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

In today's 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)





Thank you to our episode sponsor:

1. Shop ⁠⁠⁠⁠⁠⁠⁠Fresh Press Farms⁠⁠⁠'⁠⁠⁠⁠ [https://www.groflo.io/fresh-press/synthesis]⁠⁠⁠⁠Peach Cider Vinegar⁠⁠⁠⁠ [https://www.groflo.io/fresh-press/synthesis] at Sprouts locations nationwide, and check out their full collection ⁠⁠⁠⁠⁠⁠⁠here⁠⁠⁠⁠⁠⁠⁠ [https://freshpressfarms.com/].







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

In this 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.



Thank you to our episode sponsor:

1. Shop ⁠⁠⁠⁠⁠⁠Fresh Press Farms⁠⁠⁠'⁠⁠⁠ [https://www.groflo.io/fresh-press/synthesis]⁠⁠⁠Peach Cider Vinegar⁠⁠⁠ [https://www.groflo.io/fresh-press/synthesis] at Sprouts locations nationwide, and check out their full collection ⁠⁠⁠⁠⁠⁠here⁠⁠⁠⁠⁠⁠ [https://freshpressfarms.com/].







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

We are honored to be joined by Forrest Smith, the CEO and Founder of Kineon. Forrest has a 20-year history of building successful startups in tech hardware. He is passionate about health, wellness, and advancing technology to help others, and he has spent his adult life building remarkable products around innovative supply chain. Aside from his founder position in multiple companies, Forrest has held several positions, from Director of Asian Operations for a Fortune 500 company to Director of Business Development. He also grew up playing competitive sports in Atlanta, regularly participates in rugby matches, and trains CrossFit, which ultimately led him to develop Kineon Lab’s Move+, a modular, targeted laser therapy device for neuromuscular pain and inflammation.



Topics:

1. Forrest's Personal Experience with Red Light Therapy

- The creation of Kineon and the MOVE+ Pro. 

 

2. Cellular Health

- Supporting healthy mitochondrial function. 

- ATP production and oxidative stress.

- The role of oxidative stress in impairing mitochondrial output. 

- Balancing ROS production and cellular repair.

 

3. Red and Infrared Light Therapy

- Photoacceptors including cytochrome c oxidase.

- Nitric oxide.

- Comparing wavelengths and their tissue penetration. 

- Clinical research on red light therapy.

- Joint health, mobility, and blood flow.

- Skin and hair scientific literature. 

- Technical specifications.

- Importance of dose control.

- LEDs vs. Lasers in light therapy devices.

- Including laser technology in the MOVE+ Pro. 

 

4. Kineon Lab’s MOVE+ Pro

- Remarkable engineering and performance.

- Modular design for targeting joints and soft tissue. 

- Joint pain, inflammation, and recovery. 

- How often and how long to use the MOVE+ Pro. 

- Sample protocols for joint pain and performance recovery. 



Shop the Kineon Move+ Pro [https://lvnta.com/lv_zNi6P7ANlHWUYNGNVe]and save $100 during Kineon's Spring Amazon Sale running from March 25th to March 31st

Check out Kineon's website here [https://kineon.io/]

Check out Kineon's Instagram @kineon_labs [https://www.instagram.com/kineon_labs/]





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171. Combating Inflammation and Pain, Supporting Joint Health, Mobility, and More with Red Light Therapy | Forrest Smith, Founder & CEO of Kineon

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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