International Data

What Say You?

How can we serve you better?

More content please... - 33.7%
A bit more pictures would be better - 19.4%
More up to date content - 12.3%
Nothing! your site is superb! - 34.6%

Crohn's Disease

Introduction

What should I know about Crohn’s Disease?

Crohn’s disease is serious chronic illness that inflicts severe damage to the intestinal tract, causing diarrhea and abdominal pain. Though it can strike anywhere along the GI tract from the mouth to the anus, Crohn’s disease usually affects the endmost portion of the small intestine, called the "ileum."

Crohn’s disease is an inflammatory condition; the delicate mucous membrane lining the intestinal wall becomes inflamed and ulcerated in spots called "skip lesions." The intestinal lining looks somewhat like an old cobblestone street, with lesions spaced between normal tissue. The inflammation can penetrate the bowel wall, leading to the development of abscesses and deep cracks. Even worse, these cracks may lengthen, forming complete openings from the inside of the intestine to the outside called "fistulas." The intestinal wall eventually becomes hardened and inflexible. In later stages of the disease, the intestine may become obstructed.

Crohn’s disease is one of two inflammatory bowel conditions that affect the intestinal lining. The other is ulcerative colitis. The exact cause of these conditions is not known for certain. Both illnesses are thought to have a genetic component. Other contributing factors have been implicated, including food allergies, stress, poor nutrition, and infection. It is also believed that an "autoimmune response," where the immune system attacks the body’s own tissue as though it were a foreign invader, may play a role in Crohn’s disease. Although Crohn’s disease is sometimes mistaken for ulcerative colitis, it has several unique features. Crohn’s disease most commonly affects the small or large intestine, while ulcerative colitis shows up in the lower intestine and the rectum. Ulcerative colitis is more common than Crohn’s disease, but the incidence of Crohn’s appears to be on the rise. (1) Although these conditions hit the gastrointestinal tract hardest, they can lead to many other conditions affecting different parts of the body. (2)

Food allergies and Crohn’s disease appear to be closely related. Inflammation and irritation of the intestinal wall cells can eventually increase sensitivity to many foods. When the cells are damaged, they leave gaps between them through which large proteins can penetrate, a phenomenon known as "leaky gut". These molecules, identified as antigens by the immune system, stimulate an inflammatory reaction in the gut lining. Many people afflicted with the disease have identified and eliminated foods that aggravate symptoms. Such foods include chocolate, dairy products, yeast, cereal grains, fats, and artificial sweeteners. In one multicenter trial, subjects with Crohn’s disease who followed a diet that excluded the foods they were allergic to remained symptom-free almost twice as long as those receiving standard therapy with corticosteroid drugs treatments. (3)

Statistic

Crohn’s and Colitis Foundation of America, 2000.

    It is estimated that there may be up to 1,000,000 Americans with IBD. Males and females appear to be affected equally. Most cases are diagnosed before age 30, but the disease can occur in the sixth, seventh, and later decades.

Signs and Symptoms

The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.

Diarrhea is the most common symptom of Crohn’s disease. About 90 percent of people with Crohn’s disease suffer from chronic diarrhea. (4) A constant discharge from the colon contributes to the diarrhea. The intestinal wall thickens with scar tissue that prevents digested food from passing through as it should, resulting in abdominal cramping after meals. Other symptoms of Crohn’s disease include severe weight loss, anorexia, right lower abdominal pain, low-grade fever, rectal bleeding, and gas. Malabsorption, anemia, and nutritional deficiencies are common.

General

  • Diarrhea
  • Abdominal cramping after meals
  • Severe weight loss
  • Decreased appetite
  • Abdominal pain
  • Low-grade fever
  • Rectal bleeding
  • Gas

Treatment Options

Conventional

Conventional treatment for Crohn’s disease targets three major goals. First, proper nutrition is of paramount importance. The inflamed and thickened intestinal lining cannot absorb nutrients properly, so extra care must be taken to keep the body’s nutrient levels up. Next, the inflammation must be reduced. Third, therapy aims at controlling the autoimmune response mentioned earlier, to keep the body from attacking itself. The following list of medications may be prescribed for inflammatory bowel disease.

    Antidiarrhea treatment consists of loperamide, which slows down peristalsis, the wave-like contraction and relaxation of the intestinal tract that propels digested material along. (Loperamide should not be used by anyone with a liver disorder). Cholestyramine removes bile acids from the intestine and is sometimes effective in controlling diarrhea. Anticholinergic drugs, such as atropine sulfate, are used to decrease GI tract activity and cramping. Side effects include mydriasis (dilated pupils), blurred vision, tachycardia (rapid heartbeat), urinary retention, and dry mouth. Tremors, irritability, hallucinations, nerve blockage in muscles, and difficult breathing are among the possible toxic side-effects. Dicyclomine hydrochloride also controls hyperactivity of the GI tract, without the side effects of anticholinergic drugs. Anti-inflammatory treatment consists of steroidal and nonsteroidal drugs. Sulfasalazine and mesalamine are NSAIDs of the sulfonamide group. Side effects include gastric irritation, headache, dizziness, nausea, fatigue, and loss of appetite. Oligospermia and infertility in men has been associated with sulfasalazine but has not been reported with mesalamine. (5) Steroidal medications may be taken during acute attacks to control inflammation and suppress the autoimmune response. Prednisone, a synthetic glucocorticoid, is often prescribed. Rapid withdrawal can affect the body in the same way as low function of the adrenal glands, and long-term use can lead to muscle wasting and osteoporosis.
  • Mercaptopurine is a powerful drug used to suppress the immune system in severe cases of Crohn’s. (This drug is also used to treat leukemia). Its ability to inhibit immune function makes it useful in the treatment of severe Crohn’s disease. Because of its immune-suppressing activity, people taking the drug have decreased resistance to infection. Mercaptopurine can be highly toxic, leading to bone marrow suppression and anemia. Taking mercaptopurine with the drug allopurinol, which decreases uric acid formation, significantly increases its potential toxicity.

Nutritional Suplementation


Multivitamin

Nutritional supplementation is vitally important in Crohn’s disease. (6) In one study of 270 patients with Crohn’s disease, 85 percent of the patients were found to have nutritional deficiencies. (7) Not only does the condition itself lead to nutrient deficiency, many of the medications used to treat Crohn’s disease deplete nutrients from the body. Consequently, a high potency multivitamin/mineral supplement is recommended. Some of the nutrients that are most commonly deficient and/or nutrients that support the healing process are reviewed below.


Vitamin A

Vitamin A plays a critical role in the growth and repair of the cells lining the gastrointestinal tract. Numerous studies have reported that patients with Crohn’s disease are deficient in vitamin A. (8) , (9) , (10) Some studies have also uncovered a deficiency of carotenes (beta carotene and others) in these people. Interestingly however, not all groups of patients with Crohn’s disease are found vitamin A deficient. There are several possible causes of vitamin A deficiency in Crohn’s disease, including poor diets, increased requirement for nutrients, and malabsorption.

Diminished night vision and other vision problems associated with vitamin A deficiency have been reported in patients with Crohn’s disease. (11) , (12) Supplementation with vitamin A orally reportedly restored visual function in these patients.


Zinc

Zinc deficiency is commonly found in Crohn’s disease. (13) , (14) Some Crohn’s disease sufferers develop skin conditions such as eczema and psoriasis. (15) Providing supplemental zinc has been reported to correct both skin and vision problems in Crohn’s disease patients. (16)


Folic Acid

Low levels of folic acid occur frequently in patients with Crohn’s disease. (17) , (18) In some of these patients, the folic acid deficiency is responsible for the development of pain, numbness, and tingling in the fingers and toes. (19) , (20) Called "peripheral neuropathy," this condition responds well when the patients receive adequate folic acid supplementation. Because many of these patients have malabsorption problems, high doses of folic acid may be required if given orally. Intramuscular and intravenous administrations are very effective.


Vitamin B12

Many patients with Crohn’s disease who have had surgical resections develop a vitamin B12 malabsorption problem, and the majority probably need B12 supplements. (21) , (22) Because these patients have such difficulty absorbing B12, physicians often prefer to administer it in nasal or sublingual (under the tongue) form, or by injection.


Vitamin E

In some studies, patients with Crohn’s disease have been found to have significantly lower levels of vitamin E compared to normal subjects. (23) In an animal study, the creation of a Crohn’s disease-like condition resulted in a substantial reduction of both vitamin E and the antioxidant enzymes superoxide dismutase and glutathione peroxidase. These results indicate that extensive free radical damage may contribute to inflammation in Crohn’s disease. Because they help neutralize free radicals, antioxidants such as vitamin E could play a therapeutic role in the treatment of Crohn’s disease.


Omega-3 Fatty Acids

Some studies report that patients with Crohn’s disease are low in omega-3 fatty acids. (24) Overall, studies on the effectiveness of omega-3 fatty acids for Crohn's disease have shown mixed results, so this remains somewhat controversial. However, omega-3 fatty acids reportedly reduce the formation of chemicals called "leukotrienes." Produced in the body, leukotrienes are potent triggers of inflammation, so omega-3 fatty acids should in theory be helpful as part of the treatment plan for Crohn’s disease. (25)


Lactobacillus, Bifidobacteria

It has been reported that the numbers of bifidobacteria, one of the friendly gut bacteria are significantly reduced in fecal samples from patients with Crohn’s disease. (26) In another study, patients with Crohn’s disease were given oral Lactobacillus supplements, containing human Lactobacillus casei, twice daily for 10 days. The results indicated that Lactobacillus GG boosted the gut’s immune defenses, making it a stronger barrier to infectious organisms. Consequently, it was suggested that Lactobacillus GG could provide added nutritional therapy for Crohn's disease. (27)

In a small study, four of five patients with Crohn's disease went into remission for 22 months after having their bowel "friendly flora" completely replaced with lactobacillus and non disease-causing Escherichia coli. Initially the five patients were treated with broad-spectrum oral and intravenous antibiotics to kill off all bacteria in the bowel. (28) Effective dosages range from 10 to 20 billion CFU or "colony forming units," (one CFU represents a single live bacteria) of a dairy free culture three times daily. It is also helpful to take a product called "FOS" along with friendly bacteria supplements. FOS is composed of non-digestible carbohydrates that provide a food source for the good intestinal bacteria, thus promoting their growth in the gut. FOS does not add to one’s caloric intake, nor does it encourage the growth of bad gut bacteria.


L-Glutamine

The gastrointestinal tract is by far the largest user of L-glutamine in the body. The small intestine absorbs more L-glutamine than any other organ. The cells that line the small intestine (termed enterocytes) use L-glutamine, eventually converting it to ATP, a common energy source in the body. (29)

Herbal Suplementation


Cat's Claw

Cat’s claw reportedly affects the immune system and acts as a free radical scavenger. (30) Cat’s claw has active ingredients called "glycosides," that may be able to reduce inflammation and edema. (31) The anti-inflammatory effects of cat’s claw are considered to be due to the sum total of the plant’s constituents. Cat’s Claw contains natural sterols that have demonstrated anti-inflammatory activity in animal studies. Cat’s Claw also contains a group of substances called "triterpenoid alkaloids" that appear to stimulate the immune system and prevent some viruses from growing and reproducing. (32) , (33)

Experts agree that "pentacyclic alkaloids" (POAs) from cat’s claw root bark are the health promoting constituents. Tetracyclic alkaloids (TOAs) do occur in the root bark, but should be kept to a minimum in the final product as to maximize the health benefits of cat’s claw as a dietary supplement.


Licorice

Licorice has been used as both a flavoring agent and a medicinal herb. It has often been used in fatigue (in the case of adrenal insufficiency), (34) as an expectorant, (35) in GI distress (particularly of benefit in ulcers), (36) , (37) , (38) and in inflammation. (39) , (40) Licorice is claimed to inhibit antibody formation and support the stress response and the inflammatory response. (41) Licorice reportedly inhibits enzymes that produce and activate inflammatory substances in the body. (42) Licorice may also stimulate interferon production in the body, which could support its antiviral activity. (43) , (44) Deglycyrrhizinated (DGL) licorice has demulcent (tissue-soothing/healing) activity, having the ability to protect irritated mucous membranes. (45) In cases where the intestinal lining is inflamed, DGL licorice reportedly stimulates the production of mucus, and is used to reduce symptoms. (46)


Olive Leaf

Olive leaf extract has been reported to be an effective antimicrobial agent against a wide variety of bacteria that cause intestinal and respiratory infections, including Salmonella, E. coli, Staph, and Klebsiella. (47) The olive leaf contains a key active ingredient called "oleuropein," which is believed to be responsible for its properties. (48) , (49) In the laboratory, Oleuropein has been found to stimulate immune cells called "macrophages" that destroy germs and other foreign substances that invade the body. (50)

Olive leaf extract may also be effective against viral infections. A by product of oleuropein called "elanolic acid" appears to account for this. Experiments have shown that calcium elenolate, a synthetic derivative of elenolic acid, is an antiviral agent. (51) , (52) As an antifungal and antiviral herb, olive leaf extract is currently used to help maintain bowel flora in patients with Crohn’s disease. (53)

Diet & Lifestyle

Nutritional support: Generally, a high protein, vitamin, and calorie diet is recommended. Long chain fatty acids found in saturated fats are minimized, as they can aggravate diarrhea and promote inflammatory pathways in the intestine. (54) However, short chain fatty acids, found in omega-3 essential fatty acids have been reported to reverse the inflammatory response. (55) Supplementation with fish oil high in omega-3 fatty acids is recommended. While low-fiber, low-residue diets are traditionally recommended, there is evidence that diets high in refined carbohydrates increase the incidence and severity of acute episodes. (56) Therapeutic regimens that include increased fiber and decreased refined carbohydrates have demonstrated a positive influence on the disease. In one study, 16 of 20 subjects on a sugar-free, fiber-rich diet remained in remission for an average of nineteen months after discontinuing drug therapy. (57) It is interesting to note that diets high in sugar and consumption of fast food are positively correlated with an increased risk of Crohn’s disease, while diets high in fiber are associated with a reduced risk. (58) Saturated fat and cholesterol have also been identified as dietary risk factors. (59)

References

  1. Marz RB. Medical Nutrition from Marz. Portland, OR: Omni-Press; 1997:375.
  2. Kirsner JB. Recent developments in ‘non-specific’ inflammatory bowel disease. N Engl J Med. 1982;306:775.
  3. View Abstract: Riordan AM, et al. Treatment of active Chrohn’s disease by exclusion diet: East Anglican multicentre controlled trial. Lancet. Nov1993;340(8880):1131-4.
  4. Smeltzer SC, Bare BG. Medical-Surgical Nursing. Philadelphia: JB Lippincott Co; 1992.
  5. PDR, 53rd ed. Montvale, NJ: Medical Economics Company; 1999:2630;3216.
  6. View Abstract: Harries AD, Heatly RV. Nutritional disturbances in Crohn's disease. Postgrad Med J. Nov1983;59(697):690-7.
  7. View Abstract: Rath HC, et al. Nutritional deficiencies and complications in chronic inflammatory bowel diseases. Med Klin. Jan1998; 93(1):6-10.
  8. View Abstract: Rumi G, Jr, et al. Decrease of serum carotenoids in Crohn's disease. J Physiol Paris. Mar2000;94(2):159-61.
  9. View Abstract: Schoelmeirch J, et al. Zinc and vitamin A deficiency in patients with Crohn's disease is correlated with activity but not with localization or extent of the disease. Hepatogastroenterology. Feb1985;32(1):34-8.
  10. View Abstract: Main AN, et al. Vitamin A deficiency in Crohn's disease. Gut. Dec1983;24(12):1169-75.
  11. View Abstract: Gans M, Taylor C. Reversal of progressive nyctalopia in a patient with Crohn's disease. Can J Ophthalmol. Apr1990;25(3):156-8.
  12. View Abstract: Kemp CM, et al. Visual function and rhodopsin levels in humans with vitamin A deficiency. Exp Eye Res. Feb1988;46(2):185-97.
  13. View Abstract: Mocchegiani E, et al. Levels of zinc and thymulin in plasma from patients with Crohn's disease. J Clin Lab Immunol. Jun1990;32(2):79-84.
  14. Sercki P, et al. Cutaneous manifestations of zinc deficiency in Crohn disease. Ann Dermatol Venereol. 1990;117(11):833-4.
  15. View Abstract: Krasovec M, Frenk E. Acrodermatitis enteropathica secondary to Crohn's disease. Dermatology. 1996;193(4):361-3.
  16. View Abstract: Myung SJ, et al. Zinc deficiency manifested by dermatitis and visual dysfunction in a patient with Crohn's disease. J Gastroenterol. Dec1998;33(6):876-9.
  17. View Abstract: Steger GG, et al. Folate absorption in Crohn's disease. Digestion. 1994;55(4):234-8.
  18. View Abstract: Kuroki F, et al. Multiple vitamin status in Crohn's disease. Correlation with disease activity. Dig Dis Sci. Sep1993;38(9):1614-8.
  19. View Abstract: Lossos A, et al. Peripheral neuropathy and folate deficiency as the first sign of Crohn's disease. J Clin Gastroenterol. Aug1991;13(4):442-4.
  20. View Abstract: Contamin F, et al. Involvement of the peripheral and pyramidal nervous system in Crohn disease. Determining role of folic acid deficiency. Sem Hop. May1983;59(18):1381-5.
  21. View Abstract: Behrend C, et al. Vitamin B12 absorption after ileorectal anastomosis for Crohn's disease: effect of ileal resection and time span after surgery. Eur J Gastroenterol Hepatol. May1995;7(5):397-400.
  22. View Abstract: Geerling BJ, Budart-Smook A, Stockbrugger Rw, Brummer RJ. Comprehensive nutritional status in patients with long-standing Crohn disease currently in remission. Am J Clin Nutr. May1998;67(5):919-26.
  23. View Abstract: Geerling BJ, et al. Comprehensive nutritional status in patients with long-standing Crohn disease currently in remission. Am J Clin Nutr. May1998;67(5):919-26.
  24. View Abstract: Kuroki F, et al. Serum n3 polyunsaturated fatty acids are depleted in Crohn's disease. Dig Dis Sci. Jun1997;42(6):1137-41.
  25. View Abstract: Endres S, et al. Lipid treatment of inflammatory bowel disease. Curr Opin Clin Nutr Metab Care. Mar1999;2(2):117-20.
  26. View Abstract: Favier C, et al. Fecal beta-D-galactosidase production and Bifidobacteria are decreased in Crohn's disease. Dig Dis Sci. Apr1997;42(4):817-22.
  27. View Abstract: Malin M, et al. Promotion of IgA immune response in patients with Crohn's disease by oral bacteriotherapy with Lactobacillus GG. Ann Nutr Metab. 1996;40(3):137-45.
  28. Substituting Bowel Flora Eases Crohn's. Medical Tribune. Jun1992;19.
  29. View Abstract: Mithieux G. New data and concepts on glutamine and glucose metabolism in the gut. Curr Opin Clin Nutr Metab Care. Jul2001;4(4):267-71.
  30. Aquino R, et al. Plant Metabolites. Structure and in Vitro Antiviral Activity of Quinovic Acid Glycosides from Uncaria tomentosa and Guettarda platypoda. J Nat Prod. 1989;52(4): 679-85.
  31. Aquino R, et al. Plant Metabolites. New Compounds and Anti-inflammatory Activity of Uncaria tomentosa. J Nat Prod. 1991;54(2):453-59.
  32. Jones K. Cat’s Claw: Healing Vine of Peru. Seattle: Sylvan Press; 1995:48-49.
  33. View Abstract: Aquino R, et al. New Polyhydroxylated Triterpenes from Uncaria tomentosa. J Nat Prod. 1990;53(3):559-64.
  34. Gibson MR. Glycyrrhiza in Old and New Perspectives. Lloydia. 1978;41(4):348-54.
  35. Bradley PR, ed. British Herbal Compendium. Dorset, Engl: Bournemouth; 1992:145-48.
  36. Wilson JA. A Comparison of Carbenoxolone Sodium and Deglycyrrhizinated Liquorice in the Treatment of Gastric Ulcer in the Ambulant Patient. British Journal of Clinical Practice. 1972;26:563-66.
  37. Van Marle J, et al. Deglycyrrhizinated Liquorice (DGL) and the Renewal of Rat Stomach Epithelium. European Journal of Pharmacology. 1981;72:219-25.
  38. Morgan AG, et al. Comparison Between Cimetidine and Caved-S in the Treatment of Gastric Ulceration, and Subsequent Maintenance Therapy. Gut. 1982;23:545-51.
  39. Tangri KK, et al. Biochemical Study of Anti-inflammatory and Anti-arthritic Properties of Glycyrrhetic Acid. Biochemical Pharmacology. 1965;14:1277-81.
  40. Akamatsu H, et al. Mechanism of Anti-inflammatory Action of Glycyrrhizin: Effect on Neutrophil Functions Including Reactive Oxygen Species Generation. Planta Medica. 1991;57:119-21.
  41. Akamatsu H, et al. Mechanism of Anti-inflammatory Action of Glycyrrhizin: Effect on Neutrophil Functions Including Reactive Oxygen Species Generation. Planta Medica. 1991;57:119-21.
  42. Kimura Y, et al. Effects of Chalcones Isolated from Licorice Roots on Leukotriene Biosynthesis in Human Polymorphonuclear Neutrophils. Phytotherapy Res. 1988;2: 140-45.
  43. Shinada M, et al. Enhancement of Interferon-gamma Production in Glycyrrhizin-Treated Human Peripheral Lymphocytes in Response to Concanavalin A and to Surface Antigen of Hepatitis B Virus. Proc Soc Exp Biol Med. 1986;181(2):205-10.
  44. Abe N, et al. Interferon Induction by Glycyrrhizin and Glycyrrhetinic Acid in Mice. Microbiol Immunol. 1982;26:535-39.
  45. Van Marle J, et al. Deglycyrrhizinated Liquorice (DGL) and the Renewal of Rat Stomach Epithelium. European Journal of Pharmacology. 1981;72:219-25.
  46. Wilson JA. A Comparison of Carbenoxolone Sodium and Deglycyrrhizinated Liquorice in the Treatment of Gastric Ulcer in the Ambulant Patient. British Journal of Clinical Practice. 1972;26:563-66.
  47. Bisignano G, et al. On the in-vitro antimicrobial activity of oleuropein and hydroxytyrosol. J Pharm Pharmacol. Aug1999;51(8):971-4.
  48. Bisignano G, et al. On the in-vitro antimicrobial activity of oleuropein and hydroxytyrosol. J Pharm Pharmacol. Aug1999;51(8):971-4.
  49. View Abstract: Visioli F. Antiatherogenic components of olive oil. Curr Atheroscler Rep. Jan2001;3(1):64-7.
  50. Visoli F, et al. Oleuropein protects low density lipoprotein from oxidation. Life Sciences. 1994;55:1965-71.
  51. Renis HE. In vitro antiviral activity of calcium elenolate. Antimicrob Agents Chemother. 1970:167-72.
  52. Heinze JE, et al. Specificity of the antiviral agent calcium elenolate. Antimicrob Agents Chemother. Oct1975;8(4):421-5.
  53. View Abstract: Aziz NH. Comparative antibacterial and antifungal effects of some phenolic compounds. Microbios. 1998;93(374):43-54.
  54. View Abstract: Miura S, et al. Modulation of intestinal immune system by dietary fat intake: relevance to Chrohn’s disease. J Gastroenerol Hepatol. Dec1998;13(12):1183-90.
  55. View Abstract: Miura S, et al. Modulation of intestinal immune system by dietary fat intake: relevance to Chrohn’s disease. J Gastroenerol Hepatol. Dec1998;13(12):1183-90.
  56. View Abstract: Brandes JW, Lorenz-Meyer H. Sugar-free diet: A new perspective in the treatment of Chrohn’s disease? Randomized, control study. J Gastroenerol. 1981;19(1):1-12.
  57. View Abstract: Brandes JW, et al. Sugar-free diet as long-term or interval treatment in the remission phase of Chrohn’s disease-a prospective study. Leber Magen Darm. Nov1982;12(6):225-8.
  58. View Abstract: Persson PG, et al. Diet and inflammatory bowel disease: a case control study. Epidemiology. Jan1992;3(1):47-52.
  59. View Abstract: Reif S, et al. Pre-illness dietary factors in inflammatory bowel disease. Gut. Jun1997;40(6):754-60.