An Integrated Approach to Managing Inflammatory Bowel Disease (part 1 of 5)

Inflammatory bowel disease (IBD) is an umbrella term used to describe a group of inflammatory disorders of the gastrointestinal tract. Each of these disorders involves some degree of inflammation (redness, swelling, erosion and sometimes bleeding) of the gastrointestinal mucosa or lining that commonly leads to ulceration of the mucosa to varying degrees. The inflammation is usually a result of an immune reaction of the body against its own intestinal tissue. Therefore, the diseases included in IBD are considered to be autoimmune disorders.

This is Part 1 of a 5-part article including:

1. An Integrated Approach to Managing Inflammatory Bowel Disease

2. Diagnostic Evaluation of IBD

3. IBD Treatment: Remove the Obstacles to Cure

4. IBD Treatment: Quiet the Inflammation

5. IBD Treatment: Repair the Gut

(or, download the PDF of the entire article.)

Ulcerative Colitis and Crohn’s Disease

IBD: Signs and Symptoms Abdominal Pain very common Urgency to Stools very common Fatigue very common Bleeding from Rectum very common in ulcerative colitis Bloating very common Weight Loss more common in Crohn's disease Stool: loose, can be constipated in Crohn's disease Mucus in Stool very common Fever very common Gastritis or Stomach Ulcers common in Crohn's disease Canker Sores in the Mouth common in Crohn's disease Anemia common (B12, folate, iron) Dehydration common in ulcerative colitis Delayed Growth in Children very common in Crohn's disease Nutritional Deficiencies very common in Crohn's disease Fissures/Fistulas common in Crohn's disease Abdominal Abscesses common in Crohn's disease Intestinal Obstruction common in Crohn's disease (stricture) Arthritis 33% IBD patients Iritis / Uveitis up to 12% of IBD patients Skin Rashes common Hepatobiliary Disease (liver and gallbladder) more common in ulcerative colitis Kidney Stones (calcium oxalate) more common in Crohn's disease Protein, Calorie Malnutrition & Micro/Macro Nutrient Deficiencies common in Crohn's disease IBD: Risk Factors Familial History of IBD up to 10 times the risk if family with IBD Spouse with IBD Increases Risk for IBD Slight Female Predominance in Crohn's disease and a Slight Male predominance in ulcerative colitis Greater Predominance in Jewish Population Greater Risk if White, More Affluent, Live in Metropolitan Areas and in the Northeast Region of the United States Recent or Excessive Use of Antibiotics History of Delayed Growth and Development History of Chronic Perceived Stress and Suppressed Anger Peak Incidence Between ages 15 and 25 Smoking is Risk Factor for Crohn's disease Diet High in Processed Foods Especially White Flour, Anti-Caking Agents and Food Preservatives (8) Appendectomy is Protective for ulcerative colitis Presence of Genetic Markers for Celiac Disease (HLA-DQ2 and DQ8)

Two major types of IBD are ulcerative colitis and Crohn’s disease. There is also a subtype of colitis called microscopic colitis commonly occurring in adults over the age of 50. As the name suggests, ulcerative colitis is limited to the large intestine or colon. Its inflammatory pathology is easily visualized via a colonoscopy. On the other hand, microscopic colitis can only be detected via microscopic examination of tissue samples of the colonic mucosa.

Crohn's disease can involve any part of the gastrointestinal tract from the mouth to the anus. However, it most commonly affects the small intestine; sometimes the colon and stomach may also be affected. Its inflammatory reaction is often deeper and can penetrate the full thickness of the intestines leading to serious infections in the abdominal cavity and intestinal strictures causing obstruction. Because Crohn’s disease involves the small intestine which is the primary site of nutrient absorption, Crohn’s disease can also lead to malabsorption, weight loss, and failure to grow when occurring in children. Both ulcerative colitis and Crohn's disease usually run a waxing and waning course in the intensity and severity of illness.

When there is severe inflammation, these diseases are considered to be in an active stage causing the person to experiences a flare-up of the condition. When the degree of inflammation is less (or absent) and the person usually is without symptoms, the disease is considered to be in remission. Both disorders are not considered to be “curable” but can be nutritionally and medically managed into remission in most people.

What Causes IBD?

Since ulcerative colitis and Crohn’s disease are autoimmune-mediated, “disregulation” of the person’s normal or innate and adaptive immune system is involved. This disregulation leads to an immune response directed against “self” i.e., the person’s own mucosal cells and proteins.

Immune Response and Genetic Predisposition

Presently, it is suspected this disregulated or inappropriate immune response against self is due to intrinsic alterations in mucosal barrier function caused/stimulated by an immune response directed against specific dietary proteins such as gliadin (the protein in gluten) or various bacteria in the intestinal tract that don’t normally cause such a response. It is becoming more evident that a genetic predisposition leads to this inappropriate, cross-reactive immune response to self-proteins. (1, 2)

Hygiene Hypothesis

The old naturopathic “hygiene hypothesis” for autoimmune disorders has gained respect in contemporary medicine as a possible explanation for this cross-reactive response and the development of IBD and other autoimmune disorders. It suggests that cleaner, hygienic environments offer less exposure to parasitic infections of the gastrointestinal tract and this may negatively affect normal development of the immune system, predisposing to disregulation and over-reaction of the immune system leading to autoimmunity and IBD. (3)

Autoimmune and Self-Inflamed

Inflammation leading to swelling, erosion and ulcerations of the gastrointestinal mucosa (superficial with ulcerative colitis and full-thickness through the intestine with Crohn’s disease) is the common feature with IBD. White blood cells (T cells) recognize gut-associated self-proteins and direct auto-antibodies against them… against one’s own “self.” This immune response stimulates the production and local release of immune-active chemicals that cause intestinal inflammation and damage leading to the symptoms and complications associated with IBD.

Leaky Gut

Besides the apparent local inflammatory damage to the intestinal mucosa in IBD, the intestines can become highly “leaky” to larger protein molecules (bacterial and dietary) that normally would stay in the intestines without leaking through the intestinal barrier. The leaked protiens alert the immune system outside of the gastrointestinal tract. This is called “leaky gut.”

When "leaky gut" happens, gut-associated proteins get into systemic circulation and become immune-activating throughout the body. This immune activation results in inflammatory reactions and disorders in other parts of the body which can further develop into other autoimmune diseases. To illustrate this point, people with IBD are at higher risk for developing:

• Arthritic disorders such as rheumatoid arthritis, arthritis of the spine, and psoriatic arthritis (arthritis associated with the skin disorder called psoriasis). (4)
• Iritis (inflammation of the iris in the eye), inflammation of the liver, and multiple sclerosis.(5-7)

IBD: Signs, Symptoms, and Risk Factors

If you're experiencing any of the common signs and symptoms of IBD (right) with or without the common risk factors (right), the next step is to meet with your healthcare practitioner for a diagnostic evaluation.

Diagnostic Evaluation and Treatment of IBD

Diagnostic evaluation of IBD includes blood work, stool samples, nutritional evaluation, and diagnostic procedures. Click here to learn more.

Treatment: Employing basic Naturopathic philosophy and guidelines, there are three primary actions to consider as part of the treatment and management of IBD. First, “remove the obstacles to cure,” then “quiet the inflammation” and finally “repair the gut.” All three can be done simultaneously. Click the links below to learn.

Remove the Obstacles to Cure

Quiet the Inflammation

Repair the Gut

Summary

Inflammatory bowel disease is a group of autoimmune, inflammatory disorders of the gastrointestinal tract all of which involve some degree of inflammation (redness, swelling, erosion and sometimes bleeding) and damage to the gastrointestinal lining to varying degrees.

The inflammation is usually a result of an immune reaction of the body against its own intestinal tissue thought to be induced and commonly worsened by various dietary and gut-bacterial immune-stimulating proteins.

Management and prevention of the inflammation and associated complications is reliant on three naturopathic factors: removing the obstacles to cure, quieting the inflammation, and healing the gut. This is achieved best through an integrated treatment approach incorporating diet, nutritional supplements, standardized botanical medicines, and conventional medications under the astute direction and guidance of a gastroenterologist and a qualified health care team.

This is Part 1 of a 5-part article including:

1. An Integrated Approach to Managing Inflammatory Bowel Disease

2. Diagnostic Evaluation of IBD

3. IBD Treatment: Remove the Obstacles to Cure

4. IBD Treatment: Quiet the Inflammation

5. IBD Treatment: Repair the Gut

(or, download the PDF of the entire article.)

References

1. The Lancet Infectious Diseases. Volume 7, Issue 9, September 2007, 607-613

2. Gastroenterology.Volume 115, Issue 6, December 1998, 1405-1413

3. Inflamm Bowel Dis. 2005 Feb;11(2):178-84

4. World J Gastroenterol. 2009 Nov 28;15(44):5517-24

5. Inflamm Bowel Dis. 2008 Jun;14(6):738-43

6. World J Gastroenterol. 2008 Jan 21;14(3):331-7

7. Inflamm Bowel Dis. 2008 Jun;14(6):775-9

8. Eur J Gastroenterol Hepatol. 2001 Feb;13(2):93-5

9. Curr Pharm Des. 2009;15(18):2087-94

10. Int J Colorectal Dis. 2001 Apr;16(2):88-95

11. Curr Med Chem. 2006;13(28):3359-69

12. J Immunol. 2006 Mar 1;176(5):3127-40

13. Int J Colorectal Dis. 2001 Apr;16(2):88-95

14. Eur J Med Res. 1997 Jan;2(1):37-43

15. Nutrition. 2001 Jul-Aug;17(7-8):669-73

16. Cancer Epidemiol Biomarkers Prev. 2008 May;17(5):1136-43

17. Cochrane Database Syst Rev. 2007 Apr 18;(2):Crohn's disease006320

18. Clin Rheumatol. 2007 Mar;26(3):289-97

19. Clin Rheumatol. 1996 Jan;15 Suppl 1:62-66

20. Clin Rheumatol. 2007 Mar;26(3):289-97

21. Z Rheumatol. 2000;59 Suppl 2:II/108-18

22. World J Gastroenterol. 2007 May 28;13(20):2826-32

23. J Clin Gastroenterol. 2006 Mar;40(3):235-43

24. Adv Exp Med Biol. 1999;472:149-58

25. Dig Dis. 2009;27(4):450-4

26. Int J Med Microbiol. 2010 Jan;300(1):25-33

27. Dig Dis. 2009;27(3):412-7

28. Rev Recent Clin Trials. 2008 Sep;3(3):167-84

29. Aliment Pharmacol Ther. 2009 Oct 15;30(8):826-33

30. J Biol Chem. 2006 Aug 25;281(34):24449-54

31. Aliment Pharmacol Ther. 2009;30(8):826-33

32. Scand J Gastroenterol. 2008;43(7):842-8

33. Dig Dis Sci. 2000 Jul;45(7):1462-4