketed sterility as hygiene, and constructed entire health systems around the assumption that the oral cavity was a plumbing problem, disconnected from the rest of the body. The science is now telling a story so different that it borders on the embarrassing. These microbial communities regulate acidity, protect enamel, and perform a function that is only recently being understood at the mechanistic level: they convert dietary nitrate into nitric oxide, the molecule that controls blood vessel tone and blood pressure. A 2025 study from the University of Exeter, published in Free Radical Biology and Medicine, demonstrated this directly. When older adults drank nitrate-rich beetroot juice twice daily for two weeks, their oral microbiome shifted: harmful Prevotella declined, beneficial Neisseria increased, and blood pressure fell. The mechanism ran through the mouth. Destroy those bacterial communities with aggressive mouthwash and one interrupts the nitrate-nitric oxide pathway. Blood pressure rises. Periodontal dysbiosis has also been associated, in observational studies, with cardiovascular events and diabetes complications. A growing body of research is investigating possible links to neurodegenerative conditions, though causal pathways remain to be established. The mouth was never a silo. It was a sentinel. We treated it like the extremity of a tube.

And within the mouth, there is a surface that strikes me as the most overlooked diagnostic site in the human body: the tongue. Its dorsum hosts dense, structured bacterial communities organised in complex biofilms, and these communities are not passive. They are a primary site for the nitrate-nitrite-nitric oxide pathway that the Exeter study exploited. A 2026 study published in npj Biofilms and Microbiomes classified tongue microbiota from 729 individuals into three distinct orotypes, each associated with different metabolic and oral health outcomes, with temporal stability observed over six years. Separately, research has linked tongue microbiome alterations to conditions ranging from rheumatoid arthritis to gastrointestinal cancers to pneumonia in the elderly. The tongue, in other words, is a readable, persistent, individually variable biological surface that may one day function as a non-invasive diagnostic interface. And we are still telling patients to scrape it and move on.

This is changing, and faster than most clinicians appear to realise. Saliva carries over three thousand identified proteins, microbial signatures, metabolites, and immune markers. It is, if one thinks about it clearly, a liquid biopsy produced continuously without a needle. Researchers are training AI to read it: models that detect early signals of diabetes, cardiovascular disease, and kidney failure from salivary patterns alone. A team in China built an AI periodontitis screening tool with ninety-four percent accuracy on panoramic X-rays, designed not for private clinics but for underserved community health centres. The oral microbiome is becoming readable, actionable, predictive. And almost nobody in mainstream healthcare is paying attention.

At-home oral microbiome test kits already exist. One can order them today. A growing number of startups ship saliva collection devices to your door, sequence your oral bacteria, and return reports identifying the specific pathogenic species driving your cavities, your gum inflammation, your chronic bad breath. They map the ratio of beneficial to harmful organisms. They recommend targeted probiotics and dietary changes based on your actual microbial profile. Your dentist, in all likelihood, has never heard of any of them.

One must be fair. This is early. Different labs use different sequencing methods. The same saliva sample can produce meaningfully different results depending on who analyses it. Reference databases are incomplete. Standardisation is thin. The clinical evidence linking specific microbial profiles to specific interventions is growing but far from settled. This is a first generation, not a finished product. But the trajectory, I think, is obvious. As AI learns to read microbial patterns at scale, as sequencing costs continue to fall, as the science of the oral ecosystem catches up with the technology built to measure it, the precision will follow. It always does.

And the oral microbiome is not arriving alone. Biosensor patches are being developed that sit on the gum and track pH, inflammatory markers, and microbial shifts in real time. Smart toothbrushes embedded with high-definition oral scanners are entering the market, with imaging analysed by AI and reviewed by remote professionals. Hydroxyapatite toothpaste, which remineralises enamel without destroying the microbiome, has been standard in Japan since 1993, born from a NASA patent for astronaut bone loss, with over 160 million tubes sold across Asia and still virtually unknown in the West. In Japan, Dr Katsu Takahashi has begun human trials for a tooth regrowth drug, a peptide that reactivates dormant stem cells in the jawbone. At King’s College London, researchers grew early tooth-like structures in a laboratory in 2025. The liquid biopsy, the smart brush, the microbiome-compatible chemistry, the regenerative biology: these are not isolated innovations. They are converging.

Which brings us to the question that, to my mind, actually matters. What happens to the dentist? Not in the abstract. Concretely. What does the profession look like in 2035 when the mouth has become a data stream, when patients arrive already knowing their microbial profile, when AI has pre-screened their imaging before the appointment begins?

I see three scenarios. 

The first is inertia. One does nothing. Dental systems continue on a model designed decades ago: episodic, reactive, centred on repair. The microbiome stays a curiosity. The tools stay consumer gadgets. Western dental workforces keep shrinking under chronic shortages while chronic oral dysbiosis silently accelerates cardiovascular disease and cognitive decline in ageing populations. Nobody connects the dots because the microbiome was never woven into the care pathway. This is the default. It requires no decision. That is precisely what makes it dangerous.

The second is augmentation. Data-driven tools are layered onto the existing model. The dentist remains central but evolves into a clinician who interprets biological data, manages microbial ecosystems, and coordinates with primary care. AI pre-analyses scans. Microbiome reads inform treatment plans. Saliva-based screening flags systemic risk alongside periodontal risk. The chair stays, but what happens in it changes fundamentally. This is the pragmatic path and probably the necessary first step.

The third scenario is harder to picture but worth taking seriously. In this version, the bathroom becomes the first diagnostic room in the house. Continuous monitoring replaces periodic visits. Toothpaste is prescribed by algorithm, matched to the current state of the ecosystem. Quarterly saliva samples, analysed by AI, screen for systemic risk months before conventional symptoms appear. The dental surgery as a standalone institution dissolves into a broader oral health node integrated into primary care. The clinician still exists, but the centre of gravity shifts from the chair to the patient’s daily routine, from repair to cultivation, from the clinic to the home. Whether this is realistic in five years, fifteen, or fifty is genuinely open. But to dismiss it entirely is to ignore where every converging technology is pointing.

Whichever scenario unfolds, one principle holds. The oral microbiome is not a dental concern. It is a medical frontier. And it demands action now, not when the science is perfect, but while the systems that will deliver it can still be shaped. One must integrate microbiome screening into primary care. Subsidise microbiome-aware tools for the populations locked out of private care: saliva tests, smart brushes, AI triage deployed in pharmacies and schools. Shift the cultural narrative from sterilisation to cultivation. A healthy mouth is not a germ-free mouth. It is a balanced one. And redesign dental training now, because whichever future arrives, the clinicians who inhabit it will need fluency in microbiology, data science, and regenerative medicine, not just restorative technique.

Seven hundred species are broadcasting. They carry data about your heart, your metabolism, your brain. The tools to listen are arriving. The profession that should be listening the hardest is, so far, the quietest in the room. If dentistry does not claim this frontier, medicine will. And dentistry will have no one to blame but itself.

Et voilà.

The findings, published in Science Immunology, suggest that leveraging gut-lung interactions could offer new ways to prevent or reduce severe complications from respiratory viral infections.

One reason people get secondary infections after flu is that the virus damages lung immune cells called alveolar macrophages (AMs). SFB can help AMs stay strong during viral infections, but it’s unknown whether these microbes protect against secondary infections and how they might do so.

Researchers led by Vu Ngo at Georgia State University in Atlanta studied whether SFB protect mice from deadly bacterial infections after flu.

Boosting immunity

The team compared mice with and without SFB in their gut. Animals without SFB lost a lot of AMs and had severe lung infections after flu. In contrast, mice with SFB had strong AMs and showed much less lung damage and fewer bacteria. But when the researchers removed AM cells, even mice with SFB became vulnerable. 

Scientists have known that mice typically acquire SFB from their mothers. Compared to pups of mice without SFB, those of mice with SFB had healthier lungs, fewer bacteria, and better survival after flu and bacterial exposure, and this protection lasted for at least four generations. 

Further experiments showed that SFB work by reprogramming the lung’s AMs to resist flu-induced damage and remain effective at killing bacteria, rather than by bringing new immune cells into the lungs. The microbes also boost antibacterial activity in immune cells throughout the body.

Transferring protection

Next, the researchers found that AMs from mice without SFB lost function in an inflamed environment, but if they were placed in the lungs of mice with SFB, they regained their antibacterial activity. 

Rather than acting only by reducing harmful inflammatory signals, SFB change AMs at the genetic and metabolic level, boosting their ability to kill bacteria, produce immune helpers, and maintain energy. Transplanting AMs from SFB-colonized mice into mice without SFB transferred protection, the researchers found.

“We speculate that defining and subsequently harnessing the mechanism by which SFB colonization reprograms AM will lead to new strategies to mitigate the [respiratory viral infection] induced disease burden,” the authors say.

The findings, published in Nature Communications, suggest that gut microbiota profiles can help support personalized dietary interventions.

Lifestyle changes such as diet and exercise can help people with prediabetes, but individual responses vary due to differences in genetics and gut bacteria. The gut microbiota plays a key role in breaking down dietary fiber to improve insulin activity. However, whether microbial features can predict individual response remains unclear. 

Researchers led by Delei Song at Shanghai Jiao Tong University in China enrolled more than 800 people with prediabetes in a clinical study to investigate whether, and how, dietary fiber supplements can help improve blood sugar control.

Prediabetes subgroups

Study participants were randomly assigned to receive standard care with or without fiber supplements. Researchers grouped participants using multiple health measures, including age, weight, and blood sugar, rather than just blood sugar, and analyzed their gut microbiota. 

This approach identified four subgroups of people with prediabetes, each with distinct health profiles, such as differences in insulin production, heart and liver health, and family history of diabetes. These subgroups also showed differences in gut bacteria and blood metabolites, with some having less diverse gut microbiotas.

Only two of these subgroups benefited from dietary fiber, and this improvement depended on whether their gut bacteria could respond to fiber, the researchers found. 

Personalized medicine 

To predict who would benefit from dietary fiber, they researchers created a score based on changes in three key blood sugar measures. Then, they used machine learning to link these outcomes to specific gut bacteria. A set of specific gut bacteria could predict with good accuracy whether a person would respond well to fiber, the team found. 

Next, the researchers tested this approach in two independent groups of people with type 2 diabetes, showing it could predict both short-term and long-term benefits.

“Our study suggests that the gut microbiota response influences the effectiveness of dietary fiber intervention and provides a clinically applicable model to guide microbiome-targeted personalized medicine for prediabetes,” the authors say.

Key themes included augmented foods to support the microbiome and astronaut performance, smart textiles integrating microbial and sensor-based solutions for skin health and physiological monitoring, and hibernation-inspired strategies informed by microbiome changes observed in animal models. The session also emphasized the reverse perspective: how the constraints of space can accelerate the clinical translation of microbiome innovation on Earth by testing robustness, feasibility, and implementation in extreme environments. This cross-disciplinary dialogue has now led to the launch of Microbiome Futures, a new think tank dedicated to human adaptation, starting in 2026 with a focus on space and the microbiome.

Visitors to booth #3C88 will find the ‘The Longevity Shift’—the company’s highly acclaimed interactive installation making its European debut at the show. Designed to spark a fundamental reframing of how the industry thinks about longevity, the experience highlights the nutrition industry’s need to shift from life expectancy to health expectancy and focuses on science-backed approaches to support health in later life and ensure that later years are some of the best.

The company will spotlight two new innovations from its health expectancy portfolio. Featured at booth #3C88 and in the New Products Zone, Age Slower targets chronic inflammation—one of the key hallmarks of aging—and is supported by landmark DO-HEALTH trial research demonstrating that life’s®OMEGA 60 and Quali®-D combined can slow biological aging by approximately three months over three years. Its second innovation—Cellular Repair—targets cellular senescence. It features natural flavonoids with senolytic properties that selectively eliminate senescent “zombie” cells without harming healthy ones. Cellular Repair will be available for visitors to sample in an innovative on-the-go format using the ‘Easy Snap’ one-hand opening technology at the Tasting Centre. 

“The science we’re presenting at Vitafoods Europe 2026—from slowing biological aging to targeting the hallmarks of aging—represents a genuine leap forward for the category, and we want attendees to experience what that means in practice in our immersive experience. Our ambition is to lead the longevity category globally, and Barcelona is where we’re going to continue building on our global position within Europe,” commented Giovanni Calderoni, VP of Dietary Supplements EMEA at dsm-firmenich. To learn more and book a meeting with the dsm-firmenich team at Vitafoods Europe 2026, visit the event page.

The findings, published in Cell, suggest that maintaining a healthy gut microbiota could be critical for preventing immune-related pregnancy complications. 

Scientists have known that the gut microbiota can influence immune function, but it’s not well understood how gut microbes shape immune responses and how microbiota-derived metabolites regulate immune cells.

So, Julia Brown at Weill Cornell Medicine in New York and her colleagues studied how the gut microbiota influences maternal-fetal immune tolerance using mice and human data.

Immune imbalance

In pregnant mice, the gut became more “leaky” and the composition of gut bacteria changed. These shifts were linked to alterations in immune cells in the intestine. Mice without gut bacteria or with disrupted gut bacteria after treatment with the antibiotic vancomycin had higher rates of fetal death and abnormal immune signals in the placenta and uterus. 

In these animals, placentas had more immune cells that attack fetal cells and higher levels of inflammatory molecules, resulting in increased pregnancy loss. Key immune cells that typically help suppress harmful immune responses in the placenta were fewer or less effective in mice lacking gut microbes. 

However, microbial metabolites derived from the amino acid tryptophan helped these immune cells work properly, the researchers found.

Pregnancy loss

Tissue from women with recurrent miscarriages showed similar immune problems, with key immune cells and gut-derived metabolites being disrupted. The findings suggest that these problems can contribute to recurrent pregnancy loss in humans, the researchers say.

Although the study shows that gut bacteria help train immune cells during pregnancy, more research is needed to understand how other body microbes contribute and exactly how these immune signals affect fetal health.

More studies are also needed to see how these results apply to people, the authors say. “Our mouse study may provide insights into specific immune pathways that are perturbed due to loss of vancomycin-sensitive gut bacteria and microbiota-derived tryptophan derivatives; this, however, needs to be further validated in controlled human studies.”

The findings, published in Science Immunology, suggest that gut Clostridia can be divided into two groups, with one group contributing to gut inflammation under certain conditions.

Scientists have known that Clostridia bacteria make proteins called flagellins, which build flagella. Flagellins can also interact with the immune system, with some triggering only weak immune responses and others causing inflammation. However, it’s unclear how differences in flagellin types affect their ability to stimulate the immune system and which flagellins promote or prevent inflammation in the gut.

To address this question, Lennard Duck at the University of Alabama at Birmingham and his colleagues set out to study more than 100,000 bacterial genomes from gut Clostridia.

Immune activation

The researchers found that the genes controlling flagella, called motility genes, are arranged differently across Clostridia bacteria, even among closely related families. Some bacteria, such as Lachnospiraceae, have multiple motility genes and more diverse flagellins, while others have fewer of these genes and less diversity. 

Based on flagellin diversity and motility gene organization, the team classified gut Clostridia into two groups, G1 and G2. Next, they tested these two groups of bacteria in germ-free mice to see how they affect the gut. 

Both groups could colonize the gut, boost protective immune cells, and stimulate the production of antibodies that help maintain normal gut balance. However, G2 bacteria triggered stronger responses in gut cells, including genes linked to inflammation and stress, while G1 bacteria mainly activated protective functions. 

Gut inflammation 

When the gut’s barrier was weakened, G2 bacteria—but not G1 bacteria—caused inflammation and tissue damage in the colon lining. The researchers found that flagellins differ between G1 and G2 gut bacteria: Most G1 bacteria produce flagellins at very low levels, while G2 bacteria produce flagellins that strongly activate the immune system. What’s more, G2 flagellins stimulate inflammatory signals, whereas G1 flagellins don’t. 

In people with Crohn’s disease, G1 bacteria are typically reduced, while G2 bacteria are more abundant in inflamed tissues, the researchers also found. This finding, they say, suggests that the balance between G1 and G2 bacteria and their flagellins may influence gut inflammation and disease. 

“This study identified key features of specific commensal bacteria that have colitogenic potential and revealed one mechanism whereby these organisms can potentially initiate intestinal inflammation,” the authors say.