In this encore episode, we detail the gut-immune axis, focusing on the protective mucus layer and the role of lactoferrin in intestinal health. We discuss endogenous secretions and how lactoferrin functions as an antimicrobial, immunomodulatory, and iron-regulating glycoprotein, influencing microbial balance and intestinal barrier integrity. Additionally, we highlight lactoferrin testing and levels. We finish by going through supplementation as a phenomenal tool.



Topics:

1. The Intestinal Barrier & Mucus Layer

- The intestinal lumen, microbiome, mucus layer, epithelial cells, and lamina propria.

- The mucus layer: antimicrobial peptides (AMPs) and secretory IgA (sIgA).

- Intestinal epithelial cells including goblet cells and enterocytes.



2. Immune Cells in the Gut

- The lamina propria.

- Macrophages, dendritic cells, neutrophils, B cells, T cells, mast cells, and more.



3. Antimicrobial Peptides & Secretory IgA

- AMPs and sIgA in the mucus layer regulate microbial balance and prevent pathogen adhesion.



4. Lactoferrin: Functions & Sources

- Iron-binding glycoprotein, antimicrobial and immunomodulatory properties.

- Found in mucosal secretions, colostrum, and more.

- Intestinal epithelial cells (IECs) and neutrophils.



5. Lactoferrin’s Role in Intestinal Health

- Regulates iron absorption via lactoferrin receptors (LFR)on enterocytes.

- Sequesters free iron, limiting bacterial growth, bacteriostatic.

- Destabilizes bacterial membranes, cell lysis, bactericidal.



6. Lactoferrin Levels

- Neutrophils release lactoferrin during infection,increasing its presence in the large intestine.

- Fecal lactoferrin levels.

- Fecal calprotectin levels.



7. Lactoferrin & Candida Overgrowth

- Fungal membranes.

- Aiding in the inhibition of biofilm formation.



8. Lactoferrin Supplementation & Benefits

- Supports gut microbiota, epithelial integrity, and immune modulation.

- Bovine colostrum and as a supplement.



9. Conclusion

- The intestinal mucus layer is key to gut barrier function.

- Lactoferrin plays a central role in microbial regulation and immune defense.







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183. The Gut-Immune Axis | Gastrointestinal Mucus & Lactoferrin, Lactoferrin Levels, a Brief Discussion on Candida Overgrowth, & More

In this encore episode, we go through the pathophysiology of hydrogen sulfide (H₂S)-dominant small intestinal bacterial overgrowth (SIBO), focusing on its role in intestinal motility disruption, microbial dysbiosis, and epithelial barrier dysfunction. We detail the interplay between the enteric nervous system (ENS), interstitial cells of Cajal (ICCs), and migrating motor complex (MMC) in regulating small intestinal transit and how excess H₂S modulates smooth muscle activity, inflammatory signaling, and gastrointestinal transit time. Lastly, we detail symptoms and related SIBO subtypes.



Topics:

1. Introduction to Hydrogen Sulfide Dominant SIBO 

   - Overview of hydrogen sulfide (H₂S) SIBO

   - Sulfate as an electron acceptor 

   - H₂S production, sulfur-containing amino acids

   - Physiological roles of H₂S vs. in excess 

 

2. Hydrogen Sulfide and Gastrointestinal Motility 

   - Impact on transit time

   - Association with IBS-like symptoms, diarrhea 

 

3. Intestinal Motility and Regulation 

   - Role of the ENS, ICCs, smooth muscle cells, and neurotransmitters in motility 

 

4. The Enteric Nervous System (ENS) and Gut Motility 

   - ENS as the "second brain" and its control over digestion 

   - Myenteric and submucosal plexuses: regulation of peristalsis, secretion, blood flow 

   - Gut-brain axis involvement via vagus nerve signaling 

   - ICCs as pacemaker cells generating slow-wave electrical activity 

   - MMC’s role in clearing debris and bacteria

 

5. Dysregulated Motility and SIBO Development 



6. Overlapping Symptoms Across SIBO Subtypes 

   - Shared symptoms

   - Hydrogen and H₂S-dominant SIBO vs. IMO

 

7. Gastric Acid and Its Role

   - HCl secretion by parietal cells and its role in digestion and microbial defense 

   - Hypochlorhydria and bacterial overgrowth 

 

8. Conclusion

   - Root cause approach.











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182. Hydrogen Sulfide Dominant Small Intestinal Bacterial Overgrowth & Gastrointestinal Motility | Contributing Factors, Symptoms, and More

In this episode, we detail the oral microbiome and its relationship with the intestinal microbiome, detailing the oral-gut microbiota axis. We discuss the stepwise development of oral biofilm, the transition from plaque to dental calculus, and potential systemic impacts of oral dysbiosis, while highlighting intestinal health and focusing on Fusobacterium nucleatum. We then detail possible symptoms of oral dysbiosis as well as testing modalities.



Topics:

1. Overview of the Oral Microbiome and the Oral-Gut Axis

 - The oral cavity and the gut: microbially dense sites.

 - These regions are anatomically distinct but connected and capable of influencing each other.

 - The oral microbiome: bacterial species, fungi, viruses, archaea, protozoa.

 - Microbial distribution is influenced by the topography and chemistry of various oral surfaces.

 

2. Oral Cavity Anatomy and Microenvironments

 - The oral cavity is divided into the vestibule and oral cavity proper.

 - Lined by oral mucosa, which varies in structure.

 - These anatomical variations create unique ecological niches that support different microbial populations.

 

3. Tooth Structure and Relevance to Microbial Colonization

 - Teeth are embedded in the alveolar processes of the maxilla and mandible.

 - Tooth structure.

 - Long-term microbial colonization and biofilm development.

 

4. Biofilm / Dental Plaque Development

 - Biofilm begins with the formation of the acquired pellicle.

- Pioneer species secreting extracellular polymeric substances (EPS).

- Secondary colonizers coaggregate.

- Coaggregation is species-specific.

- Example.

- Aerobes can lower local oxygen levels, creating micro anaerobic niches that support obligate anaerobes.

 

5. Maturation of the Biofilm

 - Biofilm composition shifting to anaerobic, proteolytic species such as P. gingivalis.

 - F. nucleatum: a bridge species.

 

6. Mineralization and Formation of Dental Calculus

 - Mineralization, calcium and phosphate deposition.

 - Dental calculus.

 - Can promote further accumulation and worsen inflammation.

 

7. Oral Dysbiosis

 - An imbalance in the oral microbial community.

 - Potential signs and symptoms.

- Halitosis, swollen or bleeding gums, tooth sensitivity, new cavities, dry mouth or altered taste, recurrent infections, coated tongue, plaque buildup near the gumline.

 

8. Oral-Gut Axis and Systemic Implications

 - Physical, chemical, biochemical, and immunological barriers aid in preventing oral bacteria from colonizing the gut.

 - Oral bacteria can potentially impact intestinal health.

 -  F. nucleatum and IBD.

 

9. Oral Microbiome Testing

10. Multi-Factorial





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181. The Oral-Gut Axis | Oral Biofilm Formation, Oral Dysbiosis and Symptoms, The Oral Microbiome and Intestinal Health, and Oral Microbiome Testing

In this encore episode, we detail the intestinal mycobiome and the mechanisms by which beneficial microbes aid in regulating opportunistic fungal species: Candida albicans. We discuss Candida overgrowth virulence and how disruptions in microbial balance, immune function, and epithelial integrity impact Candida's pathogenicity. Additionally, we discuss the role of mast cells in the lamina propria, their involvement in mucosal immunity, and how Mast Cell Activation Syndrome (MCAS) can be exacerbated by fungal dysbiosis / microbial imbalances.





Topics:



1. Introduction

- The intestinal mycobiome and its role in intestinal health. 

- Regulating populations of opportunistic fungal species like Candida albicans.

- Mast cell activation syndrome (MCAS) intro. 

 

2. Structure of the Intestinal Barrier

- The microbiome and mucus layer: microbes, mucins, antimicrobial peptides, sIgA.

- The epithelial monolayer: enterocytes, goblet cells, Paneth cells, enteroendocrine cells…

- Tight junction proteins and paracellular transport.

- The lamina propria beneath the epithelium: immune cells and more.

 

3. Candida’s Pathogenicity and Barrier Disruption

- Exists primarily in its yeast form, regulated by microbial competition, host immune defenses, antifungal peptides. 

- Secretory IgA (sIgA) and immune surveillance mechanisms help regulate fungal populations.

- Chronic stress, immune suppression, and dysbiosis can deplete sIgA, increasing susceptibility to Candida proliferation. 

- Environmental triggers such as immune suppression, microbial depletion, inflammatory cytokines.

- Yeast-to-hyphal transition, deeper tissue invasion. 

- Secreted aspartyl proteinases (SAPs), phospholipases, candidalysin: epithelial damage.

- Pattern recognition receptors (PRRs) and overgrowth detection.

 

4. Impact of Beneficial Bacteria on Candida Overgrowth 

- Beneficial bacteria compete with Candida for nutrients and epithelial adhesion sites. 

- Short-chain fatty acids (SCFAs) produced by beneficial bacteria.

- Depletion of beneficial bacteria removes ecological resistance, allowing Candida to proliferate unchecked. 

 

5. Mast Cells in the Lamina Propria and Their Role in Intestinal Immunity

- Mast cell location

- Upon activation, mast cells release histamine, cytokines, proteases, and more that regulate gut immune responses. 

- Histamine can increase gut permeability and modulate local immune activation. 

- Tryptase and chymase.

- Pro-inflammatory cytokines.

 

6. Mast Cell Activation Syndrome (MCAS)

- Mast cell hyperactivation.

- Environmental triggers, toxins, chronic infections, and stress.

- Candida overgrowth and mast cell activation.

- Addressing microbial imbalances and reducing the body’s total microbial, chemical, and toxin burden.

- A diverse microbiome. 

 

7. Conclusion

- Candida overgrowth and regulation via immune defenses and beneficial bacterial competition.

- MCAS, root cause approach.









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180. Intestinal Mycobiome | The Role That Beneficial Microbes Play in Regulating Pathogenic Fungal Species, Candida Overgrowth, & a Conversation on Mast Cell Activation Syndrome

In this encore episode, we detail the pathophysiology of intestinal methanogen overgrowth (IMO), hydrogen-dominant small intestinal bacterial overgrowth (H₂-SIBO), and hydrogen sulfide-dominant SIBO (H₂S-SIBO), discussing their mechanistic interactions and overlap. We discuss methanogenic archaea, as well hydrogen sulfide- and hydrogen-producing microbes and their contributions to altered gastrointestinal motility, epithelial barrier function, and neuromuscular signaling. We detail host endogenous defense mechanisms, including gastric acid secretion, pancreatic enzymatic activity, bile flow, intestinal motility, and more.



Topics:

1. Introduction

- Overview of intestinal methanogen overgrowth (IMO), hydrogen sulfide-dominant SIBO, and hydrogen-dominant SIBO 

- Discussion of overlap

 

2. Intestinal Methanogen Overgrowth (IMO)

- Characterized by an overabundance of methane-producing archaea 

- Methane and intestinal transit

- Bloating, abdominal discomfort, constipation 

- Associated with irritable bowel syndrome with constipation (IBS-C) 

 

3. Overlap Between IMO and SIBO Subtypes

- Hydrogen as a substrate for methane and/or hydrogen sulfide production

- Shared potential root causes

 

4. Small Intestinal Bacterial Overgrowth (SIBO) and Protective Mechanisms

- The small intestine remains relatively free of bacteria due to protective mechanisms 

- Gastric acid secretion 

- Pancreatic enzymes and bile

- Intestinal motility

- Structural abnormalities

 

5. Hydrogen-Dominant SIBO

- Increased hydrogen and intestinal transit

- Potential symptoms, diarrhea, postprandial bloating 

- Different forms of SIBO can coexist

 

6. Hydrogen Sulfide-Dominant SIBO

- H₂S and intestinal motility

- H₂S and intestinal epithelial integrity

- Symptoms, associations with IBS diarrhea   

 

7. Host Defense Mechanisms Regulating Microbial Balance

- Gastric acid secretion, pancreatic enzyme activity, bile flow, intestinal motility, and more

 

8. Gastric Acid and Its Role in Microbial Regulation

- Parietal cells secrete hydrochloric acid (HCl) and intrinsic factor 

- Chief cells secrete pepsinogen, conversion into pepsin in acidic conditions 

- Gastric acid, digestion and antimicrobial defense 

 

9. Hypochlorhydria

- Low gastric acid impairs microbial defense

- Reduced acidity disrupts digestion and downstream pancreatic enzyme and bile release 

 

10. Pancreatic Enzymes and Their Role in Microbial Regulation

- Pancreatic enzymes, digestion, antimicrobial activity

- Enzymes modify chyme to limit fermentable substrates that fuel microbial proliferation 

 

11. Intestinal Motility

- Coordinated contractions propel food, microbes, and waste through the GI tract 

- The enteric nervous system (ENS) and gut motility

- The myenteric plexus controls peristalsis, while the submucosal plexus regulates secretion and absorption 

 

12. Conclusion

- Intestinal methanogen overgrowth (IMO), hydrogen-dominant SIBO, and hydrogen sulfide-dominant SIBO 

- Overlap in symptoms and microbial interactions 

- Host defense mechanisms, including gastric acid, pancreatic enzymes, and motility 

- Intestinal motility and ENS function in microbial homeostasis 

- Hydrogen sulfide as a gasotransmitter





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179. Intestinal Motility & SIBO | Interactions Among Intestinal Methanogen Overgrowth (IMO), Hydrogen-Dominant Small Intestinal Bacterial Overgrowth, and Hydrogen Sulfide-Dominant SIBO

In this episode, we highlight the stomach's role in vitamin B12 absorption and bioavailability, detailing the cellular composition of the gastric mucosa and further highlighting mucous cells, parietal cells, and chief cells. We also briefly discuss Helicobacter pylori and common symptoms, while detailing H. pylori's survival mechanisms in the acidic gastric environment as well as potential impacts on the gastric mucosal barrier.

 

Topics:

1. Introduction

- Overview of the stomach's role in B12 absorption

- Helicobacter pylori

 

2. H. pylori Overview

- Gram-negative bacterium, can colonize the stomach lining

- Many individuals remain asymptomatic

- Symptoms

- Can contribute to gastritis and peptic ulcers

- Produces urease, hydrolyzes urea into ammonia (NH₃) andcarbon dioxide (CO₂)

- Ammonia neutralizes stomach acid locally, protective microenvironment

- H. pylori damages the mucosal barrier and contributes to persistence

- Possesses additional virulence factors

 

3. Gastric Anatomy 

-  Stomach is divided into the cardia, fundus, body, and pylorus

- The gastric mucosa

- The epithelial lining; mucous cells, parietal cells, chief cells, and more

 

4. Mucous Cells and Mucosal Protection 

- Line the gastric pits and secrete thick, viscous mucus

- Mucus composed of water, mucin glycoproteins, and other low-molecular-weight molecules

- Traps bicarbonate ions (HCO₃⁻)

- Shields the stomach lining

 

5. Parietal Cells 

- Located in the gastric glands, predominantly in the fundus and body

- Secrete hydrochloric acid (HCl)

- Secrete intrinsic factor (IF)

 

6. Vitamin B12 Overview 

- Cobalamin: DNA synthesis, red blood cell formation, neurological function, methylation, and more

- Methylcobalamin and 5-deoxyadenosylcobalamin

- Non-active forms include hydroxocobalamin and synthetic cyanocobalamin

 

  7. Vitamin B12 Absorption Pathway 

- B12 is released from proteins by HCl and pepsin

- Binds first to haptocorrin

- In the small intestine, pancreatic enzymes degrade haptocorrin

- B12 binds intrinsic factor

- Absorption in the ileum

- Impairment

 

8. Chief Cells 

- Located in the gastric glands

- Secrete pepsinogen, activated by acid into pepsin

- Also secrete gastric lipase

 

9. Hydrochloric Acid (HCl) 

- Secreted by parietal cells

- Denatures dietary proteins and activates pepsinogen

- Acts as a defense mechanism by aiding in sterilizing ingested food

 

10. Relevance of H. pylori

- Produces urease that breaks down urea into NH₃ and CO₂

- Ammonia neutralizes acid locally, forming a protective “bubble”

- Enhances mucosal damage and microbial persistence

 

11. B12 Absorption 

- Multiple factors and root causes can impair absorption

- H. pylori

 

12. Hypochlorhydria 

- Symptoms

- Absorption: vitamin B12, iron, calcium, magnesium, more

- Small Intestinal Bacterial Overgrowth (SIBO)

 

13. Conclusion

- Multi-factorial, root cause approach



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178. The Stomach & Gastric Acid | Vitamin B12 Absorption and a Brief Conversation on H. pylori

In this episode, we highlight vitamin D₃ in gastrointestinal health, with a focus on intestinal barrier function and the gut-immune axis. We discuss how vitamin D is metabolized into its active form, 1,25-dihydroxyvitamin D, and how 1,25-dihydroxyvitamin D can support the intestinal mucosa, while highlighting the intestinal epithelium and immune cells in the lamina propria. Through this, we further detail the role of regulatory T cells in supporting immune balance and modulating immune function.



Topics:

1. Introduction

- Highlighting intestinal barrier function and the gut-immune axis with a focus on vitamin D₃

 

2. Vitamin D Synthesis and Metabolism

- Skin and 7-dehydrocholesterol; dietary intake.

- Transported through the bloodstream bound to vitamin D binding protein.

- First hydroxylation in the liver to form 25-hydroxyvitamin D₃ (25(OH)D₃).

- Testing.

- Second hydroxylation in the kidney to form the active 1,25 dihydroxyvitamin D₃ (1,25(OH)₂D₃).

- Local activation also occurs.

 

3. Intestinal Barrier Anatomy

- The intestinal epithelium forms a selectively permeable monolayer that interfaces with the gut lumen.

- Covered by a mucus layer: mucins, antimicrobial peptides, secretory IgA.

- Mucus layer provides physical and biochemical protection.

- Tight junction proteins and paracellular permeability.

- Molecules crossing the epithelium.

- Disruption of tight junctions, immune cell exposure to luminal contents.

- The lamina propria and Gut-Associated Lymphoid Tissue (GALT).

- Maintaining tolerance while defending against pathogens.

 

 4. Vitamin D’s Role in Barrier Support and Immune Modulation

- 1,25-dihydroxyvitamin D₃, tight junction integrity, immune regulation, and more.

- Regulatory T Cells (Tregs) and immune balance.

 

 5. Vitamin D₂ and D₃

- D₃ (cholecalciferol) is more biologically effective and binds DBP more strongly.

 

 6. Vitamin D Levels

- Levels observed in autoimmune conditions, IBS, and more.

- Symptoms.

- Insufficient and excessive levels of vitamin D can be detrimental.

- Multi-system.

 

 7. Conclusion

- Multifactorial: Numerous factors regulate vitamin D levels.

- Gastrointestinal health root cause approach.



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177. The Gut-Immune Axis, Intestinal Barrier Function, & Vitamin D₃ | Activated 1,25-dihydroxyvitamin D₃ and Immune Function, Vitamin D Testing, & More

In this episode, we discuss the gut-immune axis and Small Intestinal Fungal Overgrowth (SIFO), with a mechanistic focus on immune activation and epithelial barrier disruption. We detail contributing factors to and symptoms of SIFO. We further discuss the anatomical positioning and immunological functions of mast cells within the lamina propria, highlighting mast cell activation syndrome, while detailing how SIFO and SIBO can serve as upstream triggers for mast cell activation.



Topics:

1. The Gut-Immune Axis and Mast Cells

- The intestinal epithelium forms the innermost selective barrier, coated in a protective mucus layer.

- Immediately beneath lies the lamina propria, rich in immune cells including mast cells.

 

2. Mast Cells in the Lamina Propria

- Mast cells are positioned near nerves, capillaries, lymphatics, and epithelial cells within the lamina propria.

- Their anatomical location enables rapid immune surveillance and inflammatory response.

- Mast cell granules store histamine and more.

 

3. Mast Cell Mediators

- Histamine: Biogenic amine, inflammatory signaling.

- Tryptase: A serine protease.

- Cytokines and lipid mediators also released upon activation.

 

4. Mast Cell Activation Syndrome (MCAS)

- Systemic: skin, respiratory tract, cardiovascular system, nervous system, and more.

- The gastrointestinal tract.

- Common triggers for mast cell activation.

 

5. Transition to Small Intestinal Fungal Overgrowth (SIFO)

- Overgrowth of fungal organisms, often candida species, within the small intestine.

- Contributing factors including hypochlorhydria, slowed motility, immune suppression, disrupted bacterial populations.

- Overlap: SIFO, SIBO

 

6. Hypochlorhydria and the Stomach’s Defense Role

- Parietal cells secrete hydrochloric acid (HCl) and intrinsic factor.

- HCl denatures proteins and sterilizes ingested pathogens.

- Chief cells secrete pepsinogen, which becomes pepsin in acidic conditions to digest proteins.

- Consequences of Reduced Gastric Acidity

 

7. The Role of Intestinal Motility

- Enteric nervous system (ENS), myenteric and submucosal plexuses.

- Coordinated contractions preventing stasis and microbial overgrowth.

 

8. Common Symptoms of SIFO and clinical overlap with SIBO

 

9. Candida and Fungal Pathophysiology in the Gut

- Yeast form, regulated by microbial competition and immune defenses.

- Hyphal transformation.

- Degrade the mucus layer, disrupt epithelial integrity, trigger inflammation.

 

10. Secretory IgA and Mucosal Defense

- Chronic stress, immune dysfunction, dysbiosis can lower sIgA levels and weaken mucosal immunity.

 

11. SIFO, SIBO, and Mast Cell Activation

 

12. Conclusion 

- Root cause approach, multi-factorial





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176. The Gut-Immune Axis and Small Intestinal Fungal Overgrowth | Contributing Factors to Fungal Overgrowth, and a Conversation on Mast Cell Activation Syndrome

In this episode, we detail the role of vitamin B1 (thiamine) in supporting gastrointestinal function, highlighting intestinal motility through vitamin B1's involvement in acetyl-CoA and acetylcholine synthesis. We discuss thiamine insufficiency as well as how small intestinal bacterial overgrowth (SIBO) can further affect thiamine availability. We further detail host defense mechanisms—including gastric acid, pancreatic enzymes, and gastrointestinal motility—that work in concert to regulate microbial balance in the small intestine.



Topics:

1. Introduction

- Focus on SIBO, intestinal motility, and vitamin B1 (thiamine)

 

2. Small Intestine and Microbial Regulation

- Low bacterial load under healthy conditions 

- Protective mechanisms: gastric acid, enzymes, motility… 

 

3. Overview of SIBO Subtypes

- H₂-SIBO, hydrogen-producing bacteria 

- IMO, methane-producing archaea 

- H₂S-SIBO, hydrogen sulfide-producing bacteria 

- Subtypes can coexist, share underlying factors 

 

4. Host Factors in Microbial Regulation

- Gastric acid, motility, pancreatic enzymes, bile acids, and immune surveillance

 

5. Gastric Acid and Parietal Cells 

- Hydrochloric acid and intrinsic factor 

- Acid environment supports digestion and microbial regulation 

- Protein denaturation and pepsin activation

 

6. Chief Cells and Enzyme Function

- Pepsinogen and gastric lipase 

- Pepsinogen activated by acidic pH 

 

7. Hypochlorhydria and Downstream Effects

 

8. Pancreatic Enzymes in the Small Intestine 

 

9. Intestinal Motility and the Enteric Nervous System (ENS)

- Coordinated smooth muscle contractions 

- Myenteric and submucosal plexuses 

 

10. Intestinal Wall Anatomy 

- Epithelium and lamina propria

- Submucosa contains the submucosal plexus 

- Myenteric plexus located between muscle layers 

 

11. Vitamin B1 (Thiamine) and Gastrointestinal Function 

- Acetylcholine synthesized from choline and acetyl-CoA 

- Acetyl-CoA formation, thiamine availability 

- Acetylcholine signaling

 

12. SIBO and Nutrient Availability

- Bacterial overgrowth can affect nutrient absorption 

- Thiaminases 

 

13. Conclusion 

- Root cause approach, multi-factorial





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175. Thiamine, Vitamin B1 | Thiamine, Gastrointestinal Function, and Gastrointestinal Motility; and a Conversation on Small Intestinal Bacterial Overgrowth

In this encore episode, we discuss the role of histamine within the gastrointestinal tract, detailing its regulation of gastric acid secretion and impact on intestinal motility. We examine how histamine-producing enterochromaffin-like (ECL) cells, mast cells, and gut microbiota contribute to histaminergic signaling, and how enzymatic degradation via diamine oxidase (DAO) maintains homeostasis. Additionally, we discuss histamine intolerance, highlighting the impacts of dysbiosis (as well as SIBO or small intestinal bacterial overgrowth) and intestinal barrier dysfunction on DAO insufficiency and histamine accumulation.



Topics:

1. Introduction to Histamine & the Gastrointestinal Tract

- Role in digestion and motility

- Impact of intestinal conditions such as SIBO

 

2. Histamine as a Biogenic Amine

- Definition and classification

- L-histidine and histidine decarboxylase (HDC)

- Presence in various tissues, including the GI tract

 

3. Sources of Histamine in the Gut

- Enterochromaffin-like (ECL) cells in the stomach

- Mast cells in the lamina propria

- Histamine-producing gut bacteria

 

4. Histamine’s Role in Digestion & Gastric Acid Secretion

- Interaction with parietal cells in the stomach

- Activation of proton pumps via H₂ receptor binding

- Maintenance of acidic pH for digestion

- Importance of proper pH within the stomach for protecting against pathogenic microbes

- Impact on downstream gut microbiota balance (e.g., SIBO)

 

5. Histamine & Intestinal Motility

- Modulation of gut motility via H₁ and H₃ receptors

- H₁ receptor activation leading to contractions (diarrhea, cramping)

- H₃ receptor-mediated inhibition of neurotransmitter release (bloating, slow motility)

 

6. Histamine Intolerance: Definition & Mechanisms

- Diamine Oxidase and histamine breakdown

- DAO secretion by enterocytes (intestinal epithelial cells)

- Enzymatic breakdown of histamine before absorption

 

7. Factors That Can Affect DAO Activity

- Genetic Polymorphisms: AOC1 gene, reduced DAO expression

- Cofactor Deficiencies: Copper, vitamin B6, and vitamin C as essential DAO cofactors

- Importance of intestinal lining integrity for DAO production

- Conditions leading to or associated with enterocyte damage

- Intestinal dysbiosis and histamine accumulation

- Intestinal dysbiosis & epithelial/enterocyte damage

- Suppression of DAO production due to epithelial dysfunction

- Small Intestinal Bacterial Overgrowth (SIBO) & Histamine

 

8. Symptoms of Histamine Intolerance

- Gastrointestinal symptoms (bloating, gas, constipation, diarrhea, acid reflux...)

- Systemic symptoms (dizziness, flushing, migraines...)

 

9. Identifying Potential Root Causes

- Tools and supplements

- Bioindividual approach





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174. Connections Between Histamine Intolerance, Intestinal Dysbiosis, & Impaired Intestinal Barrier Function | Diamine Oxidase Enzyme Production and More

I’m a Model, Engineer, Researcher, and Entrepreneur. Here at The Synthesis of Wellness, I want to shed light on the newest health and wellness practices, research, biohacks, and knowledge! As an engineer and researcher, I am wired to dive deep into these easily misconstrued topics so I can provide the most accurate life-enhancing information. Feel free to reach out with questions or requests and follow me on Instagram to see my modeling work and more @chloe_c_porter Support this podcast: https://anchor.fm/chloe-porter6/support

Chloe Porter

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