Inflammatory Bowel Disease Overview:
Inflammatory bowel disease is a recurring inflammatory condition in the lower gastrointestinal tract. There are 2 main types of inflammatory bowel conditions; Crohn's disease, and ulcerative colitis.
T cell regulation:
- vitamin D
Experienced by about 33,000 Australians and is most prevelent in the Jewish descent.
In both of these conditions, an inflammatory response is triggered when contents of the intestinal tract (lumen) enter the inner layers of the epithelial tissue (lamina propria) where immunomodulatory macrophages are located. When these macrophages are activated, inflammatory cytokines are released including TNF-a, IL-1, IL-6, and interferon-gamma. This causes further inflammation, promotes coagulation of blood, and increases the release of free radical compounds from the macrophages in the area.
Depending on the condition (Crohns or Ulcerative colitis), the distribution of TNF-a reactive macrophages are different, which results in slightly different symptoms.
Ultimately, the end result of each condition is a self-perpetuating state of inflammation in the digestive tissue, causing contents to leak out from the lumen, and into the deeper layers of the intestinal tissue. Eventually, this damage becomes so severe, contents begin leaking into the blood stream directly, which then interferes with other organs like the liver, brain, lungs, and skin.
+ Crohn's Disease
Increased TNF-a activity reduces anticoagulant mediators (such as thrombomodulin), , and promotes procoagulant factors  TNF-a activated macrophages clustering around the arterioles and venules infiltrate and disrupt the vascular endothelium .
In effect, Crohns has a stronger affect on the vascular tissues of the digestive tract, and tnds to form clusters of inflammation around these areas. It can appear anywhere along the digestive tract, from the mouth to the anus.
+ Ulcerative Cholitis
In ulcerative colitis, the majority of inflammatory activity can be attributed to the epithelioid macrophages, and is more evenly distributed within the lamina propria .
The result is a more widely distributed inflammatory picture with ulcerative colitis than Crohns, with less clotting and infiltration of the vascular tissue. Ulcerative colitis also has a higher affinity for the large intestines, which is likely the reason why bleeding from the rectum is more common in this condition (closer proximity).
Ulcerative colitis comes with an increased of colon cancer, perforations and obstructions in the digestive tract. Systemically this condition is linked with rheumatoid arthritis, liver disorders, and inflammation involving the sclera of the eyes.
This condition is sometimes included under the category of inflammatory bowel disease, but has slightly different pathology. it involves the formation of outpounchings (diverticulae) in the digestive mucosa, which pokes through musclular layers. This usually occurs in the sigmoid colon. Faeces and bacteria can accumulate in these pouches, resulting with infection. This infection si what we refer to as diverticulitis.
This condition is associated with a low fiber diet, poor gut wall integrity, increased intestinal pressure, and a narrowing of the intestinal lumen diameter.
Diverticulitis may be asymptomatic, but most commonly has similar symptoms to other forms of inflammatory bowel disease or IBS.
This condition comes with several red flags, including gastrointestinal hemorrhage, fistula formation, perforations, and abscess formations.
Urgency With Bowel Movements
Irregular Menstrual Cycle
From this pathophysiological process, Crohns has some distinct differences to ulcerative colitis including:
* The affected location can appear anywhere in the digestive tract, compared to ulcerative colitis mainly affecting the large intestine.
* Inflammation tends to form patches, compared to large, uninterupted sections of inflammation with ulcerative colitis
* Rectal bleeding is much more common with ulcerative colitis than Crohns
Differences Between Crohns & Ulcerative Colitis
|Inflammation Patterns||Multiple, separated sections of inflamed and damaged tissue.||Large, ininterrupted area of inflammation.|
|Location||Anywhere along the digestive tract.||Most common in the large intestine.|
|Rectal Bleeding||Not common.||Common.|
|Inflammatory Factors Involved||IL-1, IL-6, TNF-a, IFN-γ||TNF-α, IL-12, IL-23, IL-17 and IFN-β|
Lab Tests For IBD
|Lab Test||Crohns||Ulcerative Colitis|
|CRP||>5 mg/L.||>5 mg/L|
|ESR||Female: >19 mm in 1 hour
Male: >10 mm in 1 hour
|Female: >19 mm in 1 hour
Male: >10 mm in 1 hour
|Bone Density Scan||Normal-Low||Normal-Low|
Cytokine Profiles Of CD and UC
|IL-1||Normal in serum, increased in mucosa||Normal in serum, increased in mucosa|
|IL-6||Increased||Normal in serum, raised in mucosa|
|IL-8||Undetectable in serum||Undetectable in serum, increased in mucosa|
|TNF-a||Increased serum, increased mucosa||Increased serum, increased mucosa|
1. Reduce Inflammation In The Digestive Tract
Regulate T cell, histamine, and inflammatory markers Systemically.
- Immunomodulators(Ganoderma, Innonotus)
- Antinflammatories(Boswellia serrata, Curcuma longa, Calendula officinalis)
- Nutrients(Selenium, Vitamin D, Zinc)
2. Repair Gut Mucosa
- Demulcents(Aloe vera, Althaea officnialis, Ulmus fulva, GLycyrhiza glabra)
- Mucorestoratives(Hydrastis canadensis)
- Astringents(Geranium maculatum)
- Nutrients(Glutamine, Vitamins (A, B, C, and D), Zinc, Calcium, Iron)
3. Regulate Immune Function In The Presence Of Autoimmune Disorders
- Immunomodulators(Ganoderma lucidum, Inonotus obliquus, Echinaceae purpurea, Andrographis paniculata, Hemidesmis indicus, Tylophora asthmatica)
- TNF-a & NF-kB Inhibitors(Curcuma longa, Boswellia serrata)
- COX/5-LOX Inhibitors(Curcuma longa, Boswellia serrata)
- Antioxidants(Silybum marianum, Curcuma longa, Vaccinum myrtillus)
- Nutrients(Zinc, Fish oil)
4. Improve Liver Function
- Hepatics(Silybum marianum, Schisandra chinensis, Cynara scolymus)
5. Fight Infection If Relevant
- Antifungals(Tabebuia impetiginosa)
6. Identify and Remove Food Intolerances
Such as dairy, gluten, fructose
6. Treat Diarrhea Symptomatically
Short term treatment only. The underlying cause should be the priority here.
- Antidiarrheals(Matricaria recutita, Agrimonia eupatoria, Filipendula ulmaria)
- Styptics(urtica dioica, Panax notoginseng, Achillea millefolium)
- Irritable bowel syndrome
- Colon cancer
- Celiac Disease
- Food intolerances/allergies
- Bacterial infection
Rule out colon cancer.
- curcuma longa
The Sunlight Experiment
Updated: March 2018
Recent Blog Posts:
- Roberts-Thomson, I. C., Fon, J., Uylaki, W., Cummins, A. G., & Barry, S. (2011). Cells, cytokines and inflammatory bowel disease: a clinical perspective. Expert review of gastroenterology & hepatology, 5(6), 703-716.
- Deem, R. L., Shanahan, F., & Targan, S. R. (1991). Triggered human mucosal T cells release tumour necrosis factor‐alpha and interferon‐gamma which kill human colonic epithelial cells. Clinical & Experimental Immunology, 83(1), 79-84.
- Doukas, J., & Pober, J. S. (1990). IFN-gamma enhances endothelial activation induced by tumor necrosis factor but not IL-1. The Journal of Immunology, 145(6), 1727-1733.
- Gross, V., Andus, T., Caesar, I., Roth, M., & Schölmerich, J. (1992). Evidence for continuous stimulation of interleukin-6 production in Crohn's disease. Gastroenterology, 102(2), 514-519.
- Hanauer, S. B. (2006). Inflammatory bowel disease: epidemiology, pathogenesis, and therapeutic opportunities. Inflammatory bowel diseases, 12(suppl_1), S3-S9.
- Kühl, A. A., Erben, U., Kredel, L. I., & Siegmund, B. (2015). Diversity of intestinal macrophages in inflammatory bowel diseases. Frontiers in immunology, 6, 613.
- Moore, K. L., Esmon, C. T., & Esmon, N. L. (1989). Tumor necrosis factor leads to the internalization and degradation of thrombomodulin from the surface of bovine aortic endothelial cells in culture. Blood, 73(1), 159-165.
- Murch, S. H., Braegger, C. P., Walker-Smith, J. A., & MacDonald, T. T. (1993). Location of tumour necrosis factor alpha by immunohistochemistry in chronic inflammatory bowel disease. Gut, 34(12), 1705-1709.
- Sandborn, W. J., & Hanauer, S. B. (1999). Antitumor necrosis factor therapy for inflammatory bowel disease: a review of agents, pharmacology, clinical results, and safety. Inflammatory bowel diseases, 5(2), 119-133.
- Wakefield, A. J., Dhillon, A. P., Rowles, P. M., Sawyerr, A. M., Pittilo, R. M., Lewis, A. A. M., & Pounder, R. E. (1989). Pathogenesis of Crohn's disease: multifocal gastrointestinal infarction. The Lancet, 334(8671), 1057-1062.