The Innovation | Gastroenterology

Coffee and tea consumption in relation to chronic disease: An epidemiological perspective the-innovation.org/article/doi/10…

🎯Just Accept/The Innovation Nutrition Coffee and tea consumption in relation to chronic disease @HarvardHealth @Harvard @harvardmed @HarvardChanSPH Open Access doi.org/10.59717/j.xin… #Nutrition #Meded #Medx #Coffee #Tea #Science #Health #Academic #PhD #PrecisionNutrition

Metabolic health is mental health. Exercise & diet must be first-line treatments.

GLP-1RAs transform T2DM care. Tirzepatide excels in glycemic control and weight loss, with multi-organ benefits. #GLP1RA #T2DM

Coffee and tea consumption in relation to chronic disease: An epidemiological perspective doi.org/10.59717/j.xin…

nejm.org/doi/full/10.10… REVIEW ARTICLE 1 April 26 @NEJM GLP-1 Receptor Agonists

📢IBS Awareness Month 2026🎉 🚨Most recent highlights on #IBS articles @NGMJournal 🔥#DiveDeep⏬ @IBS_Maastricht @AndreaShin_GI @nicolascenac @NehaSantucciMD @KristenSEdwards #AllisonMalcolm #DavidReed @Pierfra_Visaggi @ThisIsButt #KristinElfers #WilmarieMorales @Rajan___Singh👏

Castells-Nobau et al. present “Gut microbial modulation of 3-hydroxyanthranilic acid and dopaminergic signalling influences attention in obesity” via bit.ly/3POWtXN (Original research, Gut microbiota section). The gut–brain axis in action. This fascinating study links microbial metabolism to dopaminergic signalling and attention, providing mechanistic insight into how the microbiome may influence behaviour in obesity. #Obesity #Microbiome

GLP-1 receptor agonists are increasingly used to treat type 2 diabetes and obesity, and trials have shown reductions in cardiovascular risk and slowing of kidney failure. Adverse events are mostly gastrointestinal. Read the Review Article “GLP-1 Receptor Agonists” by Clifford J. Rosen, MD, and Julie R. Ingelfinger, MD, from @tuftsmedschool and the Maine Medical Center Institute for Research: nejm.org/doi/full/10.10…

New! Online now: The gut microbiota alleviates depression by remodeling gut-brain energy metabolism dlvr.it/TRp62v

pubmed.ncbi.nlm.nih.gov/41689434/ H. pylori induces production of the pan-immunosuppressive cytokine IL-37 to enhance colonization, modulate gastritis and suppress innate, cellular and humoral immunity to ultimately promote pathogenesis in the host.

Castells-Nobau et al. present “Gut microbial modulation of 3-hydroxyanthranilic acid and dopaminergic signalling influences attention in obesity” via bit.ly/3POWtXN (Original research, Gut microbiota section). The gut–brain axis in action. This fascinating study links microbial metabolism to dopaminergic signalling and attention, providing mechanistic insight into how the microbiome may influence behaviour in obesity. #Obesity #Microbiome

Where are we on the management of diarrhea with gut microbiome manipulation? Giovanni Barbara et al. explore what's new and interesting @TAGastroenterol: tinyurl.com/24ejk8nd

The interplay between environmental and human microbiomes is fascinating! From soil to skin, from oceans to gut—microbial communities shape our planet's health and our own. 🌍🦠 #Microbiome #OneHealth #EnvironmentalScience #HumanHealth #Biotechnology doi.org/10.59717/j.xin…

🌡️ [Hepatology Breakthrough] Cell Metabolism publishes comprehensive MASH inflammation review: 1️⃣ Three major inflammatory pathways dissected 2️⃣ New multi-omic classification strategy 3️⃣ Next-gen anti-inflammatory metabolic drugs emerge #LiverDisease #MetabolicSyndrome

Excess alcohol = fatty liver → cirrhosis. Fatty liver = MASLD (metabolic) / MetALD (mix) / ALD (alcohol: >3W/4M drinks/day)

B) Hepatitis B infection

@MondayNightIBD @joshsteinbergMD @ibddoctor @LoriPlung @berinsj @DrRosenIBD @IBDGastroDocSg @rogeriosparra @ibdseb @JamesHaddadMD @puentesfabi @fgomollon @Youcantmakethi4 @srmbeauroy #IBDAlgorithm 🧠 #ASUC 🚨 📍Day0️⃣: R/o 🦠CDI/CMV ➕scope early 💉IV steroids ➕DVT prophylaxis 📊Reassess daily (PRO + CRP) ⏳Day3️⃣: No response ➡️Rescue w IFX/ CsA/ JAKi 🎯Day6️⃣: Response? ✔️ Transition & maintain ❌ Don’t delay surgery Rx choice🟰availability➕💰➕access

Leung et al. present the paper “Asian Pacific Association of Gastroenterology task force recommendations on surveillance for Helicobacter pylori associated gastric premalignant conditions” via bit.ly/4sY2YWP (Guideline section) This comprehensive guideline provides clear, practical recommendations for surveillance of gastric premalignant conditions, supporting risk-based approaches to improve early cancer detection. #GUTGuidelines #Hpylori #HelicobacterPylori

The gut is a mitochondrial organ. Every function it performs requires ATP at a cellular level and this is the piece that gets completely ignored in conventional gastroenterology AND most functional gut protocols tbh. Motility, enzyme secretion, mucus production, barrier maintenance, immune tolerance, nutrient absorption. These are ALL powered by mitochondria in your enterocytes, colonocytes, goblet cells & enteric neurons. When mitochondrial function drops in the gut, everything breaks simultaneously. ↓ mito in colonocytes → ↓ O2 consumption → ↑ luminal oxygen → obligate anaerobes die off → ↓ butyrate → colonocytes lose their primary fuel source. Vicious cycle right there. ↓ mito in goblet cells → ↓ MUC2 mucin output → thinning mucus layer → direct bacterial contact with epithelium → immune activation. This one is a very underrated as a driver of gut inflammation btw. ↓ mito in crypt stem cells → ↓ epithelial renewal (your gut lining replaces every 3-5 days which is a HUGE energy demand) → older damaged cells with ↓ brush border enzymes and absorptive capacity. So potentially your gut is not renewing itself as often as is expected. ↓ mito in enterocytes → ↓ tight junction maintenance (occludin, claudins, ZO-1 all require constant ATP) → ↑ permeability → LPS → endotoxemia → which tanks mito function further and drives systemic inflammation. Also gonna be a big driver of neuroinflammation too. Every layer fails and every failure feeds back into worse mitochondrial output. That is the understanding that systems biology gives us. This is the central vicious cycle underlying most chronic gut pathology imo and its prob why so many people cycle through gut protocols without lasting results. And its also why gut issues tend to co-exist with almost any other health problem/ Many work more directly on the microbiome composition but the cellular infrastructure or terrain which holds that microbiome doesnt have teh energy or conditions to maintain and self-regulate it so nothing sticks. What I look at with clients: - Metabolomix+ or OAT to map metabolic bottlenecks - ETC cofactor status - CoQ10, B2, B3, iron, copper, Mg for ATP itself - Gut function testing to assess butyrate producer populations - Mitotoxin exposure (especially thngs like PPIs which simultaneously ↓ HCl AND have direct mito effect) - Light/circadian environment cus mito function IS circadian - Basically any other environmental mismatch