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:
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:
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
No comments:
Post a Comment