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.

Thanks for tuning in!

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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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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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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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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.

Get Chloe's Book Today! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠"

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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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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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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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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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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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