NeuroGASTRO Conference 2025

All about the gut-brain axis

What follows is my personal account of the latest findings in neurogastroenterology, grounded in the research presented, with an eye to how it will shape our clinical practice in nutrition and functional medicine.

"A Case Story to Begin the event: Consider Jane, a 35-year-old patient who exemplifies this confluence. She has IBS – chronic abdominal pain and erratic bowel habits – along with fibromyalgia and anxiety. She often feels lightheaded (suggesting dysautonomia) and has hypermobile joints hinting at Ehlers-Danlos syndrome. Throw in a history of poor sleep and weight struggles, and Jane’s case might leave any specialist scratching their head. "

The event opened by challenging us to break these silos. In a hall full of gastroenterologists, neurologists, dietitians, and researchers, we set out to connect the dots between gut, brain, microbiome, metabolism, and circadian rhythms. The tone was set: this was not a dry series of lectures, but a shared quest to rewrite the story of gut health in a more personal, integrated way.

Unmasking IBS: From Gut-Only to Multisystem Disorder

The first plot twist came from Professor Javier Santos, who leads the DISCOvERIE project on IBS comorbidities. He painted a striking picture: up to 60–70% of IBS patients have significant mental health (anxiety, depression) or somatic comorbidities (e.g. fibromyalgia, chronic fatigue) [1]. This isn’t the “ IBS” we read about in textbooks as a purely gut-limited functional disorder. These patients’ abdominal pain and bowel dysfunction are magnified by concomitant anxiety or body-wide pain syndromes. Prof. Santos shared how such comorbid IBS patients often suffer more severe symptoms and poor treatment outcomes, essentially “turning up the volume” on their GI distress. It was a powerful reminder that when an IBS patient like Jane reports widespread pain or panic attacks, those aren’t mere footnotes – they are integral to her illness experience. The DISCOvERIE team is unravelling gut–brain mechanisms behind this overlap, searching for biomarkers and personalized interventions for the IBS patient who also carries the burdens of a hyperactive mind and hypersensitive body. 

As I listened, I realized we must approach IBS not as an irritable bowel in isolation, but as a disorder of the gut-brain axis influenced by mood, pain processing, and immunity.

Professor Magnus Simrén took this concept further, posing a question that lingered in the auditorium: Is IBS a gut-specific condition with some extraintestinal “add-ons,” or is it truly a multisystem disorder with the gut as one player? His answer leaned toward the latter. He cited new epidemiological data from a 54,000-person global study: having any organic GI disease (from reflux to inflammatory bowel disease) significantly raises the odds of also meeting criteria for a disorder of gut–brain interaction (DGBI) like IBS. For instance, individuals with inflammatory bowel disease (IBD) were over three times more likely to have IBS-type symptoms compared to those without IBD [2]. Surprisingly, the associations extended beyond organ borders – even people with conditions like celiac or peptic ulcer had higher rates of esophageal or bowel DGBI symptoms. And crucially, the presence of these overlapping DGBI symptoms correlated with higher psychological distress and worse quality of life in patients, whether or not an “organic” disease was present.

Taken together, these findings undermine the old dualism of “organic vs. functional” GI disorders. Symptom profiles alone cannot neatly separate an IBS patient from one with IBD. As Prof. Simrén argued, we should move beyond labeling patients as having either a structural disease or a psychosomatic disorder – many have both, and all have genuine symptoms that impact their whole well-being. 

For practitioners like me, this was a call to action: we must treat the whole patient. In Jane’s case, that means acknowledging her anxiety and fibromyalgia as inseparable from her IBS like this study published in Nature explain very well [7] – all possibly rooted in a common dysregulation of the gut–brain axis.

Fig. 1: Immunological changes in the gut–joint axis of inflammation in SpA: In healthy gut tissue (left), innate and adaptive type 3 immune cells maintain epithelial barrier homeostasis in collaboration with intraepithelial lymphocytes. Type 3 immune cell activity is regulated in part by commensal microorganisms and dietary metabolites, such as aryl hydrocarbon receptor (AHR) agonists and retinoic acid. This homeostasis limits the translocation of microorganisms and their products through the epithelial barrier through maintenance of the mucus layer and tight junctions between epithelial cells. Mononuclear phagocytes and regulatory T (T_reg) cells keep type 3 immunity in check. In spondyloarthritis (SpA), gut ‘leakiness’ can increase without appreciable histological changes (centre left), and dysbiosis and subclinical inflammatory events are likely to occur. In early inflammatory bowel disease (IBD) and in most cases of SpA, acute inflammation can be subclinical (centre right). This subclinical inflammation is typified by a loss of barrier function (with reduced mucus thickness and damage to epithelia), increased neutrophil and mononuclear phagocyte recruitment, enhanced type 3 immunity and increased antibody production. Concentrations of cytokines such as TNF, IL-23 and IL-17 are elevated. In the majority of patients with IBD, and some patients with SpA, chronic inflammation is present (right). With chronic inflammation, epithelial integrity can be lost, transmural inflammation is present and tissue remodelling and fibrosis occur. Changes to type 3 immune cells, cytokines and other soluble factors can be detected in the blood, but how they relate to the degree of gut inflammation is not known. Immune cells and cytokines are detectable in bone, entheseal tissue in peripheral and axial joints, and in the synovial fluid of peripheral joints. Although IL-23 is detectable in both skeletal locations, this cytokine does not seem to have a pathogenic role in the axial skeleton. Microorganisms and their products can be detected in the peripheral joints in patients with reactive arthritis. APRIL, a proliferation-inducing ligand; BAFF, B cell activating factor; CRP, C-reactive protein; MAIT, mucosal associated invariant T; T_H17, T helper 17. [7]

It means collaborating across specialties to address her pain and mood along with her bowel symptoms. The narrative of IBS is expanding from a local gut tale to a body-wide saga.

The Hidden Culprits: Proteases and the Gut’s Pandora’s Box

One fascinating subplot in the IBS story involves microscopic culprits: proteases – enzymes that cut proteins. Professor Nathalie Vergnolle has long studied how excess proteases in the gut can wreak havoc, and her talk asked, “Proteases in gut physiology and pathophysiology: can old dogs learn new tricks?” The “old dogs” here are well-known digestive enzymes (like trypsin or pancreatic elastase) and proteases from bacteria or immune cells. Their “new tricks” are roles in signaling and inflammation. We learned that IBS patients often have elevated levels of serine proteases in their intestines, and these enzymes can directly activate pain-sensing nerves and disrupt the gut barrier. In essence, an imbalance in proteolytic activity may be a central driver of the visceral hypersensitivity that characterizes IBS. When proteases break down the normal barriers and activate receptors on gut nerves (such as protease-activated receptors, PARs), they can cause the nerves to fire pain signals in response to stimuli that would not normally hurt [3]. This mechanism helps explain why IBS patients feel exaggerated pain from bowel stretching or diet triggers – their sensory nerves are chemically sensitized.

Fig 2.  Proposed mechanisms by which gut-derived proteases contribute to visceral pain in IBS. (A) The bidirectional gut–brain axis can be perturbed by factors like gut infections, microbiome changes, barrier disruption, and psychological stress. (B) In IBS, excess proteases (orange and purple boxes) from food, pancreas, gut bacteria, or immune cells can increase intestinal permeability and activate receptors on nerves (protease-activated receptors, PAR1–4) and on mast cells. This leads to release of pain mediators (like histamine, tryptase, bradykinin) and activation of nerve channels (TRPV1, TRPA1, etc.), lowering the threshold for pain and causing visceral hypersensitivity. [3]

What excited me is the therapeutic potential here: protease inhibitors as a novel treatment for IBS. Dr. Vergnolle and others are identifying specific proteases (tryptase from mast cells, proteases from dysbiotic flora, etc.) that are overactive in IBS. Early studies suggest that targeting these enzymes (for example, with selective tryptase inhibitors or dietary protease blockers) can reduce abdominal pain in animal models of IBS. It’s akin to closing Pandora’s box by neutralizing the very molecules that escaped and caused chaos. In fact, a recent review highlighted that protease inhibitors are emerging as promising tools to manage IBS pain, though we still need to pinpoint the main offending proteases in each patient. 

For clinicians, this line of research encourages us to think outside the box: maybe the next IBS therapy won’t be an analgesic or an antidepressant, but a gut-specific enzyme blocker that calms the inflammatory noise at its source. 

When Tech Meets Gut: Smart Capsules and Hidden Rhythms

The conference then shifted gears to innovative technologies shining light on gut function. Dr. Mark Scott gave an update on telemetric capsule measurement of gut motility. If that sounds futuristic, it is – think “smart pills” that travel through the GI tract, measuring pressures, pH, and transit times, all while the patient goes about their day. He asked, “Where are we now?” and answered with encouraging results. One such system, the 3D-Transit electromagnetic capsule, allows us to track gut movement in real-time. Patients swallow a capsule the size of a large multivitamin; as it journeys from stomach to colon, an external belt receiver records its path [4]. This provides a readout of gastric emptying, small bowel transit, and colonic motility patterns without the need for X-rays or wires. Dr. Scott even presented a pilot study where they combined the capsule with overnight sleep polysomnography to see how the gut moves during sleep. 

Figure 3: Data synchronization: Posture changes obtained through the accelerometer inside the 3D-Transit receiver (red, green, and blue lines) are associated with an increased heart rate achieved through the portable sleep monitor. This way data were easily time-linked (ovals).2

Remarkably, this ambulatory setup made it possible to observe that during certain sleep stages, gut contractions diminish – a reminder that our gut has its own circadian rhythm and “light–dark” cycle of activity. The telemetric capsule is a game-changer for diagnosing motility disorders: patients with unexplained constipation or bloating can avoid hospital admissions for motility tests and instead carry on normal life while the capsule does the work.

For clinicians, these tools mean we can objectively measure what was once elusive, like subtle gastroparesis or colonic inertia that might be contributing to a patient’s IBS symptoms. 

In Jane’s case, for instance, a smart capsule could reveal if her gut transit is abnormally slow during the daytime or if her nighttime motility is disrupted (perhaps linking to her poor sleep).

As someone deeply interested in circadian nutrition, I found this thrilling – we are now able to capture the gut’s rhythmic dance quantitatively. The consensus was that within a few years, wireless motility capsules might become as routine as wearing a Holter monitor, helping tailor treatments (dietary fiber, prokinetics, etc.) to a patient’s specific motility profile. We are essentially giving the gut a “voice” through data, and it’s telling us when and how it likes to move.

Gut Feelings and the Brain: Parkinson’s Disease and Beyond

No neurogastroenterology meeting would be complete without tackling the gut–brain axis in neurological disease. A highlight for me was Dr. François Cossais’s talk on the microbiome–gut–brain axis in Parkinson’s disease (PD). Parkinson’s is typically viewed as a brain disorder of movement, but here we learned it might start in the gut in some patients. Dr. Cossais pointed out that many PD patients have years of constipation and gut dysfunction before their first tremor [5]. Even more compelling, research shows a compromised intestinal barrier (“leaky gut”) and altered gut microbiome in Parkinson’s, reinforcing the idea that PD is partly a gut–brain disorder. He summarized large metagenomic studies: while results vary, a few microbial trends emerge in PD. Patients often have an overrepresentation of certain bacteria like Akkermansia (mucus-degraders), Lactobacillus, and Bifidobacterium, and a reduction in key short-chain fatty acid (SCFA) producers like Faecalibacterium and Roseburia [6]. The consequence is a gut microbiome that may produce less beneficial SCFAs (like butyrate) and more pro-inflammatory or neuroactive compounds. Indeed, lower levels of faecal butyrate have been consistently found in PD and even in REM-sleep behaviour disorder (a prodromal condition), hinting that a deficiency of microbiome-derived nutrients could contribute to PD progression.

Fig 4: Microbial therapies for Parkinson’s disease (a). Probiotics, prebiotics, synbiotics, and fecal microbiota transplantation are the most commonly used microbial therapies for PD. These therapies can be administered through oral, nasogastric, rectal, or colonoscopic route (b). Microbial therapies have neuroprotective effects on the brain by reducing the blood–brain barrier damage, decreasing microglial and astrocytic activation, suppressing neuroinflammation, and inhibiting α-syn aggregation, thereby preventing the death of dopaminergic neurons (c). In the gut, microbial therapies can regulate gut microbes, improve intestinal metabolism, modulate the intestinal mucosal immune system, inhibit gut inflammation, and restore gut barrier damage, resulting in improved intestinal symptoms (d). In conclusion, microbial therapies relieve nonmotor symptoms of PD, particularly constipation, as well as the motor symptoms through multiple pathways. [6]

One of the most hopeful parts of this story is the interventional trials. Dr. Cossais described an elegant study where Parkinson’s patients were given a prebiotic fibre (resistant starch) for 8 weeks. The result? Their faecal butyrate levels rose significantly and markers of gut inflammation (like calprotectin) fell. Clinically, some patients reported improved bowel regularity. Essentially, feeding the good bugs helped patch the “leak” in the gut and modulate inflammation – a small step that could potentially influence neurological health down the line. And in rodent models of PD, faecal microbiota transplantation (FMT) from healthy donors has been shown to restore gut microbiota balance, reduce neuroinflammation, and even alleviate motor symptoms. While FMT is still experimental in PD (ongoing clinical trials are evaluating it), the concept is revolutionary: treating a brain disease through the gut [5].

As I absorbed this, I reflected on how we might apply it in practice. Could we, for example, screen patients with longstanding constipation for early signs of neurodegeneration? Or advise dietary interventions (like high-fibre diets or probiotics) to at-risk patients (such as those with a family history of PD who have gut issues)? For Jane – who thankfully doesn’t have Parkinson’s, but perhaps struggles with anxiety – similar principles may apply: a healthier gut microbiome might ease her extra-intestinal symptoms. The microbiome is emerging as the master weaver between neurology and gastroenterology, and we are learning to gently tug its threads for therapeutic benefit.

Parallel to Parkinson’s, Professor Jordi Serra explored gastrointestinal manifestations of rheumatological diseases. This was a tour of how autoimmune and connective tissue disorders often hit the gut. We heard about systemic sclerosis(scleroderma), in which the esophagus can become a rigid tube and intestinal muscles weaken, leading to severe reflux and pseudo-obstruction [7]. In lupus, intermittent bowel ischemia or impaired motility (so-called “lupus gastroenteritis”) can cause pain and malabsorption. Prof. Serra reminded us that many rheumatologic patients have been dismissed when they report GI symptoms – chalked up to medication side effects or stress – when in fact there may be an underlying pathological process. A striking example is the link between ankylosing spondylitis (AS) and inflammatory bowel processes. Up to 50–70% of AS patients have subclinical gut inflammation on biopsy, even if they don’t have overt Crohn’s or colitis. About 5–10% of them will eventually develop full IBD, essentially unmasking the gut component that was brewing all along [8]. This gut–joint axis means that gastrointestinal evaluation and early dietary management (like anti-inflammatory diets) might be relevant even in a “back pain” patient. I found this illuminating – it reinforced that systemic disorders truly affect multiple systems. If a patient with rheumatoid arthritis complains of chronic diarrhea, we should not reflexively blame NSAIDs; they might have a concurrent microscopic colitis or simply an IBS that merits attention. 

For us nutrition and functional medicine practitioners, it underscores the importance of anti-inflammatory and microbiome-friendly diets in our rheumatology patients, as their gut may be a common denominator in systemic inflammation.

Tying the Threads: Autonomic Cross-Talk and Chrononutrition

By Saturday morning, the conference narrative had built up many threads – IBS, pain pathways, motility, microbiome, systemic disease – and now it brought in two more pivotal characters: the autonomic nervous system and the circadian clock. Dr. Andrea Shin’s lecture on EDS, POTS, and Mast Cell Activation – what gastroenterologists should know was greeted with nodding heads from the audience.

These conditions have been the talk of patient support groups and are now entering mainstream GI discussions. She addressed the cluster of hypermobile Ehlers-Danlos syndrome (hEDS), postural orthostatic tachycardia syndrome (POTS), and mast cell activation syndrome (MCAS) that is seen in some patients with functional GI disorders. The take-home message was clear: gastroenterologists should be aware of the strong association between hypermobility disorders and autonomic or allergic dysfunction – and how they manifest in the gut.

Patients (often young women) with hEDS can present with refractory nausea, bloating, dyspepsia, and alternating bowel habits. These GI symptoms overlap with their episodes of tachycardia, dizziness (from POTS), and flushing or allergic flares (from MCAS). Dr. Shin emphasized that while the mechanistic links are still being studied, we should not dismiss these connections as coincidence. For example, mast cell mediators like histamine can directly affect gut nerve function and permeability, potentially causing IBS-like symptoms. And POTS, a disorder of autonomic blood flow, might predispose to pooling of blood in the abdomen and sluggish GI transit in some cases.

Crucially, the AGA Clinical Practice Update co-authored by Dr. Shin provides best-practice advice. It suggests that GI providers screen for joint hypermobility (using the Beighton score) in patients with difficult DGBI cases. I found this immediately useful – I can incorporate a quick hypermobility screening in my clinic for patients like Jane who have chronic GI complaints plus symptoms hinting at dysautonomia. The guidelines also advise targeted testing: if a patient with hypermobility has unexplained bouts of flushing, hypotension, and GI pain, consider evaluating for MCAS (e.g. serum tryptase during an attack) rather than doing the tenth colonoscopy. And if they report chronic lightheadedness or palpitations on standing, checking orthostatic vitals or referring for POTS evaluation (tilt-table test) could yield a diagnosis. The beauty of this approach is integrated care: treating these patients often requires a network of specialists – cardiologists for POTS, allergists for MCAS, physical therapists for EDS – but someone has to connect them, and gastroenterologists are in a prime position when GI symptoms are the presenting complaint. 

For my practice, Dr. Shin’s talk was empowering. I now feel equipped to validate these patients’ experiences (“Yes, your IBS, fainting spells, and hives might be connected”) and to coordinate a multidisciplinary plan. Often, a combination of dietary modifications (low-histamine diet for MCAS, high-salt and fluid for POTS), medications (H1/H2 blockers, mast cell stabilizers, midodrine or beta-blockers for POTS), and gentle nutrition and exercise plans can dramatically improve quality of life. The key is to recognize the pattern – to see that Jane’s joint hypermobility and fast heart rate aren’t unrelated quirks but clues to a unifying syndrome affecting her gut-brain interaction.

Finally, as the conference drew to a close, we zoomed out to the grandest scale of all: time. Professor Inge Depoortere delivered a fascinating lecture on chronodisruption and gastrointestinal homeostasis. As a circadian nutritionist, this was music to my ears. We learned that virtually every aspect of gut physiology has a 24-hour rhythm, driven by both the central clock in the brain and local clocks in the gut [9]. Our digestive tract and its accessory organs (liver, pancreas) anticipate meal times – day vs. night – and optimize digestion and absorption accordingly. Disrupt those rhythms (say, by eating at 2 AM regularly or doing shift work), and you invite trouble: impaired motility, altered appetite hormones, leaky gut barrier, and glucose dysregulation [9].

Fig. 5: Circadian regulation of glucose homeostasis: The suprachiasmatic nucleus (SCN) signals via neuroendocrine pathways to the peripheral clocks in pancreas, gut, fat, skeletal muscle and the liver. The circadian clocks of pancreatic β-cells and α-cells coordinate diurnal plasma levels of insulin and glucagon. In the active phase (fed), glucagon-like peptide 1 (GLP1) and glucose-dependent insulinotropic polypeptide (GIP) secretion are upregulated by the gut circadian clock, stimulating the diurnal rhythm of insulin. Insulin signals to the gut, fat, skeletal muscle and liver to stimulate glucose uptake via activation of its receptor, which is diurnally expressed. The uptake of glucose by these organs is dictated by their respective circadian oscillators, which regulate diurnal expression of glucose transporters (GLUTs). In the liver and muscle, glucose is stored as glycogen. The rate-limiting enzyme of glycogen synthesis, glycogen synthase 2 (GYS2), is controlled by the CLOCK–BMAL1 heterodimer. In the resting phase (fasting), glucagon signals via the diurnally expressed glucagon receptor to the liver to increase plasma glucose levels by glycogen breakdown and gluconeogenesis. The key enzyme of gluconeogenesis, phosphoenolpyruvate carboxykinase 1 (PCK1), is rhythmic and stimulated by glucagon signalling, which in turn is inhibited by the clock component CRY. [9]

Prof. Depoortere highlighted emerging evidence that circadian disturbances contribute to disorders ranging from obesity to dyspepsia, and conversely, that reinforcing circadian cues can be therapeutic. One striking research example she mentioned was the use of specific nutraceuticals to “reset” or strengthen circadian clocks. In a head-to-head comparison, nobiletin, a flavonoid from citrus peel, outperformed the plant compound berberine in its ability to entrain peripheral clocks.

Nobiletin is like a molecular clock tuner – it binds to retinoid orphan receptors (RORα/γ) and boosts the expression of core clock genes like BMAL1, thereby enhancing the amplitude of circadian rhythms in cells. In mouse models of metabolic syndrome, giving nobiletin resulted in remarkable benefits: it counteracted obesity, improved insulin sensitivity, and even increased energy expenditure – all in a clock-dependent manner. In other words, nobiletin only worked its magic if the animal’s circadian clock machinery was intact, underscoring that its effect was indeed through clock modulation.

This finding has profound implications. It suggests we might treat metabolic and GI diseases not just by targeting the end symptoms, but by rewiring the body’s timing system. Prof. Depoortere hinted that human trials could be on the horizon – imagine a future “chronotherapy” supplement derived from oranges that helps synchronize your gut clocks for better digestion and metabolic health. I was particularly fascinated by an insight she shared: patients with IBS or functional disorders often have disrupted daily routines (irregular meals, sleep deprivation, etc.), and part of our therapeutic arsenal should be restoring a consistent rhythm. Time-restricted feeding (e.g. eating within a 10-hour daytime window) is one practical intervention gaining evidence for improving GI symptoms and overall metabolic parameters, essentially by reinforcing the alignment between our eating schedule and our internal clocks [10]. 

Fig. 6: The Small Molecule Nobiletin Targets the Molecular Oscillator to Enhance Circadian Rhythms and Protect against Metabolic Syndrome: Dysregulation of circadian rhythms is associated with metabolic dysfunction, yet it is unclear whether enhancing clock function can ameliorate metabolic disorders. In an unbiased chemical screen using fibroblasts expressing PER2::Luc, we identified Nobiletin (NOB), a natural polymethoxylated flavone, as a clock amplitude-enhancing small molecule. When administered to diet-induced obese (DIO) mice, NOB strongly counteracted metabolic syndrome and augmented energy expenditure and locomotor activity in a Clock gene-dependent manner. In db/db mutant mice, the clock is also required for the mitigating effects of NOB on metabolic disorders. In DIO mouse liver, NOB enhanced clock protein levels and elicited pronounced gene expression remodeling. We identified retinoid acid receptor-related orphan receptors as direct targets of NOB, revealing a pharmacological intervention that enhances circadian rhythms to combat metabolic disease via the circadian gene network. [10]

As I mulled over this, I looked back at Jane’s case – she’s a busy nurse who frequently rotates night shifts and skips meals. Perhaps a piece of her puzzle is chronodisruption. By helping her establish regular eating times, a pre-bed wind-down routine, and maybe considering chronobiotics (like nobiletin) in the future, we might alleviate some of her GI turmoil that has resisted conventional treatment. The conference made clear that when we eat may be as important as what we eat for gut health, echoing the classic wisdom that timing is everything.

Personalizing the Future: Microbiome and Nutrition – “Time to Make it Personal"

The grand finale was delivered by Professor Sarah Berry of King’s College London, aptly titled “Nutrition, the Gut Microbiome and the Future of Healthcare: Time to Make it Personal.” It felt like the perfect culmination of the story – having explored the many factors that influence gut health, we arrived at the paradigm of personalized nutrition.

Prof. Berry has been a leader in the PREDICT studies, which have revealed astonishing variability in how individuals respond to the same foods. She opened by reminding us that no two people have identical metabolic responses to a given meal– one person’s blood sugar might spike with a banana while another’s barely budges. These differences are partly due to genetics, but also profoundly shaped by the gut microbiome and even the time of day [11]. The problem with traditional dietary guidelines, she argued, is that they assume a one-size-fits-all model, which clearly is not working when diet-related diseases are still on the rise.

Fig. 7: Impact of dietary intervention on the gut microbiome: a, Bray–Curtis dissimilarity at baseline, week 12 and week 18, for the control (red) (n = 118) and PDP (blue) (n = 112) groups. Data presented include the first quartile, median and third quartile. KSp between treatment groups (P = 0.04). ***P < 0.001 determined using a paired, one-sided Wilcoxon rank-sum test for within-individual change in Bray–Curtis dissimilarity. b,c, Relative abundance of favorable microbial species at baseline (blue), week 12 (green) and week 18 (red) for PDP (n = 112) (b) and control (n = 118) (c) groups (minimum to maximum shown).

She presented data from a recent randomized trial where participants followed either a personalized diet (tailored to their postprandial glucose/lipid responses and microbiome profile) or a standard healthy diet. The personalized diet led to significantly better outcomes in triglycerides, insulin sensitivity, and weight compared to controls [12].

Notably, adherence was higher too – when people are given foods that suit their biology (and preferences), they naturally stick to the plan better. One of the most intriguing aspects was the role of the gut microbiome as a predictor and mediator in these responses. Prof. Berry showed how certain microbial signatures correlate with how a person handles fats or carbs.

For instance, having a high abundance of Prevotella might predict a better postprandial glucose control on whole grains, whereas another microbe might indicate a propensity to spike on the same meal. Moreover, personalized dietary changes led to improvements in microbiome diversity and an enrichment of beneficial microbes, which in turn were linked to improvements in inflammation and blood markers. It’s a positive feedback loop: tailor the diet to the person, you feed the right microbes, which then produce metabolites that improve host metabolism [12].

For those of us in the audience (clinicians and nutritionists), the message was empowering. We now have tools – from at-home blood glucose monitors to stool sequencing – that enable this personalization. Prof. Berry’s vision (which I share) is that in the near future, dietitians will routinely incorporate microbiome analysis and perhaps even circadian assessment into nutritional planning. Instead of generic advice like “eat more fiber,” we’ll be saying “increase Bifidobacterium-friendly fibers for your gut, and have them in the morning when your body handles glucose best.” It struck me that throughout NeuroGASTRO 2025, one refrain was constant: the future of gut health care is precision and personalization. Whether it was identifying which IBS patient needs a protease inhibitor, which Parkinson’s patient might benefit from a prebiotic, or which diet best suits a given microbiome profile – the age of trial-and-error is receding. We are moving toward evidence-guided, individualized therapy.

Professor Berry ended on a hopeful note that resonated deeply with my own practice: “It’s time to make healthcare personal.” I couldn’t agree more. In the closing moments of the conference, I looked around and saw excitement in my colleagues’ eyes (and perhaps a few neurons firing with new ideas!). We are participants in a rapidly evolving narrative – one where the patient is not a passive character but the central protagonist with unique traits, and where clinicians act more like skilled editors, refining the story of health for each individual.

Fig. 8: Targeting the gut to treat obesity – example of personalized nutraceutical approach. In a clinical trial, researchers delivered specific nutrients in delayed-release capsules to the colon to stimulate satiety hormones. Graphs (A,C) show changes in blood PYY and GLP-1 levels over 8 hours in obese adults given the nutrient capsules (red) vs. placebo (blue). Arrows indicate capsule ingestion and meal times. The nutrient therapy led to significantly higher PYY release (p<0.05, panel B) compared to placebo, indicating enhanced satiety signaling, whereas GLP-1 did not differ significantly. This approach, pioneered by Dr. Madusha Peiris, reduced calorie intake by ~13% per meal in participants and exemplifies how understanding gut hormones can inspire novel obesity treatments [13].

My Perspective as a Nutritionist

Leaving NeuroGASTRO 2025, I felt a sense of narrative closure – and a spark for new chapters to write back at the clinic. The lectures had intertwined like a well-crafted novel, reinforcing that the gut is central but never solitary.

As a Circadian Nutritionist, I see immediate ways to apply this knowledge. For patients like Jane, I will broaden my assessments: checking for hypermobility or POTS if her story hints at it, screening for anxiety or trauma that might amplify her IBS, and certainly inquiring about her meal timing and sleep patterns. The concept of “chrononutrition” will take a front seat – I’ll encourage her to anchor meals at consistent times and perhaps experiment with time-restricted feeding to resynchronize her gut clocks. If her symptoms flare with stress, I now have greater confidence to explain the biology (e.g. mast cells and proteases releasing under stress, sensitizing nerves) and to incorporate stress-management or even mast cell stabilization strategies.

In practice, I foresee developing personalized gut-health plans that integrate multiple facets: diet (tailored to one’s microbiome and metabolic responses), lifestyle (sleep and circadian habits), and targeted therapeutics (maybe a probiotic for the Parkinson’s patient, or an enzyme inhibitor for the IBS patient with protease-driven pain, or nobiletin for the metabolic syndrome patient with circadian disruption). The conference armed me with citations and science to back up these integrative approaches. Perhaps most importantly, it reinforced a mindset: to always think of the patient in 360 degrees. The gut might be where their symptom screams the loudest, but the echoes are everywhere – in the brain, in the immune cells, in the microbes, and in the ticking of genes.

NeuroGASTRO 2025 felt like a glimpse into a future of healthcare that is holistic and precise at once. It’s a future where we begin a clinical story not with “Here’s the standard IBS diet, come back in 6 weeks,” but rather with, “Tell me about your whole self – your sleep, your stressors, your other conditions – because it’s all relevant. Let’s craft a plan tailored to you.” 

As I return to my patients, I carry with me the enriching stories and science shared by Prof. Berry, Prof. Santos, Prof. Simrén, Dr. Peiris, Prof. Depoortere, Dr. Cossais, Prof. Vergnolle, Dr. Scott, Prof. Serra, Dr. Shin, and others. Their research has equipped me to be a better healer, one who can integrate nutrition, microbiome, mind, and time. And so, our story continues – in each clinic visit and each research endeavor – with a clearer narrative arc: the gut connected to the whole, and the care of the patient made personal.

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References

1. Vall d’Hebron University Hospital. (2020, February 11). The DISCOvERIE project will provide enhanced understanding on IBS and comorbidities and the risk factors. https://www.vallhebron.com/en/news/discoverie-project-will-provide-enhanced-understanding-ibs-and-comorbidities-and-risk-factors

2. Keszthelyi, D. (2024). Organic versus functional dichotomy in gastroenterology: Are we ready to move the needle? United European Gastroenterology Journal, 12(7), 824–825. https://doi.org/10.1002/ueg2.12588

3. Decraecker, L., Boeckxstaens, G., & Denadai-Souza, A. (2022). Inhibition of serine proteases as a novel therapeutic strategy for abdominal pain in IBS. Frontiers in Physiology, 13, 880422. https://doi.org/10.3389/fphys.2022.880422

4. Haase, A. M., Gregersen, T., Christensen, L. A., & Krogh, K. (2015). Gastrointestinal motility during sleep assessed by tracking of telemetric capsules combined with polysomnography: A pilot study. Clinical and Experimental Gastroenterology, 8, 327–335. https://doi.org/10.2147/CEG.S91964

5. Pérez-Pardo, P., Dodiya, H. B., Engen, P. A., Naqib, A., Green, S. J., Garssen, J., Kraneveld, A. D., & Keshavarzian, A. (2020). Faecal transplantation, pro- and prebiotics in Parkinson’s disease—Hope or hype? Journal of Parkinson’s Disease, 10(3), 1061–1083. https://doi.org/10.3233/JPD-191802 journals.sagepub.com(Your list mentioned a Neurology 2019 abstract by Pérez-Pardo on prebiotics/FMT; the full peer-reviewed article covering that work is this JPD review.)

6. Cossais, F., Rees, A., Sundaram, A., & Malek, N. (2022). Microbiome and metabolome insights into the GI–brain axis in Parkinson’s disease. Metabolites, 12(12), 1222. https://doi.org/10.3390/metabo12121222 ScienceDirect

7. Gracey, E., Vereecke, L., McGovern, D. et al. Revisiting the gut–joint axis: links between gut inflammation and spondyloarthritis. Nat Rev Rheumatol 16, 415–433 (2020). https://doi.org/10.1038/s41584-020-0454-9

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