IBD Treatment - Repair the Gut (part 5 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.

IBD Treatment - Repair the Gut

This is Part 5 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)

The following nutritional and botanical products have been demonstrated to be safe, effective anti-inflammatory compounds beneficial in the treatment and management of IBD (according to the existing peer-reviewed scientific literature). As stated above, any use of additional medications or changes in treatment should only be made with your physician’s guidance and knowledge.

Butyrate and Short-Chain Fatty Acids (SCFAs)

SCFAs are produced in the colon by the digestive action of “good bacteria” on dietary fiber. Butyrate is a SCFA that acts as the fuel or food for the mucosal cells of the colon (colonocytes) and promotes their regeneration and repair. SCFAs, particularly butyrate, can modulate inflammation and promote regeneration of the colonocytes damaged by ulcerative colitis or Crohn’s colitis. (22)

Butyrate stimulates sodium and water absorption in the colon and promotes intestinal mucosal restitution and repair. It also prevents the development of colon cancer by promoting healthy cell differentiation and destruction of cancer-transformed colonocytes. (23) SCFAs can be given orally or used in an enema, particularly when there is proctitis and/or distal colitis. As researchers found, SCFA enemas are “a new and promising treatment for ulcerative colitis.” (24) I commonly prescribe butyrate enemas through a compounding pharmacy and suggest daily use for 2 to 4 weeks in acute flare-ups.

L-Glutamine

L-glutamine is a single amino acid that is an important metabolic fuel for the mucosal cells of the small intestine (enterocytes) and has been shown to preserve the intestinal barrier functions and reduce leakiness of the gut. L-glutamine also stimulates repair and regeneration of the small intestinal mucosa important in Crohn’s disease and celiac disease.

Zinc

Zinc is commonly deficient in children with Crohn’s disease. This is a contributing factor to poor growth and development in children with Crohn’s. Zinc has also been shown to improve intestinal barrier function (leaky gut) in Crohn’s disease. (25)

Gastrocrom (oral chromolyn)

Gastrocrom is the oral form of chromolyn, a safe and effective antihistamine flavonol used safely for years in the treatment of asthma. It is a synthetic cousin of the natural, medicinal flavonoid called quercitin. Research has shown Gastrocrom strengthens the epithelial/mucosal barrier reducing “leaky gut.” (25) It also reduces local mucosal allergic inflammation and is used to treat eosinophilic gastroenteritis, a form of allergic inflammation of the gastrointestinal tract.

Probiotics (Lactobacillus, Bifidobacterium and others)

Simply put, probiotics are “friendly bacteria” to the gastrointestinal tract. People have more bacteria in their colon then they have cells in their body. These bacteria produce beneficial immunomodulatory effects in the gastrointestinal tract and induce immune homeostasis (balance). Due to this “normalizing action,” researchers have suggested probiotics can be “a suitable treatment for mild to moderate IBD.” (26)

The evidence for the use of probiotics in the treatment of IBD is strongest in the case of ulcerative colitis and pouchitis (inflammation of the remaining pouch after removal of the colon). (27) By far, the research has shown a human-sourced, multi-agent mixture of various friendly bacteria “may be better suited in ulcerative colitis and pouchitis.” (28)

Probiotics (Saccharomyces boulardi)

S. boulardii is a spore-forming yeast that commonly does not set up home in the colon. However, S. boulardii and its secreted-protein(s) inhibit gut inflammation and reduce IBD pathology. This is especially true in Crohn’s disease and pseudomembranous colitis, a form of antibiotic-induced infectious colitis caused by the bacteria Clostridium difficile. S. boulardii inhibits the production of the proinflammatory chemicals called cytokines by interfering with the global mediator of inflammation, nuclear factor kappa B. (29) S. boulardii further protects against intestinal inflammation by modulating host inflammatory signaling pathways to exert its beneficial effects. (30)

The list of S. boulardii’s beneficial actions in IBD is impressive. It suppresses bacterial overgrowth in the small intestine and inhibits adherence of invasive bacteria to the intestinal mucosal cells. It releases an enzyme (protease) that cleaves C. difficile toxin A and its intestinal receptor then stimulates antibody production against toxin A so that it cannot damage the colon resulting in a bloody colitis. S. boulardii also interferes with the development of IBD by trapping specific lymphocytes (T cells) in intestinal-related lymph nodes thereby, stopping their ability to induce an immune reaction against self-proteins. (31) Finally, in clinical studies, S. boulardii was found to reduce gut permeability and relapse of symptoms (6% vs. 36%) in Crohn’s disease patients. (32, 33)

This is Part 5 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

IBD Treatment - Quiet the Inflammation (part 4 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.

IBD Treatment - Quiet the Inflammation (reduce production of inflammatory mediators)

This is Part 4 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)

The following nutritional and botanical products have been demonstrated to be safe, effective anti-inflammatory compounds beneficial in the treatment and management of IBD (according to the existing peer-reviewed scientific literature). Their use can help to limit reliance on heavier doses of medications known to have more side effects.

That said, each case of IBD is different in its presentation and degree of severity. I am in no way suggesting the following nutritional and botanical therapies can successfully treat and manage IBD by themselves. I commonly use them in combination with conventional medications and conservative medical management. However, a number of my patients have successfully weaned off the more potent medications such as Azathioprine, 6-mercaptopurine, prednisone and others after being symptom-free for 6-12 months or longer on the integrated treatment regime described below.

Please remember, any use of additional medications or changes in treatment should only be made with your physician’s guidance and knowledge.

Curcuma longa (Curcumin)

Curcumin is a flavonoid extract from the spice turmeric (Curcuma longa). It is one of the most studied natural compounds in the world due to its marked anti-inflammatory and anticancer activity. It safely and actively inhibits production and release of numerous pro-inflammatory chemicals that are involved in the inflammatory process of IBD.

Curcumin causes:

• Inhibition of cyclooxygenases/COX-2 (This is how sulfasalazine and mesalamine work.)
• Inhibition of lipoxygenase (LOX)
• Inhibition of TNF-alpha (This is how Remicade works.)
• Inhibition of IFN-Gamma
• Inhibition of the transcriptional nuclear factor kappa B (NF-kappa B) - a key factor in the upregulation of inflammatory cytokines

Clinical research demonstrates Curcumin can significantly reduce clinical relapse in patients with quiescent IBD. Quoting researchers from the Center for Gastroenterology and Inflammatory Bowel Disease Research at Hamamatsu South Hospital, Hamamatsu, Japan, “The inhibitory effects of curcumin on major inflammatory mechanisms like COX-2, LOX, TNF-alpha, IFN-gamma, NF-kappaB and its unrivalled safety profile suggest that it has bright prospects in the treatment of IBD.” (9)  

Gum Resin Extract from Boswellia serrata

The gum resin extract from Boswellia serrataa (Frankincense) has also been shown to be of value in the treatment of IBD and chronic inflammation overall. According to researchers, “Oral therapy with the Boswellia extract or AKBA significantly reduces macroscopic and microcirculatory inflammatory features of inflammation in IBD.”¹⁰ The anti-inflammatory actions of Boswellia extract appear to be primarily due to its ability to inhibit 5-lipoxygenase, a potent activator of inflammation. This is the same anti-inflammatory activity that makes the aminosalicylate (aspirin-related) drugs such as sulfasalazine, olsalazine, mesalamine and azulfidine commonly used to treat IBD so beneficial. Boswellia has been further shown to inhibit other activators of inflammation such as NF-kappa B. (11, 12)

In clinical studies, medicinally effective oral doses of Boswellia reduced mucosal injury by inhibiting activity and adherence of activated leukocytes to intestinal mucosal cells in patients with IBD. (13) In one clinical study of Boswellia and IBD, Boswellia serrata gum resin preparation (350 mg TID for 6 weeks) was given to ulcerative colitis patients. Stool properties, biopsies, and various blood parameters were studied. Patients receiving sulfasalazine (1 g thrice daily) served as controls. “All parameters tested improved after treatment with Boswellia serrata gum resin, the results being similar compared to controls: 82% out of treated patients went into remission; in case of sulfasalazine remission rate was 75%.” (14)

Fish Oils (EPA/DHA)

Fish oils have been studied for nearly 30 years for their health giving benefits, their anti-inflammatory capability in particular. They have been shown to effect the production of the chemical mediators of inflammation called prostaglandins by reducing those that promote inflammation while increasing those that reduce inflammation. Quoting researchers from the scientific journal, Nutrition,

“Fish oils have been used successfully in the management of several inflammatory and autoimmune diseases. The potential for the use of fish oils in the management of these diseases is tremendous…" (15)

Experimental/epidemiological studies show fish/n-3 polyunsaturated fatty acids have anti-carcinogenic effects in the colon as well. (16) This is particularly important for people with IBD as they are at much higher risk than the normal population for developing colon cancer.

In studies with IBD, fish oils have been found to be safe and effective nutritional therapies for maintaining remission. After reviewing the published medical studies using fish oils in the treatment of IBD, the researchers concluded, “Omega 3 fatty acids are safe and may be effective for maintenance of remission in Crohn’s disease when used in enteric coated capsules." (17)

Deglycyrrhizinated licorice (DGL)

Licorice root has had a long history of medicinal use. In clinical studies, it has been shown to reduce inflammation in gastric mucosa and promote healing of ulcers while reducing recurrence. Human studies have found it to be as effective as leading anti-ulcer medications in relieving pain associated with stomach ulcers and preventing the ulcers from recurring. It also promotes the healing of canker sores commonly associated with Crohn’s disease while reducing the associated pain.

Specific Carbohydrate Diet (SCD)

The Specific Carbohydrate diet is my first choice in the treatment of IBD and should include organic, whole foods and free-range, grass-fed animal protein. It reduces exposure to high dietary intakes of sucrose, refined carbohydrates, and microparticles (anti-caking agents, food additives) which may combine with various gut bacteria such as Klebsiellala thereby enhancing their ability to cause cross-reactive immune responses leading to inflammation locally in the gut and systemically.

People with Crohn’s disease and reactive arthritis such as ankylosing spondylitis, have been found to have elevated levels of antibody against the whole bacteria or preparations from Klebsiella along with antibodies to the connective tissues of their joints and cartilage (collagen) due to molecular similarities between their genetic markers for certain proteins and Klebsiella. (18) Therefore, reducing the immune reactivity and cross-reactivity to these bacteria may reduce the body-wide inflammation IBD can cause.

A “low starch diet” like the Specific Carbohydrate Diet has been shown to reduce the levels of specific bacterial cross-reactive antibodies in both healthy controls and patients with IBD and reactive arthritis. Further, it has also been shown to decrease the inflammation and symptoms in those patients.¹⁹ Researchers suggest, “Early treatment of Crohn’s disease patients with anti-Klebsiella measures is proposed, which may involve the use of antibiotics and low starch diet together with other traditionally used immunomodulatory, immuno-suppressive, or biologic agents.” (20)

Corticosteroids (Prednisone or Budesonide)

Corticosteroids, such as prednisone, are prescriptive, suppressive, anti-inflammatory medications used to treat acute exacerbations of IBD. Every clinician I know prefers not to use these drugs for long-term management of IBD if at all possible, due to their eventual side effects such as diabetes, osteoporosis, stomach ulcers and others when used over prolonged periods. However, with that said, prednisone can save lives when given at the right time, with the right patient, in the right tapering doses. Prednisone tapers for acute exacerbation of IBD commonly begin with doses in the range of 40 to 60 mg daily, slowly tapering down over 6 to 12 weeks. Budesonide is an intra-luminal (stays within the intestine) steroid that is commonly effective in treating IBD, particularly microscopic colitis. Its benefit over prednisone is it isn’t absorbed into systemic circulation and, therefore, has less systemic side effects.

DHEA (co-treat prednisone therapy with DHEA)

DHEA is an anabolic steroid produced naturally in our adrenal gland. It has been termed the “youth hormone” because it helps to keep us younger with less risk of developing the common degenerative diseases like diabetes, heart disease, and osteoporosis. Studies have shown serum levels of DHEA are significantly lower in patients with chronic inflammatory diseases and chronic prednisone treatment. Therefore, I commonly recommend patients receiving prednisone therapy also take DHEA as it can reduce the side effects caused by prednisone. (21)

Aminosalicylates

Aminosalicylates are aspirin-like anti-inflammatory drugs often used as the first-line treatment in early disease states of IBD. Sulfasalazine and mesalamine are more commonly used in the treatment and management of ulcerative colitis for inducing and maintaining controlled remission. Mesalamine (Canasa, Rowasa) is commonly used as a retention enema or suppository to treat proctitis (inflammation of the rectal pouch) and distal colitis. Blood tests to check liver and kidney function and blood counts to check white blood cells should be done every 3-6 months in patients being treated with these medications. Also, folic acid must be supplemented when using sulfasalazine as it inhibits the absorption of folic acid.

Generic Names of Aminosalicylates

• balsalazide disodium
• mesalamine
• olsalazine sodium
• sulfasalazine

Immunosuppressive Drugs

Immunosuppressive drugs such as 6-mercaptopurine (6-MP), azathioprine and Remicade are commonly used as second-level therapy in patients who are not well managed on just aminosalicylates and diet/nutritional intervention alone. These immunosuppressive drugs can help maintain a remission and reduce the dose of and reliance on corticosteroids. 6-MP and azathioprine have a longer history of use and are safer than Remicade (Infliximab). Remicade is still somewhat the “new kid on the block” and is used when “all else fails” or when progressive pathology is serious enough to warrant its use. Remicade has MANY side effects including cancer. But, it saves lives and reduces risks of serious complications when the time is right for its use.

This is Part 4 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

IBD Treatment - Removing the Obstacles (part 3 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.

IBD Treatment - Removing the Obstacles to Cure

This is Part 3 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)

Eliminating Disruptive Foods

Identifying and removing food intolerances and dietary promoters of inflammation is one of the first steps to take in the treatment of IBD. This means removing gluten if celiac is suspected and removing allergic foods. The intestinal reactions from these food products can worsen already present symptoms of IBD and further fuel the already existing inflammation making it harder to resolve.

Lactose intolerance is another aggravating factor that doesn’t necessarily promote the inflammatory process but does complicate symptoms by contributing to more gassiness, diarrhea and intestinal discomfort.

Removing pro-inflammatory fats (hydrogenated fats, omega-6 fats and saturated fats) as well as processed and “fast” foods from the diet, especially white flour, anti-caking agents and food preservatives can be helpful as these are known to be causatively associated with IBD.

Following the Specific Carbohydrate Diet has helped many people with IBD, especially those with Crohn’s disease. (www.breakingtheviciouscycle.info) This diet removes many of the aforementioned foods, especially processed flours and refined carbohydrates.

Removing Infectious Agents

There are a number of infectious agents that can promote gastrointestinal inflammation. They should be identified and successfully treated. Some of these agents include Helicobacter pylori(causes stomach inflammation and ulcers), Clostridium difficile (causes infectious/pseudomembranous colitis), intestinal parasites like Giardia, and other microorganisms such as Mycobacterium avium subsp. paratuberculosis (MAP), adherent invasive E. coli, Pseudomonas, Citrobacter, Proteus, and Klebsiella, all of which are known to be disruptive to the intestinal tract and cross-reactive.

Addressing Leaky Gut 

Identifying and removing known promoters of “leaky gut” is especially important in those people with IBD who are experiencing associated inflammatory disorders in other parts of their body. Promoters of leaky gut include alcohol, needless or recurrent antibiotics, bisphosphates used to treat osteoporosis, and other medications that disrupt gastrointestinal integrity such as non-steroidal anti-inflammatories (NSAIDS) like ibuprofen. Dietary promoters of inflammation as mentioned earlier can also promote leakiness of the gut.

 Nutritional Deficiencies

Nutritional deficiencieses should be identified and resolved as they can inhibit gastrointestinal repair and healing. These important nutrients include vitamin D, zinc and other trace minerals, B12 and folic acid, iron, and omega-3 fats. Protein/Calorie malnutrition is most common with Crohn’s disease and can lead to marked weight loss.

Electrolytes such as potassium, sodium and chloride can be easily lost with the diarrhea associated with IBD especially in ulcerative colitis. Some of the medications used to treat IBD, such as sulfasalazine, can cause folic acid deficiency by inhibiting its absorption.

Eliminating Stress 

Many people with IBD experience major flare-ups in their disease when confronted with stress. Therefore, identifying and managing major stress factors are also very important.

This is Part 3 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

Diagnostic Evaluation for IBD (part 2 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.)

Blood work must be done and should include complete blood count, blood chemistry, iron studies, nutrient evaluation, and inflammatory markers. In agreement with the latest scientific research, I highly recommend screening for celiac disease. This includes genetic testing and blood tests for immune reactions as well as intestinal biopsies. It is important to note here according to the latest research, biopsies can be negative in patients with latent celiac disease. Celiac screening is especially important with microscopic colitis. A blood test called IBD serology (pANCA and pASCA) may be done if there are questions over the biopsy results regarding diagnosis of ulcerative colitis versus Crohn’s disease.

Stool samples should be examined to rule out infectious (bacterial or parasitic) causes of symptoms. This may include Complete Stool Diagnostic Analysis (CSDA) which checks for multiple stool factors to determine quality of digestion, absorption, bacterial environment, parasites, blood, inflammation, etc.

Nutritional evaluation should be done, especially with Crohn’s disease. This should include evaluation of electrolytes, zinc, folic acid, iron, B12, vitamin D25, total protein, albumin, and others. I highly recommend being tested for food allergies and intolerances such as celiac disease and lactose intolerance. This nutritional evaluation can include blood tests (IgE RAST and IgG4 RAST) or skin scratch testing to identify allergic foods.

Diagnostic Procedures will definitely include a colonoscopy and biopsy as this is the “Gold Standard” for diagnosing IBD. Sometimes a CT scan will be done to check for strictures, abdominal abscesses, fistulas, or obstruction of the intestines when the symptoms indicate it. Plain X-Rays of the abdomen could be done as a quick, easy, and inexpensive way to show narrowing of the intestines or an intestinal blockage. Contrast X-Rays such as barium swallow (small intestine) and barium enema (large intestine) might be done as well.

This is Part 2 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

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.)

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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