Our FODZYME clinician team attended FOOD: The Main Course 2026, a conference that focuses on medical nutrition therapy and integrated care in gastroenterology (GI). This article covers some of my biggest takeaways. As a dietitian, I was excited to see how digestive enzymes like FODZYME align with one of the core messaages shared across all sessions: the less restrictive approach to diet, the better.
Dr. Bill Chey (Michigan Medicine) opened the conference with a deep dive into Rome V, the first major revision to these diagnostic guidelines in 10 years. The updates reflect a decade of evidence and are aimed at making the criteria more clinically actionable.
Biggest terminology shift: "Functional" is largely being dropped. We're moving to more descriptive, less stigmatizing language. "Functional Constipation" is now "Chronic Constipation," for example. This aligns with how patients experience and describe their conditions, and may reduce the sense that symptoms are "in their head."
Four new diagnoses were added:
Inability to Belch - a recognized condition, not just a quirk
Abdominal Migraine - particularly relevant in pediatric practice
Rectal Hyposensitivity - reduced rectal sensation contributing to defecatory dysfunction
Rectal Hypersensitivity - heightened rectal sensation, distinct from generalized visceral hypersensitivity
IBS Rome V update: The pain criterion now specifies "recurrent but not continuous" abdominal pain or discomfort ≥3 days/month. This helps differentiate IBS from centrally mediated abdominal pain syndrome (CAPS) and other conditions with continuous pain. There was also the addition of "and discomfort" to provide more inclusive language across many different countries. This will likely increase rates of IBS diagnoses.
Dr. Prashant Singh (University of Michigan) gave a measured and evidence-grounded talk on what we actually know about the gut microbiome in IBS, and what remains hype.
The microbiome absolutely plays a role, with supporting data shared: fecal transplant from IBS-D patients induces anxiety-like behavior in germ-free mice (De Palma et al. 2017), and bacterial lipopeptides have been shown to modulate visceral hypersensitivity (Petitfils et al. Gut 2022). New data also shows low FODMAP diet improves gut barrier function and reduces colonic mast cell infiltration in IBS-D (Gao et al. Gastroenterology 2025), which is both a mechanistic win for the diet and a highlight of the potential role of the microbiome.
But the bottom line is sobering: no consistent microbial signature has been found for IBS. Probiotics and prebiotics are not recommended by ACG or AGA. Rifaximin offers only a 9% advantage over placebo (Pimentel, NEJM 2011). FMT shows unclear benefit in the latest meta-analysis (Aumpan et al. Gastroenterology 2026).
Dr. Singh's conclusion: the microbiome is one component of a broader brain-gut-microbiome ecosystem. Behavioral therapies may be as effective as microbiome-based approaches. Our evidence-based foundations remain the most reliable tools, so it's important we use them first.
This session, led by GI dietitian Kate Scarlata, was a standout for practical clinical application. A network meta-analysis of 28 RCTs (n=2,338) found that specific carbohydrate/sucrose-restricted diets (SSRD) had the strongest overall effect size, but with only 2 trials to support it. The low FODMAP diet carries the most evidence with 23–24 trials, and outperforms British Dietetic Association/NICE dietary advice (Cuffe MS et al. Lancet Gastroenterology & Hepatology).
Two noteworthy variations on the standard low FODMAP approach:
FODMAP Simple (fructans + GOS only): Restricts just two FODMAP subgroups : fructans and galacto-oligosaccharides. Improves symptoms in the majority of IBS-D patients and is better tolerated than the full LFD, with an adverse event rate of 12.5% vs. 26.3% (Singh P et al. Clinical Gastroenterology and Hepatology 2024).
FODMAP Gentle: Reduces a few high-concentration foods without full elimination, which is useful in clinical practice for patients who aren't ready for or cannot tolerate a full LFD (Halmos EP et al. Journal of Gastroenterology & Hepatology 2019).
I'd propose another variation of the standard LFD: Using FODZYME as a digestive enzyme for FODMAPs may be an effective first step for symptom reduction, before FODMAP restriction is considered.
Hot off the press: A FODMAP-lowering app RCT (Domino, n=459) showed a 71% vs. 61% responder rate versus antispasmodics, with earlier improvement at 4 weeks (Routhiaux K et al. DDW 2026, #338).
Reintroduction data is now stronger. One study finds fructans (56%) and mannitol (54%) are the most common FODMAP triggers, with an average of 2.5 triggers per patient, while another identifies fructans and GOS as the most common triggers (Van den Houte K et al. Gastroenterology 2024; Eswaran S et al. CGH 2025). This is an important reminder: the goal is a personalized, sustainable diet, not long-term full elimination.
ARFID risk on LFD deserves attention: 18% of IBS patients met ARFID criteria before starting the low FODMAP diet, and 5 developed new ARFID-like behaviors during elimination. Dietitian-guided reintroduction is essential, both for identifying triggers and protecting against over-restriction.
In consideration of relieving symptoms with less restrictive approaches: FODZYME is a digestive enzyme blend targeting lactose, GOS, and fructan. According to our peer-reviewed prospective data, 78.0% of participants report clinically significant improvements to bloating after 4 weeks of FODZYME use.
On the medical side (Dr. Shrinivas Bishu, Michigan Medicine): Anti-IL-23 agents (ustekinumab, risankizumab, guselkumab, and mirikizumab) are rapidly becoming first-line for IBD, offering a favorable safety and efficacy profile compared to older biologics. JAK inhibitors (tofacitinib, upadacitinib) are highly effective for colonic disease but carry the highest risk. Anti-TNFs remain in the toolkit but carry 30–40% antibody formation rates.
Critically: 20–40% of IBD patients have residual IBS-like symptoms even when inflammation is well-controlled. Diet can play a role in managing these functional symptoms, but that's distinct from its anti-inflammatory role. Keeping these goals separate is clinically important.
If IBS-like symptoms are driven by diet, FODMAPs could be worth looking at as possible triggers. If that's confirmed, FODZYME digestive enzymes for FODMAPs can help reduce these symptoms, without further dietary restriction.
On the nutrition side (GI Dietitian Stacey Collins, UCHealth):
Exclusive Enteral Nutrition (EEN): ~80% remission in pediatric Crohn's, steroid-sparing, 6–12 weeks. Preferred for pediatric CD per ESPGHAN/ECCO guidelines. Also works in pregnancy.
Crohn's Disease Exclusion Diet (CDED): A phased approach - Phase 1 (strict exclusion + partial EN, limits insoluble fiber) → Phase 2 (gradual reintroduction) → Phase 3 (long-term individualized). Growing evidence base.
Specific Carbohydrate Diet (SCD): Evidence does not support it for reliable remission induction. Symptom improvement ≠ disease remission, an important distinction. Not recommended as a standalone therapy.
DINE-CD Trial (n=194): SCD vs. Mediterranean diet over 12 weeks found no significant difference in symptomatic remission. The Mediterranean diet is now preferred, given its lower restriction burden and cardiometabolic benefits (Hashash JG et al. AGA Clinical Practice Update, Gastroenterology 2025).
Mediterranean diet for IBD: Appropriate across all phases, with texture modifications during flares (fork-tender, soft). Limit additives with evidence of harm: carrageenan, carboxymethylcellulose, polysorbate-80, and titanium dioxide.
Malnutrition screening matters: IBD patients are 5× more likely to experience malnutrition when hospitalized. Use validated tools (MST, MUST, ASPEN/GLIM criteria) routinely. Don't wait for visible signs of malnutrition to intervene.
Low Sulfur Diet in IBD (Allen Lee, Michigan): At high concentrations, hydrogen sulfide (H2S) causes mitochondrial dysfunction, barrier disruption, and visceral pain. The 4-SURE Diet increased resistant starch/fermentable fiber, reduce animal protein, avoid sulfite/sulfate/nitrite/nitrate/carrageenan. This diet showed 36% endoscopic improvement in a UC pilot (n=28, Day et al. Journal of Nutrition 2022). However, the double-blind RCT (n=53) showed reduced H2S but no clinical superiority over sham (15% composite response in both arms, Day et al. JCCO 2026). Most promising application: quiescent Crohn's disease with persistent symptoms - pilot data showed significant improvement in abdominal pain and bloating (Golob, Advances in Gastroenterology & Hepatology 2024). Early-stage, but worth watching.
Two back-to-back EoE sessions - one medical (Dr. Joy Chang, Michigan Medicine / ACG 2025 Guidelines) and one nutritional (GI Dietitian Amanda Lynett, Michigan Medicine) - gave us a thorough current-state picture.
EoE overview: Chronic immune-mediated disease with progressive eosinophilic inflammation → fibrosis.
Treatment ladder:
PPIs (first-line): ~40% response; omeprazole 20mg BID or 40mg daily
Topical steroids: 53–80% efficacy; budesonide oral suspension (BOS) FDA-approved February 2024; patients must be NPO 30–60 min after dosing
Dupilumab: First FDA-approved biologic for EoE (ages 1+), 300mg SC weekly; anti-IL-4Rα; significant efficacy for both histologic and symptomatic endpoints
Coming soon: Cendakimab (anti-IL13), tezepelumab, APT-1011 (fluticasone orodispersible tablet), and less invasive monitoring tools are in the pipeline.
Dietary therapy efficacy (histologic remission rates):
Elemental diet: 94.5% efficacy (great!), but low real-world feasibility (Arias et al. Nutrients 2024)
6-Food Elimination Diet (SFED): 61% efficacy
The step-up approach to the elimination diet is now recommended: start with 1FED (dairy elimination) or 2FED, escalate as needed. The ACG explicitly does not recommend allergy testing to guide food elimination because skin prick testing identifies only 13% of true dietary triggers. Each reintroduction step requires endoscopy with biopsy.
Most common triggers: Milk (50–60%), wheat, soy - though significant individual variation exists. Reintroduction data must drive clinical decisions, not assumptions.
Nutritional concerns: Supplement calcium, vitamin D, B vitamins, zinc, magnesium, selenium, and fiber - especially when multiple food groups are eliminated. Screen for ARFID and eating disorder overlap, particularly in patients with comorbid GERD, functional dyspepsia, or achalasia.
Reminder: EoE without treatment leads to recurrence. Maintenance therapy (medication or diet) is required long-term. 14-year DDW 2026 data shows highest remission rates with PPI + diet combination (Dhingra et al. DDW 2026). For patients managing with diet alone, SFED is the most cost-effective strategy over a 5-year horizon (Hiramoto B et al. American Journal of Gastroenterology 2025).
Dr. Kyle Staller (Mass General/Harvard) delivered one of the most myth-busting talks of the conference. A few things he wants us to stop saying to patients:
"Just drink more water" - Additional water is absorbed systemically. It doesn't remain in the GI lumen. Water alone does not treat constipation.
"Exercise will fix it" - Association exists, but effect size is small.
"Not all fiber is equal" - Correct. Soluble, gel-forming fiber (psyllium) outperforms insoluble fiber for constipation symptom improvement.
"IBS-C and CIC are distinct" - False. Constipation is a spectrum: normal-transit → IBS-C/mixed → slow-transit → obstructed defecation. These categories overlap.
He also flagged a clinically important issue: GLP-1 agonists are driving new constipation in a significant portion of users. 31.6% of obese patients on GLP-1s develop constipation, with a hazard ratio of 1.49 for new constipation (Wang K et al. Clinical Gastroenterology and Hepatology 2026). This is now a routine clinical consideration.
Pelvic floor dysfunction is frequently missed in "refractory" constipation. Dyssynergia should be diagnosed via anorectal manometry, balloon expulsion testing, and/or defecography, not assumed or dismissed. Referral to pelvic floor PT is often the most impactful intervention in this population.
Nutrition focus (GI Dietitian Megal Villareal): The first comprehensive evidence-based BDA Dietary Guidelines for Chronic Constipation (Dimidi E et al. Journal of Human Nutrition and Dietetics 2025) were the centerpiece of her talk. Key recommendations:
Psyllium: Best overall fiber supplement - increases stool frequency, softens consistency, reduces straining
Kiwifruit: 2–3 daily for ≥4 weeks; more effective than psyllium for stool frequency; preferred if psyllium causes side effects; comparable on straining
Magnesium oxide: 0.5–1.5g/day for ≥4 weeks; increases stool frequency, softens consistency, improves global symptoms and QoL
Inulin-type fructans: Soften stool; note increased flatulence
Rye bread: 6–8 slices daily for ≥3 weeks; effective but high volume may not be realistic for most patients
High mineral-content water: 0.5–1.5L/day; improves overall clinical response (Gerolsteiner, San Pellegrino have the highest magnesium and sulfate content in commercially available options)
Probiotics: Limited evidence; trial a specific strain for ≥4 weeks; Bifidobacterium lactis and Bacillus coagulans Unique IS-2 show some benefit
The SMART Constipation Diet - a new hypothesis-generating framework - integrates fiber optimization, hydration/mineral balance, fat quality and bile stimulation, microbiota support, and chrono-nutritional timing into a coordinated approach. It's not a validated clinical protocol yet, but it offers a useful scaffold for individualized counseling. Key practical habits: consistent meal timing, good toilet position (squatty potty), not sitting longer than 5–10 minutes, not ignoring the urge to go. Don't overcomplicate it: build good foundations first.
From clinical practice: those with chronic constipation and IBS-C tend to experience more discomfort with gas buildup, particularly with FODMAPs. FODZYME can help break down some of these FODMAPs (lactose, GOS, and fructan) before they reach the colon and lead to excess gas production. So for these patients, FODZYME may be a valuable add alongside these other strategies.
GI Dietitian Nancee Jaffe (UCLA/NJNS) gave a rich talk on how reproductive hormones influence GI function across a woman's lifespan, a topic that's underrepresented in most GI training.
Menstrual cycle effects: Progesterone inhibits colonic motility and slows gastric emptying. Estradiol reduces visceral hypersensitivity and strengthens the intestinal barrier. The result: GI symptoms follow a predictable monthly pattern for many women.
Menstruation/perimenstrual phase: Progesterone drops → prostaglandin surges → loose stools, abdominal pain, bloating, increased stool frequency. Particularly pronounced in IBS-D.
Follicular phase: Estradiol rises → fewest GI symptoms — best time to trial reintroduction of potential trigger foods.
Luteal phase: Progesterone peaks → constipation, bloating, slowed gastric emptying, possible GERD worsening. More pronounced in IBS-C.
Note on motility testing: Menstrual cycle phases can affect GI motility testing results - the luteal phase tends to slow transit. Consider follicular-phase testing if results are borderline, particularly for breath hydrogen transit testing and gastric electrophysiology (BSGM).
Practical clinical tip: Ask patients about their menstrual cycle. Track symptoms across the cycle. This single step can validate patient experience, identify patterns, and allow you to time dietary interventions strategically (e.g., reintroductions during the follicular phase).
Perimenopause and menopause: Erratic estrogen fluctuations in perimenopause produce unpredictable swings in GI symptoms - both constipation and diarrhea can occur. Sustained estrogen loss in menopause drives slower colonic transit, increased intestinal permeability, and worsening of pre-existing GI conditions (Ley & Saha, Nature Reviews Gastroenterology & Hepatology 2025).
The estrobolome - the collection of gut microbes capable of metabolizing estrogen - is a key concept here. A Western diet reduces beneficial estrobolome bacteria; a plant-forward diet increases fecal estrogen excretion and may support healthier estrogen recycling. This is one mechanism by which diet influences systemic estrogen levels in postmenopausal women.
Diet strategies for peri/menopause: plant-forward eating (fruits, vegetables, whole grains, legumes) to support microbiome diversity; isoflavone-rich foods (soy) to support the estrobolome; prebiotic and probiotic foods (fermented foods, yogurt); pelvic floor PT for postmenopausal pelvic floor atrophy. Think about the whole person - bones, brain, muscles, heart, and GI.
What happens if increasing dietary plant intake leads to more bloating and gas throughout these changes in the cycle? It could be fermentation of FODMAPs - FODZYME can help reduce the FODMAP-related symptoms, while still achieving a plant-rich diet!
Three speakers tackled the eating disorder (ED)-GI overlap in depth, and the clinical picture they painted was both sobering and actionable.
Dr. Jordan Shapiro (Gentle GI) framed the problem: DGBIs are the most common GI disorders in EDs - functional dyspepsia (90%), IBS (30–59%), constipation (38%), and 3+ DGBIs in 35–49% of patients. GI symptoms often precede recognition of the eating disorder, which means we in GI are frequently the first point of clinical contact.
GI Dietitian Emily Arkin (RD Emily & Team) highlighted the mechanisms driving ED-GI overlap:
Dieting and low energy availability alter GI motility - delayed gastric emptying, constipation, stool leakage, abdominal pain. Dieting may be the strongest predictor of new ED onset in adolescents.
Overfocus on food in managing GI conditions increases ED risk: high LFD adherence doubles ARFID risk; patients with exclusion diet history are 3× more likely to meet ARFID criteria (Atkins et al. Neurogastroenterology & Motility 2023).
Recommendations that collude with ED thinking - reinforcing food fear, weight stigma, or hypervigilance - may limit GI benefit and worsen mental health outcomes.
Practical reframe: "The nutrition information is neutral. The brain it lands on is not always equipped to keep it neutral." (Emily Arkin, quoting Sharon Chirban). When prescribing dietary interventions for GI conditions, consider who you're prescribing to - de-emphasize food where possible, consider non-diet therapies first, and watch for restriction creep.
GI Psychologist Helen Burton-Murray (MGH/Harvard) provided the clinical tools for screening:
Nine-Item ARFID Survey (NIAS) for ARFID screening: A brief, validated self-report tool covering picky eating, appetite issues, and fear-based avoidance. ARFID is distinct from other EDs. The distinguishing features are persistent food restriction, compromised dietary intake, and failure to reintroduce despite clinical improvement.
For broader ED screening: EDE-Q8 (likely ED: global score ≥4.0; possible ED: ≥2.3) and the SCOFF questionnaire (2+ "yes" = likely ED) are practical options. Note: neither SCOFF nor EDE-Q8 screens for ARFID specifically.
What to say: "It sounds like your GI symptoms are making it really difficult to eat... I hear similar concerns from other patients who've benefited from working with a dietitian or behavioral health provider. The first step is an evaluation to learn more about your symptoms and make recommendations." - A warm, non-judgmental referral framing from Dr. Burton-Murray
Dr. Lin Chang (UCLA) gave a comprehensive deep dive into the vagus nerve as a bidirectional gut-brain conduit, and the growing evidence for vagal-targeted interventions in GI conditions.
Why it matters in DGBI: The vagus nerve integrates interoceptive signals from the gut and modulates motility, secretion, immune activity, and visceral sensory processing. In IBS and other DGBIs, altered autonomic and interoceptive regulation - measurable via heart rate variability (HRV) - may underlie symptoms. Dysregulation co-occurs with fibromyalgia, POTS, migraines, joint hypermobility (EDS), and interstitial cystitis.
Anti-inflammatory role: Vagal nerve stimulation activates the cholinergic anti-inflammatory pathway, suppressing cytokine release and reducing systemic inflammation, a key mechanism linking the nervous system to immune regulation in DGBI.
HRV as a clinical marker: Wearable-derived HRV provides accessible insight into autonomic nervous system (ANS) balance. Reduced HRV has been shown to predict IBD flares and COVID-19 symptom onset (Hirten R et al. Gastroenterology 2025). Upcoming data: wearable-based HRV measurement in IBS is pointing to lower vagal tone and a blunted HRV peak specifically in IBS-D - early research but clinically relevant.
Behavioral interventions work via vagal pathways: CBT significantly increased cardiovagal tone in IBS-C patients vs. general medical information control, and improvements were sustained at 24 weeks (Jang A et al. Journal of Neurogastroenterology & Motility 2017).
Emerging neuromodulation approaches:
taVNS (transcutaneous auricular vagus nerve stimulation): In a 4-week RCT in IBS-C (n=42), taVNS achieved 81% responder rate vs. 26.3% sham (p=0.001), improved CSBMs, pain, and IBS-SSS, and significantly increased HF-HRV, with the HRV improvement correlating with more bowel movements (Shi X et al. JCI Insight 2021).
PENFS (peripheral electrical nerve field stimulation/IB-Stim): Reduces abdominal pain in pediatric FGID (Lancet GH 2017); adult IBS pilot data are emerging.
Cervical nVNS: A pilot study in chronic nausea/vomiting (n=41) showed use during nausea episodes reduced rescue antiemetics from 1.19 to 0.45 pills/day, with improvements in abdominal pain, reflux, constipation, and indigestion, but not diarrhea (Barahona G et al. Digestive Diseases and Sciences 2026).
Gut-brain link: Microbial metabolites including bile acids, short-chain fatty acids, and 3-indoxyl sulfate, directly stimulate vagal afferent neurons via receptor-dependent signaling (Jameson K et al. iScience 2024). This means gut health impacts autonomic nervous system regulation, and diet may offer a future lever for targeted vagal modulation.
For GI dietitians: the vagal neuromodulation data reinforces that mind-body and behavioral interventions aren't just "soft" add-ons, they have measurable physiologic effects. Diaphragmatic breathing, CBT, gut-directed hypnotherapy, and structured relaxation all target this system. These belong in our clinical toolkit. And beyond device-based stimulation: when managing a dysregulated ANS, gut-brain behavioral therapy, ideally via a GI psychologist, remains a core tool. Improving symptoms through these modalities physically resets the sensitivity set-point.
And what else can help reducing stress for an already struggling ANS? More diet flexibility and freedom to enjoy food in social and cultural settings. FODZYME digestive enzymes can help with this, while still providing relief from FODMAP-related symptoms.
GI Dietitian Natalie Manitius (Salvo Health/Biograph) gave a well-organized, evidence-grounded Complementary and alternative medicine (CAM) overview, acknowledging patient preference while staying honest about what the data actually supports.
23-44% of GI patients use CAM, and over 80% report it helpful for overall wellbeing. In those with IBD, 75% may not disclose CAM use to their physicians. This is a gap we can bridge by asking non-judgmentally.
Brain-gut interventions with good evidence:
Diaphragmatic breathing: First-line for rumination syndrome (2018 AGA), supragastric belching, aerophagia. 74-90% improvement in rumination (Pomenti et al. Current Gastroenterology Reports 2025). Practice 5–10 min daily; for rumination, initiate within 30–60 min of eating. Takes 4–6 weeks. No cost, no risk.
Yoga: Improved IBS-SSS and QoL comparable to low FODMAP diet (Schumann et al. Alimentary Pharmacology & Therapeutics 2018). In IBD: reduced anxiety, depression, and perceived stress; trend toward lower calprotectin and CRP (meta-analysis, 7 RCTs, Pan L et al. 2025).
Tai Chi: Pilot in IBS-C (n=27, Mass General): improved IBS-SSS, bloating, constipation, food fear scores, and abdominal circumference over 8 weeks (Staller et al. Neurogastroenterology & Motility 2022).
Supplements & therapies with some evidence:
Melatonin (1–5 mg): Analgesic, anti-inflammatory, motility support. Improved IBS severity, pain, and QoL in 4 RCTs (Chen HK et al. Journal of Formosan Medical Association 2023). Consider when first-line pain interventions fail in IBS. Limit to <3 months. Start at 1 mg and titrate.
Curcumin (1–3g/day): Anti-inflammatory via NF-κB inhibition; adjunct in UC - clinical and endoscopic remission superior to placebo (13 RCTs, Mohseni et al. Frontiers in Nutrition 2025). Not yet recommended via ACG 2025 mild-moderate UC guidelines. Monitor liver function tests and avoid formulations with bioperine or nanoparticles due to higher toxicity risk.
Acupuncture: For functional dyspepsia (FD): high/moderate evidence in 23 RCTs (n=2,454), superior QoL vs. prokinetics (Li et al. Frontiers in Medicine 2026). For IBS: improved QoL and severity, though abdominal pain improvement was not significant (14 studies, n=2,038; Zhou et al. PLoS One 2025).
Ginger (0.5–2g/day): Halves gastric emptying time and increases antral contractions in healthy volunteers. Useful for FD, nausea, and possibly gastroparesis. Use caution with antiplatelet therapy and avoid in severe GERD.
HMOs (Human Milk Oligosaccharides, 5g/day): Multicenter open-label trial (n=317): IBS-SSS ↓54.2%, abdominal pain/bloating ↓59.4%, QoL improved significantly (Palsson et al. Clinical and Translational Gastroenterology 2020). Consider for stubborn IBS bloating/pain after first-line interventions.
SBI (Serum-Derived Bovine Immunoglobulins / Bovine-derived IGG): Acts on luminal bacterial antigens, prevents bacterial translocation, modulates inflammation, enhances tight junction expression. Two studies in IBS exist (Good L et al. World J Gastroenterol 2015; Valentin S et al. Physiol Rep 2017). Best supported for IBS-D and chronic diarrhea; no data for constipation.
GI Dietitian Therezia AlChoufete (UPMC IBD Center) closed the program with a practical and values-grounded talk on culturally inclusive GI nutrition care.
The core premise: standard GI nutrition therapies including the low FODMAP diet, Mediterranean diet, and IBD exclusion diets, are largely built on Western dietary patterns. Cultural food practices, symptom interpretation, and beliefs about treatment all influence clinical outcomes. Building inclusive care doesn't require expertise in every culture; it requires awareness, curiosity, and adaptability.
Two practical frameworks:
T.R.U.S.T.: Tell me more about what you eat → Rituals and traditions → Usual staples in the diet → Symptom-food correlations → Tailor the diet based on individual needs. A patient-led history tool that builds rapport while capturing clinically relevant information.
G.P.S.: Get a better idea (open-ended questions) → Partner up (collaborative problem-solving) → Simplify the goals (one small, manageable change at a time). A counseling framework for adapting dietary recommendations to cultural context without abandoning therapeutic goals.
A note on AI in GI care: AlChoufete raised an important point about AI tools that are trained on non-diverse datasets. These may perpetuate rather than reduce health disparities. As we incorporate AI tools into practice, equity should be part of the evaluation criteria, not an afterthought (Uche-Anya E et al. Gut 2022).
At FODZYME, this topic is really important to us. With digestive enzyme therapy, we believe it is possible for patients to enjoy the foods they love, that are available, and are aligned with their culture. Instead of sticking to an "approved" meal plan or restrictive food list, FODZYME allows patients to continue eating the food they love, while still reducing FODMAP-related symptoms.
The through-lines from this year's FOOD conference: the gut is not a siloed organ system. Hormones, psychiatric comorbidities, cultural identity, the nervous system, and the microbiome all shape how our patients experience and respond to GI conditions. Our dietary interventions need to reflect that complexity: precise where evidence supports it, flexible where it doesn't, and always individualized.
This is exactly where FODZYME is positioned as a resource for your patients. As we move forward, we look forward to learning with you and supporting your care of patients through further research, product development, clinician education, and advocacy. If you'd like free samples to offer patients in your practice, you can request those here.