In this encore episode, we detail overlap among intestinal methanogen overgrowth (IMO), hydrogen-dominant small intestinal bacterial overgrowth (H₂-SIBO), and hydrogen sulfide-dominant SIBO (H₂S-SIBO), discussing their mechanistic interactions. 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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190. IMO, SIBO Subtypes | Interactions Among Intestinal Methanogen Overgrowth (IMO), Hydrogen Sulfide-Dominant Small Intestinal Bacterial Overgrowth, and Hydrogen-Dominant SIBO

In this encore episode, we highlight the role of vitamin B1 (thiamine) in supporting gastrointestinal function, focusing on intestinal motility while detailing vitamin B1's involvement in acetyl-CoA and acetylcholine synthesis. We discuss thiamine insufficiency as well as how small intestinal bacterial overgrowth (SIBO) may 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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189. Gastrointestinal Motility | The Role of Vitamin B1 (Thiamine) in Motility and Supporting Gastrointestinal Function, and a Brief Conversation on SIBO

In this episode, we detail connections between H. pylori and hypochlorhydria, while highlighting possible downstream effects on nutrient absorption. We examine how reduced gastric acidity can impair the liberation and assimilation of certain micronutrients, including iron, calcium, vitamin B12, and more; and we further discuss the impact of low stomach acid upon downstream digestive enzyme activation and gut microbial balance. The discussion also highlights the role of compromised gastric acidity in conditions such as small intestinal bacterial overgrowth (SIBO).



Topics:

1. Hypochlorhydria

- Low stomach acid.

- Aging, autoimmune gastritis, chronic PPI use, H. pylori infection.



2. H. pylori

- Common gram-negative bacterium that colonizes the stomach lining.

- Symptoms.

- Produces urease.

- Ammonia neutralizes acid, creating a protective microenvironment.

- Additional virulence factors and ability to form biofilms contribute to persistence.



3. Gastric Anatomy & Layers

- The stomach: hollow, muscular organ for mechanical and chemical digestion.

- Regions: Cardia, fundus, body, and pylorus.

- Layers: Mucosa, Submucosa, Muscularis externa, Serosa



4. Mucosal Layer

- Surface mucous cells secrete a thick bicarbonate-rich, protective mucus.

- Gastric pits lead to gastric glands, which contain specialized secretory cells.



5. Specialized Gastric Cells

- Parietal Cells: Secrete hydrochloric acid (HCl) and intrinsic factor (IF).

- Chief Cells: Secrete pepsinogen (converted to pepsin by HCl) and gastric lipase.

- Role of HCl: Activates pepsin, denatures proteins, and contributes to nutrient absorption.

- Intrinsic factor and vitamin B12 absorption.



6. Vitamin B12 Absorption

- Essential for DNA synthesis, RBC formation, neurological function.

- Released from food proteins by gastric acid and pepsin.

- Impaired absorption.



7. Role of Gastric Acid in Broader Micronutrient Absorption

- Absorption of minerals.

- Soluble, ionized state.

- Iron: HCl aids in preventing insoluble precipitates and supports iron absorption.



8. Protective Role of Gastric Acid

- Acts as a line of defense against ingested pathogens.

- Maintains low microbial diversity in the stomach.

- Low HCl and SIBO (Small Intestinal Bacterial Overgrowth).



9. Symptoms of Low Stomach Acid

- Bloating, early satiety, excessive belching.

- Undigested food in stool, chronic constipation.

- May reflect impaired enzymatic activation and digestive insufficiency.



10. Conclusion

- Multifactorial causes and downstream effects.

- Optimal range of stomach acid: neither high nor low.





Thank you to our episode sponsor:

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188. The Stomach | Symptoms of H. pylori & Hypochlorhydria, and a Conversation on the Effects of Low Stomach Acid on Micronutrient Absorption

In this episode, we detail Small Intestinal Fungal Overgrowth (SIFO), with a focus on fungal biofilm formation and its role in promoting microbial persistence and evasion of host immune responses. We discuss the phenotypic plasticity of Candida species, as well as biofilm matrices adherent to the intestinal mucosa. We further highlight common symptoms of SIFO as well as the effects of hypochlorhydria, reduced pancreatic enzyme and bile output, impaired motility, diminished commensal bacterial populations, and weakened mucosal immunity.



Topics:

1. Introduction

- Focus on the gut mucosal barrier.

- Emphasis on Small Intestinal Fungal Overgrowth (SIFO) and biofilms.



2. Intestinal Barrier Anatomy

- The mucosa: epithelium, lamina propria, and a thin band of smooth muscle.

- The epithelial layer.

- Covered by protective mucus composed of mucin glycoproteins secreted by goblet cells.

- In the small intestine: less dense mucus.



3. Epithelial Integrity

- Tight junctions.

- Paracellular barrier preventing uncontrolled antigen passage.



4. Lamina Propria



5. Overview of Small Intestinal Fungal Overgrowth (SIFO)

- SIFO involves fungal overgrowth in the small intestine, commonly Candida species.

- Small intestines: Low microbial density due to motility, gastric acid, bile acids, immune surveillance, and more.

- Contributing factors: hypochlorhydria, impaired motility, reduced digestive enzymes, diminished competitive flora, lowered immunity, and more.



6. Candida Pathogenicity

- Candida exhibits phenotypic plasticity: yeast and hyphal forms.

- Biofilm formation.



7. Biofilm Formation

- Biofilms are structured communities of microbes within a self-produced extracellular matrix.

- Resistance to antimicrobials and immune defenses.

- Can develop on intestinal mucosa and in various other regions.



8. SIFO and SIBO Overlap

- Root causes and overlap between SIFO and Small Intestinal Bacterial Overgrowth (SIBO).

- Common symptoms.



9. Gastric Acid in More Detail

- Stomach epithelium includes mucous, parietal, chief, and enteroendocrine cells

- Parietal cells secrete hydrochloric acid.

- HCl denatures proteins and aids in inhibiting pathogens.

- Hypochlorhydria: possible causes.



10. Downstream Effects of Low Acid



11. Gut Motility in More Detail

- Motility involves rhythmic smooth muscle contractions.

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

- Dysautonomia and motility.



12. SIFO Contributing Factors



13. Candida Regulation

- Candida generally remains in unicellular yeast form under homeostatic regulation.

- Controlled by microbial competition, host defenses, antifungal peptides, and more.



14. Role of Mucus and sIgA

- Mucosal immunity (including sIgA) aids in regulating Candida populations.

- Low sIgA levels (due to stress, immune suppression, dysbiosis,…) weaken defense



15. Conclusion

- Mucosal barrier structure.

- SIFO and Candida.

- Biofilm formation, microbial persistence, and mucosal disruption.

- SIFO and SIBO.

- Multifactorial nature of fungal dysbiosis, types of biofilms, and small intestinal overgrowth.



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187. Intestinal Mycobiome | Small Intestinal Fungal Overgrowth, Biofilm Formation & Microbial Persistence, and Intestinal Barrier Integrity

In this encore 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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186. The Gut-Immune Axis, Intestinal Barrier Function, & Vitamin D₃ | Activated 1,25-dihydroxyvitamin D₃ and Immune Function, Vitamin D Testing, & More

In this encore episode, we detail the enteric nervous system and regulation of gastrointestinal motility. We discuss factors including dysautonomia, stress, microbial overgrowth, and more, with regards to potential effects upon gastrointestinal motility. We further detail symptoms of altered GI motility.





Topics:

1. Introduction to Gastrointestinal Motility

- Orchestrated contraction of smooth muscles that propel contents along the digestive tract. 

- Roles in mixing, absorption, and preventing bacterial overgrowth.

- Disruptions in motility.

 

2. The Enteric Nervous System (ENS) and Its Role

- Myenteric and submucosal plexus.

- Coordinating contractions and relaxations for effective motility.

- Mucosa includes epithelium, lamina propria, and muscle. 

- Submucosa houses the submucosal plexus. 

- Muscularis externa.

- Inner circular and outer longitudinal muscle layers with the myenteric plexus in between. 

 

3. The Role of Interstitial Cells of Cajal (ICCs)

- Specialized pacemaker cells in muscular layers 

- Generate slow-wave electrical activity to synchronize smooth muscle contractions 

- Critical for peristalsis.

- Work with neural inputs to fine-tune gut motility 

 

4. Dysautonomia and Its Impact on Gut Motility

- Dysfunction of the autonomic nervous system (ANS) 

- Motility impacts

- Microbial overgrowth, SIBO

 

5. Gastrointestinal Dysmotility

- Neurological dysregulation

- Structural abnormalities and smooth muscle dysfunction 

- Hormonal imbalances

- Microbial overgrowth

- Autoimmunity

 

6. The HPA Axis

- Hypothalamus, pituitary gland, adrenal glands 

- Central to the stress response and interlinked with gut function 

- The amygdala and PVN of the hypothalamus 

- CRH stimulates ACTH, leading to cortisol release from adrenal glands 

 

7. Cortisol and Gut Barrier Function

- Cortisol is a glucocorticoid that modulates immune function and gut physiology 

- Chronic cortisol exposure can impair tight junction (TJ) integrity 

- Increases paracellular permeability and allows passage of antigens and endotoxins 

 

8.Stress-Induced Changes in Gut Motility

- Slow gastric motility 

- Increased colonic motility 

 

9. Symptoms of GI Dysmotility



10. Addressing Root Cause(s)





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185. Gastrointestinal Dysmotility | The Effects of Dysautonomia, Intestinal Dysbiosis, Stress, & More

In this encore episode, we detail the cellular make-up of the gastric lining, highlighting hydrochloric acid (HCl) secretion and its role in digestion, micronutrient absorption, and microbial defense. We discuss potential pathophysiological consequences of hypochlorhydria, including impaired digestive signaling, bacterial overgrowth in the small intestine (SIBO), and more. Lastly, we detail upstream microbial control, focusing on the influence of the oral microbiome and oral dysbiosis.



Topics:

1. Introduction

- Highlighting the stomach and hypochlorhydria / low stomach acid, as well as microbial balance, dysbiosis, and overgrowth.

- Discussion of intestinal microbiome and oral microbiome.

 

2. Gastric Anatomy and Mucosal Layers

- The stomach: cardia, fundus, body, pylorus.

- The gastric mucosa: epithelial lining, lamina propria, muscularis mucosae.

- The epithelial layer: mucous cells, parietal cells, chief cells, enteroendocrine cells.

- Beneath the mucosa: submucosa and muscular layers that contribute to gastric motility, mechanical digestion, and more.

 

3. Mucous Cells

- The surface epithelium and gastric pits.

- Secretion of thick, viscous mucus.

- Protecting the epithelium.

- The mucus traps bicarbonate ions: neutral microenvironment that protects against acid-induced damage.

 

4. Parietal Cells and Gastric Acid Secretion

- Secretion of hydrochloric acid (HCl): denatures dietary proteins, sterilizes ingested food.

- Parietal cells produce intrinsic factor: binds vitamin B12 to facilitate absorption in the ileum.

 

5. Chief Cells and Pepsinogen

- Secretion of pepsinogen: activated by low pH into the proteolytic enzyme pepsin.

- Pepsin and protein digestion.

- Release of gastric lipase.

 

6. Hydrochloric Acid: Digestive and Protective Roles

- Immune defense.

- Pepsinogen activation.

- Adequate gastric acidity essential for properly acidified chyme.

- Priming release of bile and pancreatic enzymes.

 

7. The Small Intestine, Stomach, and Microbial Regulation

- The pyloric sphincter.

- The stomach supports minimal microbial diversity.

- Acidic barrier aids in limiting the entry of opportunistic microbes into the small intestine.

 

8. Hypochlorhydria, Low Stomach Acid

- Hypochlorhydria can compromise one of the body's defense mechanisms.

- Colonization of the small intestine.

- Insufficient pepsinogen activation and possible protein digestion impairment.

- Suboptimal chyme formation and downstream digestive capacity.

- Possible symptoms of hypochlorhydria.

- Possible impaired absorption of micronutrients including vitamin B12, iron, calcium, magnesium.

- H. pylori infection, autoimmunity, aging.

 

9. The Oral Microbiome, Intestinal Microbiome, and Dysbiosis

- Oral and environmental microbes.

- Altered gastric pH, bile, digestive enzymes, and more.

- The oral cavity as the gateway to the GI tract.

- Oral microbial species.

- Oral hygiene and oral microbiome health.

 

10. Conclusion

- Root-cause approach.









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184. Hypochlorhydria & Small Intestinal Bacterial Overgrowth | Low Stomach Acid, Microbial Dysbiosis, & a Brief Conversation on the Oral Microbiome

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

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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